Phenotype	Phenotype Details	Title	Abstract	Journal	Year		Author(s)	PMID	Age	Sex	N Range	Units	C57BL/6J	C3H/HeJ	BXH2	BXH3	BXH4	BXH6	BXH7	BXH8	BXH9	BXH10	BXH11	BXH12	BXH14	BXH19

brain weight		"Eye1 and Eye2: gene loci that modulate eye size, lens weight, and retinal area in the mouse."		Invest Ophthalmol Vis Sci	1999		"Zhou G, Williams RW"	10102277	100 days	both		mg			433	441.9	474.6	428.5	459.1	444.9	447.5	441.8	420.1	434.3	424.3	429
body weight		"Eye1 and Eye2: gene loci that modulate eye size, lens weight, and retinal area in the mouse."		Invest Ophthalmol Vis Sci	1999		"Zhou G, Williams RW"	10102277	100 days	both		g			23.2	22.4	25.7	17.4	21.8	23.5	22.3	20.1	21.5	21	19.5	20.6
cerebellum weight				<www.nervenet.org>	2000		"Airey DC, Williams RW"		100 days	both		mg			53.3	60.2	58.6	60.6	58.5	56.9	67.5	56.3	56	57.7	55.3	53.9
eye weight		"Eye1 and Eye2: gene loci that modulate eye size, lens weight, and retinal area in the mouse."		Invest Ophthalmol Vis Sci	1999		"Zhou G, Williams RW"	10102277	100 days	both					17.1	16.3	17.9	16.7	16.7	16.7	15.2	15.4	18.7	19.2	16.3	16.2
hippocampus weight				<www.nervenet.org>	2000		Lu L et al		100 days	both					25.8	25.8	29.8	28.5	27.7	26.6	28.6	29.5	27.5	29.4	24.2	27.4
olfactory bulb weight				<www.nervenet.org>	2000		Williams RW et al		100 days	both					17.2	19.5	18	20.4	17.8	17.2	19.8	17.8	21.4	19.3	19	17.3
forebrain plus mid weight	mean value calculated 7/5/00			<www.nervenet.org>	2000		Williams RW et al		100 days	both					299.3	305.3	331.6	300.8	327	322.6	307.5	314.8	313.7	302.3	289.8	297.4
medulla weight	mean value calculated 7/5/00			<www.nervenet.org>	2000		Williams RW et al		100 days	both					4.3	U	U	U	4.6	3.7	U	3	U	4.7	U	U
hindbrain weight	mean value calculated 7/6/00	"Eye1 and Eye2: gene loci that modulate eye size, lens weight, and retinal area in the mouse."		<www.nervenet.org>	2000		Williams RW et al		100 days	both					42.9	41.5	42.1	42.6	41.3	40.2	47.6	40.8	43.2	41.5	41.3	39.4
lens weight	mean value calculated 7/6/00	"Eye1 and Eye2: gene loci that modulate eye size, lens weight, and retinal area in the mouse."		Invest Ophthalmol Vis Sci	1999		"Zhou G, Williams RW"	10102277	100 days	both					6	5.8	6.1	6	5.6	5.6	5.7	5.2	6.3	5.8	5.7	5.1
retinal area	mean value calculated 7/6/00	"Eye1 and Eye2: gene loci that modulate eye size, lens weight, and retinal area in the mouse."		Invest Ophthalmol Vis Sci	1999		"Zhou G, Williams RW"	10102277	100 days	both		mm^2			17.5	16.8	18	18	17.2	17.3	16.4	15.1	18.8	19.7	17.1	16.3
%CAFC day 7 in S-phase 	strain distribution pattern	Genetic analysis of hemopoietic cell cycling in mice suggests its involvement in organismal life span.	"Normal somatic cells undergo replicative senescence in vitro but the significance of this process in organismic aging remains controversial. We have shown previously that hemopoietic stem cells of common inbred strains of mice vary widely in cycling activity and that this parameter is inversely correlated with strain-dependent mean life span. To assess whether cell cycling and life span are causally related, we searched for quantitative trait loci (QTLs) that contributed to variation of these traits in BXH and BXD recombinant inbred mice. Two QTLs, mapping to exactly the same intervals on chromosomes 7 and 11, were identified that were associated with variation of both cell cycling and life span. The locus on chromosome 11 mapped to the cytokine cluster, a segment that shows synteny with human chromosome 5q, in which deletions are strongly associated with myelodysplastic syndrome. These data indicate that steady-state cell turn-over, here measured in hemopoietic progenitor cells, may have a significant effect on the mean life span of mammals."	FASEB	1999	Apr	"De Haan G, Van Zant G."	10094931	42 - 56 days	female		%	8	31	26.6	0.6	26.1	29.9	0.6	0.7	12	13.1	50.9	9	27	0.6
Baseline ventilatory characteristics of BXH recombinanat inbred strains	Wt	Genetic control of differential baseline breathing pattern.	"The purpose of the present study was to determine the genetic control of baseline breathing pattern by examining the mode of inheritance between two inbred murine strains with differential breathing characteristics. Specifically, the rapid, shallow phenotype of the C57BL/6J (B6) strain is consistently distinct from the slow, deep phenotype of the C3H/HeJ (C3) strain. The response distributions of segregant and nonsegregant progeny were compared with the two progenitor strains to determine the mode of inheritance for each ventilatory characteristic. The BXH recombinant inbred (RI) strains derived from the B6 and C3 progenitors were examined to establish strain distribution patterns for each ventilatory trait. To establish the mode of inheritance, baseline breathing frequency (f), tidal volume, and inspiratory time (TI) were measured five times in each of 178 mature male animals from the two progenitor strains and their progeny by using whole body plethysmography. With respect to f and TI, the two progenitor strains were consistently distinct, and segregation analyses of the inheritance pattern suggest that the most parsimonious genetic model for response distributions of f and TI is a two-loci model. In similar experiments conducted on 82 mature male animals from 12 BXH RI strains, each parental phenotype was represented by one or more of the RI strains. Intermediate phenotypes emerged to confirm the likelihood that parental strain differences in f and TI were determined by more than one locus. Taken together, these studies suggest that the phenotypic difference in baseline respiratory timing between male B6 and C3 mice is best explained by a genetic model that considers at least two loci as major determinants."	J Appl Physiol	1997	Mar	"Tankersley CG, Fitzgerald RS, Levitt RC, Mitzner WA, Ewart SL, Kleeberger SR."	9074977	68 - 96 days	male	10-Apr	g			20.4	26.2	28.7	21.2	28	25.6	25.5	21.3	22.8	20.9	22.9	25.8
Baseline ventilatory characteristics of BXH recombinanat inbred strains	f	Genetic control of differential baseline breathing pattern.	"The purpose of the present study was to determine the genetic control of baseline breathing pattern by examining the mode of inheritance between two inbred murine strains with differential breathing characteristics. Specifically, the rapid, shallow phenotype of the C57BL/6J (B6) strain is consistently distinct from the slow, deep phenotype of the C3H/HeJ (C3) strain. The response distributions of segregant and nonsegregant progeny were compared with the two progenitor strains to determine the mode of inheritance for each ventilatory characteristic. The BXH recombinant inbred (RI) strains derived from the B6 and C3 progenitors were examined to establish strain distribution patterns for each ventilatory trait. To establish the mode of inheritance, baseline breathing frequency (f), tidal volume, and inspiratory time (TI) were measured five times in each of 178 mature male animals from the two progenitor strains and their progeny by using whole body plethysmography. With respect to f and TI, the two progenitor strains were consistently distinct, and segregation analyses of the inheritance pattern suggest that the most parsimonious genetic model for response distributions of f and TI is a two-loci model. In similar experiments conducted on 82 mature male animals from 12 BXH RI strains, each parental phenotype was represented by one or more of the RI strains. Intermediate phenotypes emerged to confirm the likelihood that parental strain differences in f and TI were determined by more than one locus. Taken together, these studies suggest that the phenotypic difference in baseline respiratory timing between male B6 and C3 mice is best explained by a genetic model that considers at least two loci as major determinants."	J Appl Physiol	1997	Mar	"Tankersley CG, Fitzgerald RS, Levitt RC, Mitzner WA, Ewart SL, Kleeberger SR."	9074977	68 - 96 days	male	10-Apr	Hz	2.8	1.8	2..36 	2.62	2.63	2.24	2.59	1.67	2.44	2.71	2.6	3.01	3.42	2.09
Baseline ventilatory characteristics of BXH recombinanat inbred strains	inspiratory time	Genetic control of differential baseline breathing pattern.	"The purpose of the present study was to determine the genetic control of baseline breathing pattern by examining the mode of inheritance between two inbred murine strains with differential breathing characteristics. Specifically, the rapid, shallow phenotype of the C57BL/6J (B6) strain is consistently distinct from the slow, deep phenotype of the C3H/HeJ (C3) strain. The response distributions of segregant and nonsegregant progeny were compared with the two progenitor strains to determine the mode of inheritance for each ventilatory characteristic. The BXH recombinant inbred (RI) strains derived from the B6 and C3 progenitors were examined to establish strain distribution patterns for each ventilatory trait. To establish the mode of inheritance, baseline breathing frequency (f), tidal volume, and inspiratory time (TI) were measured five times in each of 178 mature male animals from the two progenitor strains and their progeny by using whole body plethysmography. With respect to f and TI, the two progenitor strains were consistently distinct, and segregation analyses of the inheritance pattern suggest that the most parsimonious genetic model for response distributions of f and TI is a two-loci model. In similar experiments conducted on 82 mature male animals from 12 BXH RI strains, each parental phenotype was represented by one or more of the RI strains. Intermediate phenotypes emerged to confirm the likelihood that parental strain differences in f and TI were determined by more than one locus. Taken together, these studies suggest that the phenotypic difference in baseline respiratory timing between male B6 and C3 mice is best explained by a genetic model that considers at least two loci as major determinants."	J Appl Physiol	1997	Mar	"Tankersley CG, Fitzgerald RS, Levitt RC, Mitzner WA, Ewart SL, Kleeberger SR."	9074977	68 - 96 days	male	10-Apr	s	0.112	0.188	0.158	0.138	0.126	0.166	0.134	0.19	0.134	0.126	0.143	0.125	0.118	0.154
Baseline ventilatory characteristics of BXH recombinanat inbred strains	VT	Genetic control of differential baseline breathing pattern.	"The purpose of the present study was to determine the genetic control of baseline breathing pattern by examining the mode of inheritance between two inbred murine strains with differential breathing characteristics. Specifically, the rapid, shallow phenotype of the C57BL/6J (B6) strain is consistently distinct from the slow, deep phenotype of the C3H/HeJ (C3) strain. The response distributions of segregant and nonsegregant progeny were compared with the two progenitor strains to determine the mode of inheritance for each ventilatory characteristic. The BXH recombinant inbred (RI) strains derived from the B6 and C3 progenitors were examined to establish strain distribution patterns for each ventilatory trait. To establish the mode of inheritance, baseline breathing frequency (f), tidal volume, and inspiratory time (TI) were measured five times in each of 178 mature male animals from the two progenitor strains and their progeny by using whole body plethysmography. With respect to f and TI, the two progenitor strains were consistently distinct, and segregation analyses of the inheritance pattern suggest that the most parsimonious genetic model for response distributions of f and TI is a two-loci model. In similar experiments conducted on 82 mature male animals from 12 BXH RI strains, each parental phenotype was represented by one or more of the RI strains. Intermediate phenotypes emerged to confirm the likelihood that parental strain differences in f and TI were determined by more than one locus. Taken together, these studies suggest that the phenotypic difference in baseline respiratory timing between male B6 and C3 mice is best explained by a genetic model that considers at least two loci as major determinants."	J Appl Physiol	1997	Mar	"Tankersley CG, Fitzgerald RS, Levitt RC, Mitzner WA, Ewart SL, Kleeberger SR."	9074977	68 - 96 days	male	10-Apr	ml/ g			9.5	6.8	7.5	8.3	7.7	9.7	9	8.6	2.6	3.01	3.42	2.09
Baseline ventilatory characteristics of BXH recombinanat inbred strains	VE	Genetic control of differential baseline breathing pattern.	"The purpose of the present study was to determine the genetic control of baseline breathing pattern by examining the mode of inheritance between two inbred murine strains with differential breathing characteristics. Specifically, the rapid, shallow phenotype of the C57BL/6J (B6) strain is consistently distinct from the slow, deep phenotype of the C3H/HeJ (C3) strain. The response distributions of segregant and nonsegregant progeny were compared with the two progenitor strains to determine the mode of inheritance for each ventilatory characteristic. The BXH recombinant inbred (RI) strains derived from the B6 and C3 progenitors were examined to establish strain distribution patterns for each ventilatory trait. To establish the mode of inheritance, baseline breathing frequency (f), tidal volume, and inspiratory time (TI) were measured five times in each of 178 mature male animals from the two progenitor strains and their progeny by using whole body plethysmography. With respect to f and TI, the two progenitor strains were consistently distinct, and segregation analyses of the inheritance pattern suggest that the most parsimonious genetic model for response distributions of f and TI is a two-loci model. In similar experiments conducted on 82 mature male animals from 12 BXH RI strains, each parental phenotype was represented by one or more of the RI strains. Intermediate phenotypes emerged to confirm the likelihood that parental strain differences in f and TI were determined by more than one locus. Taken together, these studies suggest that the phenotypic difference in baseline respiratory timing between male B6 and C3 mice is best explained by a genetic model that considers at least two loci as major determinants."	J Appl Physiol	1997	Mar	"Tankersley CG, Fitzgerald RS, Levitt RC, Mitzner WA, Ewart SL, Kleeberger SR."	9074977	68 - 96 days	male	10-Apr	ml . min-1 . g-1   			1.35	1.05	1.17	1.1	1.19	0.96	1.32	1.36	1.06	1.14	1.28	1.02
Baseline ventilatory characteristics of BXH recombinanat inbred strains	TI	Genetic control of differential baseline breathing pattern.	"The purpose of the present study was to determine the genetic control of baseline breathing pattern by examining the mode of inheritance between two inbred murine strains with differential breathing characteristics. Specifically, the rapid, shallow phenotype of the C57BL/6J (B6) strain is consistently distinct from the slow, deep phenotype of the C3H/HeJ (C3) strain. The response distributions of segregant and nonsegregant progeny were compared with the two progenitor strains to determine the mode of inheritance for each ventilatory characteristic. The BXH recombinant inbred (RI) strains derived from the B6 and C3 progenitors were examined to establish strain distribution patterns for each ventilatory trait. To establish the mode of inheritance, baseline breathing frequency (f), tidal volume, and inspiratory time (TI) were measured five times in each of 178 mature male animals from the two progenitor strains and their progeny by using whole body plethysmography. With respect to f and TI, the two progenitor strains were consistently distinct, and segregation analyses of the inheritance pattern suggest that the most parsimonious genetic model for response distributions of f and TI is a two-loci model. In similar experiments conducted on 82 mature male animals from 12 BXH RI strains, each parental phenotype was represented by one or more of the RI strains. Intermediate phenotypes emerged to confirm the likelihood that parental strain differences in f and TI were determined by more than one locus. Taken together, these studies suggest that the phenotypic difference in baseline respiratory timing between male B6 and C3 mice is best explained by a genetic model that considers at least two loci as major determinants."	J Appl Physiol	1997	Mar	"Tankersley CG, Fitzgerald RS, Levitt RC, Mitzner WA, Ewart SL, Kleeberger SR."	9074977	68 - 96 days	male	10-Apr	ms			157	138	127	165	133	190	134	125	141	124	118	155
Baseline ventilatory characteristics of BXH recombinanat inbred strains	TE	Genetic control of differential baseline breathing pattern.	"The purpose of the present study was to determine the genetic control of baseline breathing pattern by examining the mode of inheritance between two inbred murine strains with differential breathing characteristics. Specifically, the rapid, shallow phenotype of the C57BL/6J (B6) strain is consistently distinct from the slow, deep phenotype of the C3H/HeJ (C3) strain. The response distributions of segregant and nonsegregant progeny were compared with the two progenitor strains to determine the mode of inheritance for each ventilatory characteristic. The BXH recombinant inbred (RI) strains derived from the B6 and C3 progenitors were examined to establish strain distribution patterns for each ventilatory trait. To establish the mode of inheritance, baseline breathing frequency (f), tidal volume, and inspiratory time (TI) were measured five times in each of 178 mature male animals from the two progenitor strains and their progeny by using whole body plethysmography. With respect to f and TI, the two progenitor strains were consistently distinct, and segregation analyses of the inheritance pattern suggest that the most parsimonious genetic model for response distributions of f and TI is a two-loci model. In similar experiments conducted on 82 mature male animals from 12 BXH RI strains, each parental phenotype was represented by one or more of the RI strains. Intermediate phenotypes emerged to confirm the likelihood that parental strain differences in f and TI were determined by more than one locus. Taken together, these studies suggest that the phenotypic difference in baseline respiratory timing between male B6 and C3 mice is best explained by a genetic model that considers at least two loci as major determinants."	J Appl Physiol	1997	Mar	"Tankersley CG, Fitzgerald RS, Levitt RC, Mitzner WA, Ewart SL, Kleeberger SR."	9074977	68 - 96 days	male	10-Apr	ms			269	246	256	296	256	413	277	253	249	211	177	335
Baseline ventilatory characteristics of BXH recombinanat inbred strains	TI/TT	Genetic control of differential baseline breathing pattern.	"The purpose of the present study was to determine the genetic control of baseline breathing pattern by examining the mode of inheritance between two inbred murine strains with differential breathing characteristics. Specifically, the rapid, shallow phenotype of the C57BL/6J (B6) strain is consistently distinct from the slow, deep phenotype of the C3H/HeJ (C3) strain. The response distributions of segregant and nonsegregant progeny were compared with the two progenitor strains to determine the mode of inheritance for each ventilatory characteristic. The BXH recombinant inbred (RI) strains derived from the B6 and C3 progenitors were examined to establish strain distribution patterns for each ventilatory trait. To establish the mode of inheritance, baseline breathing frequency (f), tidal volume, and inspiratory time (TI) were measured five times in each of 178 mature male animals from the two progenitor strains and their progeny by using whole body plethysmography. With respect to f and TI, the two progenitor strains were consistently distinct, and segregation analyses of the inheritance pattern suggest that the most parsimonious genetic model for response distributions of f and TI is a two-loci model. In similar experiments conducted on 82 mature male animals from 12 BXH RI strains, each parental phenotype was represented by one or more of the RI strains. Intermediate phenotypes emerged to confirm the likelihood that parental strain differences in f and TI were determined by more than one locus. Taken together, these studies suggest that the phenotypic difference in baseline respiratory timing between male B6 and C3 mice is best explained by a genetic model that considers at least two loci as major determinants."	J Appl Physiol	1997	Mar	"Tankersley CG, Fitzgerald RS, Levitt RC, Mitzner WA, Ewart SL, Kleeberger SR."	9074977	68 - 96 days	male	10-Apr	%			36.3	35.9	33.4	35.7	34.5	31.6	31.9	33.4	36.1	37.4	40	31.8
Correlation between HO - 1 mRNA induction with MM-LDL in ECs and aortic atherosclerotic lesions 	Aortic Lesions	Determinants of atherosclerosis susceptibility in the C3H and C57BL/6 mouse model: evidence for involvement of endothelial cells but not blood cells or cholesterol metabolism.	"Lipids, monocytes, and arterial wall cells are primary components involved in atherogenesis. Using the inbred mouse strains C57BL/6J (B6) and C3H/HeJ (C3H), which have been extensively studied as models of the genetic control of diet-induced atherosclerosis, we examined which of these components determine genetic susceptibility. To test whether dietary responsiveness is involved, a congenic strain of C3H carrying an apoE-null allele (apoE(-/-)) was constructed. Although C3H.apoE(-/-) mice had higher plasma cholesterol levels, they developed much smaller lesions than their B6.apoE(-/-) counterpart on either chow or Western diets. Reciprocal bone marrow transplantation between the strains, with congenics carrying the same H-2 haplotype, was performed to examine the role of monocytes. The atherosclerosis susceptibility was not altered in the recipient mice, indicating that variations in monocyte function were not involved. Endothelial cells isolated from the aorta of B6 mice exhibited a dramatic induction of monocyte chemotactic protein-1, macrophage colony-stimulating factor, vascular cell adhesion molecule-1, and heme oxygenase-1 in response to minimally modified LDL, whereas endothelial cells from C3H mice showed little or no induction. In a set of recombinant inbred strains derived from the B6 and C3H parental strains, endothelial responses to minimally modified LDL cosegregated with aortic lesion size. These data provide strong evidence that endothelial cells, but not monocytes or plasma lipid levels, account for the difference in susceptibility to atherosclerosis between the 2 mouse strains."	Circulation Research	2000	May	"Shi W, Wang NJ, Shih DM, Sun VZ, Wang X, Lusis AJ"	10827138	105 days	both	5-Feb	mm2	25000	840	42000	---	680	---	---	---	430	2500	8500	--	--	25000
Correlation between HO - 1 mRNA induction with MM-LDL in ECs and aortic atherosclerotic lesions 	HO - 1induction (Fe - LDL: R= 0.57; P= 0.0001)	Determinants of atherosclerosis susceptibility in the C3H and C57BL/6 mouse model: evidence for involvement of endothelial cells but not blood cells or cholesterol metabolism.	"Lipids, monocytes, and arterial wall cells are primary components involved in atherogenesis. Using the inbred mouse strains C57BL/6J (B6) and C3H/HeJ (C3H), which have been extensively studied as models of the genetic control of diet-induced atherosclerosis, we examined which of these components determine genetic susceptibility. To test whether dietary responsiveness is involved, a congenic strain of C3H carrying an apoE-null allele (apoE(-/-)) was constructed. Although C3H.apoE(-/-) mice had higher plasma cholesterol levels, they developed much smaller lesions than their B6.apoE(-/-) counterpart on either chow or Western diets. Reciprocal bone marrow transplantation between the strains, with congenics carrying the same H-2 haplotype, was performed to examine the role of monocytes. The atherosclerosis susceptibility was not altered in the recipient mice, indicating that variations in monocyte function were not involved. Endothelial cells isolated from the aorta of B6 mice exhibited a dramatic induction of monocyte chemotactic protein-1, macrophage colony-stimulating factor, vascular cell adhesion molecule-1, and heme oxygenase-1 in response to minimally modified LDL, whereas endothelial cells from C3H mice showed little or no induction. In a set of recombinant inbred strains derived from the B6 and C3H parental strains, endothelial responses to minimally modified LDL cosegregated with aortic lesion size. These data provide strong evidence that endothelial cells, but not monocytes or plasma lipid levels, account for the difference in susceptibility to atherosclerosis between the 2 mouse strains."	Circulation Research	2000	May	"Shi W, Wang NJ, Shih DM, Sun VZ, Wang X, Lusis AJ"	10827138	105 days	both	5-Feb	fold (with multiple values)	"10.6, 9.6, 7.5, 7.2, 2.5"	"3.4, 2.5, 2.0"	---	---	"2.8, 1.3, 1.0"	---	---	"7.3, 7.0"	"2.5, 1.3"	"6.7, 4.9, 4.4"	"7.9, 3.7, 3.1"	---	---	"9.1, 4.8, 4.0"
Total BAL recovered from BXH RI mice	72 hr exposure to 0.3 ppm O3	Genetic susceptibility to ozone-induced lung hyperpermeability: role of toll-like receptor 4.	"The pollutant ozone (O(3)) induces lung hyperpermeability and inflammation in humans and animal models. Among inbred strains of mice, there is a 3-fold difference in total protein (a marker of permeability) recovered in bronchoalveolar lavage (BAL) fluid after a 72-h exposure to 0.3 ppm O(3). To determine the chromosomal locations of susceptibility genes, we performed a genome screen using recombinant inbred (RI) strains of mice derived from O(3)-susceptible C57BL/6J (B6) and O(3)-resistant C3H/HeJ (HeJ) progenitors. Each RI strain was phenotyped for O(3)-induced hyperpermeability, and linkage was assessed for 558 markers using Map Manager QTb27. A significant quantitative trait locus (QTL) was identified on chromosome 4. The likelihood ratio chi(2) statistic (16.6) for the peak of the QTL was greater than the significance threshold (16.3) determined empirically by permutation test. This QTL contains a candidate gene, Toll-like receptor 4 (Tlr4 ), that recently has been implicated in innate immunity and endotoxin susceptibility. The amount of the total trait variance explained by the QTL at Tlr4, the gene with the highest likelihood ratio statistic in the QTL, was approximately 70%. To test the role of Tlr4 in O(3)-induced hyperpermeability, BAL protein responses to O(3) were compared in C3H/HeOuJ (OuJ) and HeJ mice that differ only at a polymorphism in the coding region of Tlr4. Significantly greater protein concentrations (430 +/- 35 &mgr;g/ml) were found in OuJ mice compared with HeJ mice (258 +/- 18 &mgr;g/ml) after exposure to O(3). Furthermore, reverse transcriptase/polymerase chain reaction analysis demonstrated differential expression of Tlr4 message levels between HeJ and OuJ mice after O(3) exposure. Together, results indicate that a QTL on mouse chromosome 4 explains a significant portion of the genetic variance in O(3)-induced hyperpermeability, and support a role for Tlr4 as a strong candidate susceptibility gene."	Am J Respir Cell Mol Biol	2000	May	"Kleeberger SR, Reddy S, Zhang LY, Jedlicka AE"	10783135	42 - 56 days	both	16-Jun	mg/ ml	525	315	330	220	330	160	280	295	320	530	715	160	455	525
PMNÕs (x103/mL BAL return)	Mean +/ - SE	Genetic susceptibility to ozone-induced lung hyperpermeability: role of toll-like receptor 4.	"The pollutant ozone (O(3)) induces lung hyperpermeability and inflammation in humans and animal models. Among inbred strains of mice, there is a 3-fold difference in total protein (a marker of permeability) recovered in bronchoalveolar lavage (BAL) fluid after a 72-h exposure to 0.3 ppm O(3). To determine the chromosomal locations of susceptibility genes, we performed a genome screen using recombinant inbred (RI) strains of mice derived from O(3)-susceptible C57BL/6J (B6) and O(3)-resistant C3H/HeJ (HeJ) progenitors. Each RI strain was phenotyped for O(3)-induced hyperpermeability, and linkage was assessed for 558 markers using Map Manager QTb27. A significant quantitative trait locus (QTL) was identified on chromosome 4. The likelihood ratio chi(2) statistic (16.6) for the peak of the QTL was greater than the significance threshold (16.3) determined empirically by permutation test. This QTL contains a candidate gene, Toll-like receptor 4 (Tlr4 ), that recently has been implicated in innate immunity and endotoxin susceptibility. The amount of the total trait variance explained by the QTL at Tlr4, the gene with the highest likelihood ratio statistic in the QTL, was approximately 70%. To test the role of Tlr4 in O(3)-induced hyperpermeability, BAL protein responses to O(3) were compared in C3H/HeOuJ (OuJ) and HeJ mice that differ only at a polymorphism in the coding region of Tlr4. Significantly greater protein concentrations (430 +/- 35 &mgr;g/ml) were found in OuJ mice compared with HeJ mice (258 +/- 18 &mgr;g/ml) after exposure to O(3). Furthermore, reverse transcriptase/polymerase chain reaction analysis demonstrated differential expression of Tlr4 message levels between HeJ and OuJ mice after O(3) exposure. Together, results indicate that a QTL on mouse chromosome 4 explains a significant portion of the genetic variance in O(3)-induced hyperpermeability, and support a role for Tlr4 as a strong candidate susceptibility gene."	Am J Respir Cell Mol Biol	2000	May	"Kleeberger SR, Reddy S, Zhang LY, Jedlicka AE"	10783135	42 - 56 days	both	16-Jun		10.1	2.4	2.8	15.3	2.1	1.7	2.3	13.2	1.6	2.8	1.3	2.7	10.8	1.9
PMNÕs (x103/mL BAL return)	Range	Genetic susceptibility to ozone-induced lung hyperpermeability: role of toll-like receptor 4.	"The pollutant ozone (O(3)) induces lung hyperpermeability and inflammation in humans and animal models. Among inbred strains of mice, there is a 3-fold difference in total protein (a marker of permeability) recovered in bronchoalveolar lavage (BAL) fluid after a 72-h exposure to 0.3 ppm O(3). To determine the chromosomal locations of susceptibility genes, we performed a genome screen using recombinant inbred (RI) strains of mice derived from O(3)-susceptible C57BL/6J (B6) and O(3)-resistant C3H/HeJ (HeJ) progenitors. Each RI strain was phenotyped for O(3)-induced hyperpermeability, and linkage was assessed for 558 markers using Map Manager QTb27. A significant quantitative trait locus (QTL) was identified on chromosome 4. The likelihood ratio chi(2) statistic (16.6) for the peak of the QTL was greater than the significance threshold (16.3) determined empirically by permutation test. This QTL contains a candidate gene, Toll-like receptor 4 (Tlr4 ), that recently has been implicated in innate immunity and endotoxin susceptibility. The amount of the total trait variance explained by the QTL at Tlr4, the gene with the highest likelihood ratio statistic in the QTL, was approximately 70%. To test the role of Tlr4 in O(3)-induced hyperpermeability, BAL protein responses to O(3) were compared in C3H/HeOuJ (OuJ) and HeJ mice that differ only at a polymorphism in the coding region of Tlr4. Significantly greater protein concentrations (430 +/- 35 &mgr;g/ml) were found in OuJ mice compared with HeJ mice (258 +/- 18 &mgr;g/ml) after exposure to O(3). Furthermore, reverse transcriptase/polymerase chain reaction analysis demonstrated differential expression of Tlr4 message levels between HeJ and OuJ mice after O(3) exposure. Together, results indicate that a QTL on mouse chromosome 4 explains a significant portion of the genetic variance in O(3)-induced hyperpermeability, and support a role for Tlr4 as a strong candidate susceptibility gene."	Am J Respir Cell Mol Biol	2000	May	"Kleeberger SR, Reddy S, Zhang LY, Jedlicka AE"	10783135	42 - 56 days	both	16-Jun		7.2 - 14.5	0.5 - 4.1	0.5 - 7.4	7.5 - 18.5	0.4 - 7.6	0.4 - 7.6	7.9 - 24.2	0.4 - 2.9	1.0 - 4.6	0.2 - 3.4	0.2 - 3.4	0.7 - 5.5	6.2 - 18.1	0.5 - 3.3
Cell number and brain weights in BXH strains	Mean  +/ - SEM	Natural variation in neuron number in mice is linked to a major quantitative trait locus on Chr 11.	"Common genetic polymorphisms-as opposed to rare mutations-generate almost all heritable differences in the size and structure of the CNS. Surprisingly, these normal variants have not previously been mapped or cloned in any vertebrate species. In a recent paper (), we suggested that much of the variation in retinal ganglion cell number in mice, and the striking bimodality of strain averages, are caused by one or two quantitative trait loci (QTLs). To test this idea, and to map genes linked to this variable and highly heritable quantitative trait, we have counted ganglion cells in 38 recombinant inbred strains (BXD and BXH) derived from parental strains that have high and low cell numbers. A genome-wide search using simple and composite interval-mapping techniques revealed a major QTL on chromosome (Chr) 11 in a 3 cM interval between Hoxb and Krt1 (LOD = 6.8; genome-wide p = 0.001) and possible subsidiary QTLs on Chr 2 and Chr 8. The Chr 11 locus, neuron number control 1 (Nnc1), accounts for one third of the genetic variance among BXH strains and more than half of that among BXD strains, but Nnc1 has no known effects on brain weight, eye weight, or total retinal cell number. Three strong candidate genes have been mapped previously to the same region as Nnc1. These genes-Rara, Thra, and Erbb2- encode receptors for retinoic acid, thyroxine, and neuregulin, respectively. Each receptor is expressed in the retina during development, and their ligands affect the proliferation or survival of retinal cells."	J Neurosci	1998	Jan	"Williams RW, Strom RC, Goldowitz D."	9412494		both	9-Apr	1000x	55.4	67	64.6	63	66.9	52.3	56.5	62.4	57.5	56.2	55	69.5	65.6	55.3
Cell number and brain weights in BXH strains	Type	Natural variation in neuron number in mice is linked to a major quantitative trait locus on Chr 11.	"Common genetic polymorphisms-as opposed to rare mutations-generate almost all heritable differences in the size and structure of the CNS. Surprisingly, these normal variants have not previously been mapped or cloned in any vertebrate species. In a recent paper (), we suggested that much of the variation in retinal ganglion cell number in mice, and the striking bimodality of strain averages, are caused by one or two quantitative trait loci (QTLs). To test this idea, and to map genes linked to this variable and highly heritable quantitative trait, we have counted ganglion cells in 38 recombinant inbred strains (BXD and BXH) derived from parental strains that have high and low cell numbers. A genome-wide search using simple and composite interval-mapping techniques revealed a major QTL on chromosome (Chr) 11 in a 3 cM interval between Hoxb and Krt1 (LOD = 6.8; genome-wide p = 0.001) and possible subsidiary QTLs on Chr 2 and Chr 8. The Chr 11 locus, neuron number control 1 (Nnc1), accounts for one third of the genetic variance among BXH strains and more than half of that among BXD strains, but Nnc1 has no known effects on brain weight, eye weight, or total retinal cell number. Three strong candidate genes have been mapped previously to the same region as Nnc1. These genes-Rara, Thra, and Erbb2- encode receptors for retinoic acid, thyroxine, and neuregulin, respectively. Each receptor is expressed in the retina during development, and their ligands affect the proliferation or survival of retinal cells."	J Neurosci	1998	Jan	"Williams RW, Strom RC, Goldowitz D."	9412494		both			L	H	H	I	H	L	I	I	I	I	L	H	H	L
Cell number and brain weights in BXH strains	Brain	Natural variation in neuron number in mice is linked to a major quantitative trait locus on Chr 11.	"Common genetic polymorphisms-as opposed to rare mutations-generate almost all heritable differences in the size and structure of the CNS. Surprisingly, these normal variants have not previously been mapped or cloned in any vertebrate species. In a recent paper (), we suggested that much of the variation in retinal ganglion cell number in mice, and the striking bimodality of strain averages, are caused by one or two quantitative trait loci (QTLs). To test this idea, and to map genes linked to this variable and highly heritable quantitative trait, we have counted ganglion cells in 38 recombinant inbred strains (BXD and BXH) derived from parental strains that have high and low cell numbers. A genome-wide search using simple and composite interval-mapping techniques revealed a major QTL on chromosome (Chr) 11 in a 3 cM interval between Hoxb and Krt1 (LOD = 6.8; genome-wide p = 0.001) and possible subsidiary QTLs on Chr 2 and Chr 8. The Chr 11 locus, neuron number control 1 (Nnc1), accounts for one third of the genetic variance among BXH strains and more than half of that among BXD strains, but Nnc1 has no known effects on brain weight, eye weight, or total retinal cell number. Three strong candidate genes have been mapped previously to the same region as Nnc1. These genes-Rara, Thra, and Erbb2- encode receptors for retinoic acid, thyroxine, and neuregulin, respectively. Each receptor is expressed in the retina during development, and their ligands affect the proliferation or survival of retinal cells."	J Neurosci	1998	Jan	"Williams RW, Strom RC, Goldowitz D."	9412494		both	13-Mar	mg	475	427	431	442	465	455	471	437	457	455	431	432	432	436
Cell number and brain weights in BXH strains	Residual Cells	Natural variation in neuron number in mice is linked to a major quantitative trait locus on Chr 11.	"Common genetic polymorphisms-as opposed to rare mutations-generate almost all heritable differences in the size and structure of the CNS. Surprisingly, these normal variants have not previously been mapped or cloned in any vertebrate species. In a recent paper (), we suggested that much of the variation in retinal ganglion cell number in mice, and the striking bimodality of strain averages, are caused by one or two quantitative trait loci (QTLs). To test this idea, and to map genes linked to this variable and highly heritable quantitative trait, we have counted ganglion cells in 38 recombinant inbred strains (BXD and BXH) derived from parental strains that have high and low cell numbers. A genome-wide search using simple and composite interval-mapping techniques revealed a major QTL on chromosome (Chr) 11 in a 3 cM interval between Hoxb and Krt1 (LOD = 6.8; genome-wide p = 0.001) and possible subsidiary QTLs on Chr 2 and Chr 8. The Chr 11 locus, neuron number control 1 (Nnc1), accounts for one third of the genetic variance among BXH strains and more than half of that among BXD strains, but Nnc1 has no known effects on brain weight, eye weight, or total retinal cell number. Three strong candidate genes have been mapped previously to the same region as Nnc1. These genes-Rara, Thra, and Erbb2- encode receptors for retinoic acid, thyroxine, and neuregulin, respectively. Each receptor is expressed in the retina during development, and their ligands affect the proliferation or survival of retinal cells."	J Neurosci	1998	Jan	"Williams RW, Strom RC, Goldowitz D."	9412494		both	9-Apr	cells 1000x	---	---	2.48	2.2	8.86	-6.94	-0.82	1	-1.5	-3.04	-7.12	7.5	.3.60	-6.22
Correlation between HO - 1 mRNA induction with MM-LDL in ECs and aortic atherosclerotic lesions 	HO - 1 induction (Cu - LDL: R= 0.79; P= 0.0013	Determinants of atherosclerosis susceptibility in the C3H and C57BL/6 mouse model: evidence for involvement of endothelial cells but not blood cells or cholesterol metabolism.	"Lipids, monocytes, and arterial wall cells are primary components involved in atherogenesis. Using the inbred mouse strains C57BL/6J (B6) and C3H/HeJ (C3H), which have been extensively studied as models of the genetic control of diet-induced atherosclerosis, we examined which of these components determine genetic susceptibility. To test whether dietary responsiveness is involved, a congenic strain of C3H carrying an apoE-null allele (apoE(-/-)) was constructed. Although C3H.apoE(-/-) mice had higher plasma cholesterol levels, they developed much smaller lesions than their B6.apoE(-/-) counterpart on either chow or Western diets. Reciprocal bone marrow transplantation between the strains, with congenics carrying the same H-2 haplotype, was performed to examine the role of monocytes. The atherosclerosis susceptibility was not altered in the recipient mice, indicating that variations in monocyte function were not involved. Endothelial cells isolated from the aorta of B6 mice exhibited a dramatic induction of monocyte chemotactic protein-1, macrophage colony-stimulating factor, vascular cell adhesion molecule-1, and heme oxygenase-1 in response to minimally modified LDL, whereas endothelial cells from C3H mice showed little or no induction. In a set of recombinant inbred strains derived from the B6 and C3H parental strains, endothelial responses to minimally modified LDL cosegregated with aortic lesion size. These data provide strong evidence that endothelial cells, but not monocytes or plasma lipid levels, account for the difference in susceptibility to atherosclerosis between the 2 mouse strains."	Circulation Research	2000	May	"Shi W, Wang NJ, Shih DM, Sun VZ, Wang X, Lusis AJ"	10827138	105 days	both	5-Feb	fold (with multiple values)	"8.8, 8.1, 4.8, 3.5, 2.0"	"2.0, 1.7, 1.4"	---	---	"1.9, 1.5, 1.4"	---	---	"11.3, 8.6, 4.6"	"4.4, 1.4, 1.3"	"3.0, 2.5"	"4.0, 2.5"	---	---	"7.5, 5.2"
BXH RI strains segregate into at least three distinct phenotypes	Survival	Genetic characterization of strain differences in the ability to mediate CD40/CD28-independent rejection of skin allografts.	"Simultaneous blockade of the CD40 and CD28 T cell costimulatory pathways effectively promotes skin allograft survival in C3H/HeJ mice, extending median survival times (MSTs) beyond 100 days. This strategy is markedly less effective in C57BL/6 mice, with MSTs ranging between 20 and 30 days. In this study, we investigate the underlying genetic causes of these distinct phenotypes. Using H-2 congenic mice, we show that the genetic basis for the varied responses between these two strains is independent of the H-2 locus and T cell precursor frequency. C57BL/6 mice treated with costimulation blockade are able to generate allospecific CTL- and IFN-gamma-producing T cells within 3-4 wk posttransplant, whereas mice with a C3H background generate neither CTL- nor IFN-gamma-producing cells. Thus, differences appear to be in the generation of the immune response and not T cell homing. Strain differences in costimulation blockade-induced hyporesponsiveness persist in the absence of CD4(+) T cells, implying a direct effect on CD8(+) T cells. We demonstrate that genetic differences are important in cells of hemopoietic origin and that the costimulation blockade-resistant phenotype is dominant. Analysis of BXH recombinant inbred strains indicates that multiple loci contribute to the phenotype, and that the blockade resistance loci are preliminarily linked to 17 markers on four chromosomes. We conclude that strain variation in allograft MSTs following CD40/CD28 blockade results from the ability of CD8(+) T cells in some strains to use alternative modes of costimulation to mount an effective alloresponse."	 J Immunol	2000	Dec	"Williams MA, Trambley J, Ha J, Adams AB, Durham MM, Rees P, Cowan SR, Pearson TC, Larsen CP."	11120808				days	"17, 18, 19, 20, 22"	"17, 100, 110, >110, >110"	"25, 34, 41, 48"	">110, >110, >110, >110, >110"	"33, 35, 50, 64, 64"	"14, 39, 50, 50, 53"	"53, 53, 68, 95"	"28, 32, 36, 50, >65"	"95, >110, >110, >110, >110"	"18, 23, 26, 27, 50"	"14, 16"	"23, 59, 59, 98"	"14, 14, 20, 26, 95"	">110, >110"
BXH RI strains segregate into at least three distinct phenotypes	MST	Genetic characterization of strain differences in the ability to mediate CD40/CD28-independent rejection of skin allografts.	"Simultaneous blockade of the CD40 and CD28 T cell costimulatory pathways effectively promotes skin allograft survival in C3H/HeJ mice, extending median survival times (MSTs) beyond 100 days. This strategy is markedly less effective in C57BL/6 mice, with MSTs ranging between 20 and 30 days. In this study, we investigate the underlying genetic causes of these distinct phenotypes. Using H-2 congenic mice, we show that the genetic basis for the varied responses between these two strains is independent of the H-2 locus and T cell precursor frequency. C57BL/6 mice treated with costimulation blockade are able to generate allospecific CTL- and IFN-gamma-producing T cells within 3-4 wk posttransplant, whereas mice with a C3H background generate neither CTL- nor IFN-gamma-producing cells. Thus, differences appear to be in the generation of the immune response and not T cell homing. Strain differences in costimulation blockade-induced hyporesponsiveness persist in the absence of CD4(+) T cells, implying a direct effect on CD8(+) T cells. We demonstrate that genetic differences are important in cells of hemopoietic origin and that the costimulation blockade-resistant phenotype is dominant. Analysis of BXH recombinant inbred strains indicates that multiple loci contribute to the phenotype, and that the blockade resistance loci are preliminarily linked to 17 markers on four chromosomes. We conclude that strain variation in allograft MSTs following CD40/CD28 blockade results from the ability of CD8(+) T cells in some strains to use alternative modes of costimulation to mount an effective alloresponse."	 J Immunol	2000	Dec	"Williams MA, Trambley J, Ha J, Adams AB, Durham MM, Rees P, Cowan SR, Pearson TC, Larsen CP."	11120808					19	110	34	>110	50	50	53	36	>110	26	16	59	20	>110
Origin of locus in BXH RI strain	Mrv1	Frequent disruption of the Nf1 gene by a novel murine AIDS virus-related provirus in BXH-2 murine myeloid lymphomas.	"Evi-2, a common site of viral integration in BXH-2 myeloid lymphomas, is located within a large intron of the Nf1 tumor suppressor gene. Viral integration at Evi-2 appears to induce disease by disrupting normal Nf1 expression. During our attempts to characterize the nature of the proviruses located at Evi-2, we found that approximately half of the proviruses were defective nonecotropic proviruses (A. M. Buchberg, H. G. Bedigian, N. A. Jenkins, and N. G. Copeland, Mol. Cell. Biol. 10:4658-4666, 1990). This was surprising, since most proviruses characterized at other BXH-2 common integration sites are full-length ecotropic viruses. In the studies described here, we found that this defective provirus carries two large deletions, one in pol and one in env, and is structurally related to another murine retrovirus, the murine AIDS retrovirus. By using oligonucleotide probes specific for this defective provirus, designated MRV, we showed that MRV-related proviruses are carried as endogenous germ line proviruses in most inbred strains. In addition, we identified the endogenous MRV provirus that gives rise to the defective proviruses identified at Evi-2. We present a model that accounts for the positive selection of MRV proviruses at Evi-2, which may allow selective identification of common viral integration sites harboring tumor suppressor genes."	J Virol	1995	Nov	"Cho BC, Shaughnessy JD Jr, Largaespada DA, Bedigian HG, Buchberg AM, Jenkins NA, Copeland NG."	7474134				"B, C57CL/6J; H, C3H/HeJ"			B	B	H	B	H	B	H	H	H	B	B	H
Origin of locus in BXH RI strain	Mrv2	Frequent disruption of the Nf1 gene by a novel murine AIDS virus-related provirus in BXH-2 murine myeloid lymphomas.	"Evi-2, a common site of viral integration in BXH-2 myeloid lymphomas, is located within a large intron of the Nf1 tumor suppressor gene. Viral integration at Evi-2 appears to induce disease by disrupting normal Nf1 expression. During our attempts to characterize the nature of the proviruses located at Evi-2, we found that approximately half of the proviruses were defective nonecotropic proviruses (A. M. Buchberg, H. G. Bedigian, N. A. Jenkins, and N. G. Copeland, Mol. Cell. Biol. 10:4658-4666, 1990). This was surprising, since most proviruses characterized at other BXH-2 common integration sites are full-length ecotropic viruses. In the studies described here, we found that this defective provirus carries two large deletions, one in pol and one in env, and is structurally related to another murine retrovirus, the murine AIDS retrovirus. By using oligonucleotide probes specific for this defective provirus, designated MRV, we showed that MRV-related proviruses are carried as endogenous germ line proviruses in most inbred strains. In addition, we identified the endogenous MRV provirus that gives rise to the defective proviruses identified at Evi-2. We present a model that accounts for the positive selection of MRV proviruses at Evi-2, which may allow selective identification of common viral integration sites harboring tumor suppressor genes."	J Virol	1995	Nov	"Cho BC, Shaughnessy JD Jr, Largaespada DA, Bedigian HG, Buchberg AM, Jenkins NA, Copeland NG."	7474134				"B, C57CL/6J; H, C3H/HeJ"			B	B	B	H	B	B	B	H	B	H	H	B
Origin of locus in BXH RI strain	Mrv3	Frequent disruption of the Nf1 gene by a novel murine AIDS virus-related provirus in BXH-2 murine myeloid lymphomas.	"Evi-2, a common site of viral integration in BXH-2 myeloid lymphomas, is located within a large intron of the Nf1 tumor suppressor gene. Viral integration at Evi-2 appears to induce disease by disrupting normal Nf1 expression. During our attempts to characterize the nature of the proviruses located at Evi-2, we found that approximately half of the proviruses were defective nonecotropic proviruses (A. M. Buchberg, H. G. Bedigian, N. A. Jenkins, and N. G. Copeland, Mol. Cell. Biol. 10:4658-4666, 1990). This was surprising, since most proviruses characterized at other BXH-2 common integration sites are full-length ecotropic viruses. In the studies described here, we found that this defective provirus carries two large deletions, one in pol and one in env, and is structurally related to another murine retrovirus, the murine AIDS retrovirus. By using oligonucleotide probes specific for this defective provirus, designated MRV, we showed that MRV-related proviruses are carried as endogenous germ line proviruses in most inbred strains. In addition, we identified the endogenous MRV provirus that gives rise to the defective proviruses identified at Evi-2. We present a model that accounts for the positive selection of MRV proviruses at Evi-2, which may allow selective identification of common viral integration sites harboring tumor suppressor genes."	J Virol	1995	Nov	"Cho BC, Shaughnessy JD Jr, Largaespada DA, Bedigian HG, Buchberg AM, Jenkins NA, Copeland NG."	7474134				"B, C57CL/6J; H, C3H/HeJ"			B	H	H	B	B	H	B	H	B	B	B	H
The prevalence of DCC in BXH strains and the correspondence of this phenotype with the parental genotype for microsatellite markers typed on proximal chromosome 7	"D7Mit294, D7Mit266"	A locus on chromosome 7 determines myocardial cell necrosis and calcification (dystrophic cardiac calcinosis) in mice.	"Dystrophic cardiac calcinosis, an age-related cardiomyopathy that occurs among certain inbred strains of mice, involves myocardial injury, necrosis, and calcification. Using a complete linkage map approach and quantitative trait locus analysis, we sought to identify genetic loci determining dystrophic cardiac calcinosis in an F2 intercross of resistant C57BL/6J and susceptible C3H/HeJ inbred strains. We identified a single major locus, designated Dyscalc, located on proximal chromosome 7 in a region syntenic with human chromosomes 19q13 and 11p15. The statistical significance of Dyscalc (logarithm of odds score 14.6) was tested by analysis of permuted trait data. Analysis of BxH recombinant inbred strains confirmed the mapping position. The inheritance pattern indicated that this locus influences susceptibility of cells both to enter necrosis and to subsequently undergo calcification."	Proc Natl Acad Sci U S A 	1996	May	"Ivandic BT, Qiao JH, Machleder D, Liao F, Drake TA, Lusis AJ."	8643601	5 months	female		"B, C57CL/6J; H, C3H/HeJ"				H	H	B	B	B	B	B	H		B	B
The prevalence of DCC in BXH strains and the correspondence of this phenotype with the parental genotype for microsatellite markers typed on proximal chromosome 7	D7Mit224	A locus on chromosome 7 determines myocardial cell necrosis and calcification (dystrophic cardiac calcinosis) in mice.	"Dystrophic cardiac calcinosis, an age-related cardiomyopathy that occurs among certain inbred strains of mice, involves myocardial injury, necrosis, and calcification. Using a complete linkage map approach and quantitative trait locus analysis, we sought to identify genetic loci determining dystrophic cardiac calcinosis in an F2 intercross of resistant C57BL/6J and susceptible C3H/HeJ inbred strains. We identified a single major locus, designated Dyscalc, located on proximal chromosome 7 in a region syntenic with human chromosomes 19q13 and 11p15. The statistical significance of Dyscalc (logarithm of odds score 14.6) was tested by analysis of permuted trait data. Analysis of BxH recombinant inbred strains confirmed the mapping position. The inheritance pattern indicated that this locus influences susceptibility of cells both to enter necrosis and to subsequently undergo calcification."	Proc Natl Acad Sci U S A 	1996	May	"Ivandic BT, Qiao JH, Machleder D, Liao F, Drake TA, Lusis AJ."	8643601	5 months	female		"B, C57CL/6J; H, C3H/HeJ"				H	H	B	B	B	B	H	H		H	H
The prevalence of DCC in BXH strains and the correspondence of this phenotype with the parental genotype for microsatellite markers typed on proximal chromosome 7	"D7Mit247, D7Mit25"	A locus on chromosome 7 determines myocardial cell necrosis and calcification (dystrophic cardiac calcinosis) in mice.	"Dystrophic cardiac calcinosis, an age-related cardiomyopathy that occurs among certain inbred strains of mice, involves myocardial injury, necrosis, and calcification. Using a complete linkage map approach and quantitative trait locus analysis, we sought to identify genetic loci determining dystrophic cardiac calcinosis in an F2 intercross of resistant C57BL/6J and susceptible C3H/HeJ inbred strains. We identified a single major locus, designated Dyscalc, located on proximal chromosome 7 in a region syntenic with human chromosomes 19q13 and 11p15. The statistical significance of Dyscalc (logarithm of odds score 14.6) was tested by analysis of permuted trait data. Analysis of BxH recombinant inbred strains confirmed the mapping position. The inheritance pattern indicated that this locus influences susceptibility of cells both to enter necrosis and to subsequently undergo calcification."	Proc Natl Acad Sci U S A 	1996	May	"Ivandic BT, Qiao JH, Machleder D, Liao F, Drake TA, Lusis AJ."	8643601	5 months	female		"B, C57CL/6J; H, C3H/HeJ"				H	H	H	H	B	B	H	H		H	H
The prevalence of DCC in BXH strains and the correspondence of this phenotype with the parental genotype for microsatellite markers typed on proximal chromosome 7	D7Mit227	A locus on chromosome 7 determines myocardial cell necrosis and calcification (dystrophic cardiac calcinosis) in mice.	"Dystrophic cardiac calcinosis, an age-related cardiomyopathy that occurs among certain inbred strains of mice, involves myocardial injury, necrosis, and calcification. Using a complete linkage map approach and quantitative trait locus analysis, we sought to identify genetic loci determining dystrophic cardiac calcinosis in an F2 intercross of resistant C57BL/6J and susceptible C3H/HeJ inbred strains. We identified a single major locus, designated Dyscalc, located on proximal chromosome 7 in a region syntenic with human chromosomes 19q13 and 11p15. The statistical significance of Dyscalc (logarithm of odds score 14.6) was tested by analysis of permuted trait data. Analysis of BxH recombinant inbred strains confirmed the mapping position. The inheritance pattern indicated that this locus influences susceptibility of cells both to enter necrosis and to subsequently undergo calcification."	Proc Natl Acad Sci U S A 	1996	May	"Ivandic BT, Qiao JH, Machleder D, Liao F, Drake TA, Lusis AJ."	8643601	5 months	female		"B, C57CL/6J; H, C3H/HeJ"				H	H	H	H	B	B	H	H		H	H
The prevalence of DCC in BXH strains and the correspondence of this phenotype with the parental genotype for microsatellite markers typed on proximal chromosome 7	D7Mit270	A locus on chromosome 7 determines myocardial cell necrosis and calcification (dystrophic cardiac calcinosis) in mice.	"Dystrophic cardiac calcinosis, an age-related cardiomyopathy that occurs among certain inbred strains of mice, involves myocardial injury, necrosis, and calcification. Using a complete linkage map approach and quantitative trait locus analysis, we sought to identify genetic loci determining dystrophic cardiac calcinosis in an F2 intercross of resistant C57BL/6J and susceptible C3H/HeJ inbred strains. We identified a single major locus, designated Dyscalc, located on proximal chromosome 7 in a region syntenic with human chromosomes 19q13 and 11p15. The statistical significance of Dyscalc (logarithm of odds score 14.6) was tested by analysis of permuted trait data. Analysis of BxH recombinant inbred strains confirmed the mapping position. The inheritance pattern indicated that this locus influences susceptibility of cells both to enter necrosis and to subsequently undergo calcification."	Proc Natl Acad Sci U S A 	1996	May	"Ivandic BT, Qiao JH, Machleder D, Liao F, Drake TA, Lusis AJ."	8643601	5 months	female		"B, C57CL/6J; H, C3H/HeJ"				H	H	H	B	B	B	H	H		H	H
The prevalence of DCC in BXH strains and the correspondence of this phenotype with the parental genotype for microsatellite markers typed on proximal chromosome 7	D7Mit229	A locus on chromosome 7 determines myocardial cell necrosis and calcification (dystrophic cardiac calcinosis) in mice.	"Dystrophic cardiac calcinosis, an age-related cardiomyopathy that occurs among certain inbred strains of mice, involves myocardial injury, necrosis, and calcification. Using a complete linkage map approach and quantitative trait locus analysis, we sought to identify genetic loci determining dystrophic cardiac calcinosis in an F2 intercross of resistant C57BL/6J and susceptible C3H/HeJ inbred strains. We identified a single major locus, designated Dyscalc, located on proximal chromosome 7 in a region syntenic with human chromosomes 19q13 and 11p15. The statistical significance of Dyscalc (logarithm of odds score 14.6) was tested by analysis of permuted trait data. Analysis of BxH recombinant inbred strains confirmed the mapping position. The inheritance pattern indicated that this locus influences susceptibility of cells both to enter necrosis and to subsequently undergo calcification."	Proc Natl Acad Sci U S A 	1996	May	"Ivandic BT, Qiao JH, Machleder D, Liao F, Drake TA, Lusis AJ."	8643601	5 months	female		"B, C57CL/6J; H, C3H/HeJ"				H	H	H	B	B	B	H	H		H	H
The prevalence of DCC in BXH strains and the correspondence of this phenotype with the parental genotype for microsatellite markers typed on proximal chromosome 7	D7Mit82	A locus on chromosome 7 determines myocardial cell necrosis and calcification (dystrophic cardiac calcinosis) in mice.	"Dystrophic cardiac calcinosis, an age-related cardiomyopathy that occurs among certain inbred strains of mice, involves myocardial injury, necrosis, and calcification. Using a complete linkage map approach and quantitative trait locus analysis, we sought to identify genetic loci determining dystrophic cardiac calcinosis in an F2 intercross of resistant C57BL/6J and susceptible C3H/HeJ inbred strains. We identified a single major locus, designated Dyscalc, located on proximal chromosome 7 in a region syntenic with human chromosomes 19q13 and 11p15. The statistical significance of Dyscalc (logarithm of odds score 14.6) was tested by analysis of permuted trait data. Analysis of BxH recombinant inbred strains confirmed the mapping position. The inheritance pattern indicated that this locus influences susceptibility of cells both to enter necrosis and to subsequently undergo calcification."	Proc Natl Acad Sci U S A 	1996	May	"Ivandic BT, Qiao JH, Machleder D, Liao F, Drake TA, Lusis AJ."	8643601	5 months	female		"B, C57CL/6J; H, C3H/HeJ"				H	H	H	B	H	B	H	H		H	H
The prevalence of DCC in BXH strains and the correspondence of this phenotype with the parental genotype for microsatellite markers typed on proximal chromosome 7	Prevalence of DCC	A locus on chromosome 7 determines myocardial cell necrosis and calcification (dystrophic cardiac calcinosis) in mice.	"Dystrophic cardiac calcinosis, an age-related cardiomyopathy that occurs among certain inbred strains of mice, involves myocardial injury, necrosis, and calcification. Using a complete linkage map approach and quantitative trait locus analysis, we sought to identify genetic loci determining dystrophic cardiac calcinosis in an F2 intercross of resistant C57BL/6J and susceptible C3H/HeJ inbred strains. We identified a single major locus, designated Dyscalc, located on proximal chromosome 7 in a region syntenic with human chromosomes 19q13 and 11p15. The statistical significance of Dyscalc (logarithm of odds score 14.6) was tested by analysis of permuted trait data. Analysis of BxH recombinant inbred strains confirmed the mapping position. The inheritance pattern indicated that this locus influences susceptibility of cells both to enter necrosis and to subsequently undergo calcification."	Proc Natl Acad Sci U S A 	1996	May	"Ivandic BT, Qiao JH, Machleder D, Liao F, Drake TA, Lusis AJ."	8643601	5 months	female		%				50	75	25	0	0	0	0	100		29	17
The prevalence of DCC in BXH strains and the correspondence of this phenotype with the parental genotype for microsatellite markers typed on proximal chromosome 7	Mice with DCC/ total	A locus on chromosome 7 determines myocardial cell necrosis and calcification (dystrophic cardiac calcinosis) in mice.	"Dystrophic cardiac calcinosis, an age-related cardiomyopathy that occurs among certain inbred strains of mice, involves myocardial injury, necrosis, and calcification. Using a complete linkage map approach and quantitative trait locus analysis, we sought to identify genetic loci determining dystrophic cardiac calcinosis in an F2 intercross of resistant C57BL/6J and susceptible C3H/HeJ inbred strains. We identified a single major locus, designated Dyscalc, located on proximal chromosome 7 in a region syntenic with human chromosomes 19q13 and 11p15. The statistical significance of Dyscalc (logarithm of odds score 14.6) was tested by analysis of permuted trait data. Analysis of BxH recombinant inbred strains confirmed the mapping position. The inheritance pattern indicated that this locus influences susceptibility of cells both to enter necrosis and to subsequently undergo calcification."	Proc Natl Acad Sci U S A 	1996	May	"Ivandic BT, Qiao JH, Machleder D, Liao F, Drake TA, Lusis AJ."	8643601	5 months	female		"B, C57CL/6J; H, C3H/HeJ"				8-Apr	8-Jun	4-Jan	0/ 8	0/ 3	0/ 7	0/ 5	9-Sep		7-Feb	7-Jan
Number of lavageable polymorphonuclear leukocytes in bronchoalveolar lavage returns from BXH RI strains 6 hours after :	acute (3h) exposure to 2 ppm ozone	Susceptibility to ozone-induced inflammation. I. Genetic control of the response to subacute exposure.	"We demonstrated previously that C57BL/6J (B6) inbred mice are susceptible and C3H/HeJ (C3) mice are resistant to airway inflammation that is induced by acute (3 h) exposure to 2 parts per million (ppm) ozone (O3). In the present study we tested the hypothesis that B6 and C3 mice are also differentially susceptible to the airway inflammatory responses to subacute (72 h) exposure to environmentally relevant concentrations of O3 (0.12 and 0.30 ppm). Male mice (20-25 g, 5-7 wk) were exposed continuously to 0.12 ppm O3, 0.30 ppm O3, or filtered air (control). Pulmonary inflammation was assessed after 24, 48, and 72 h by differential cell count and total protein in bronchoalveolar lavage (BAL) returns. Exposure to 0.12 ppm O3 caused significant influx of alveolar macrophages, polymorphonuclear leukocytes (PMNs), lymphocytes, and total BAL protein in both strains, but no differences in the magnitude of the responses were found between B6 and C3 mice. In contrast to the effect of 0.12 ppm O3, exposure to 0.30 ppm O3 elicited significantly greater numbers of inflammatory cells and BAL protein concentration in B6 mice relative to C3 mice. The phenotypes of the B6 and C3 mice were termed susceptible and resistant, respectively. To further evaluate the potential genetic contribution to the inflammatory response to 0.30 ppm O3, the F1, F2, and backcross progeny from B6 and C3 progenitors were examined. The ratios of susceptible and resistant phenotypes of these progeny support the hypothesis that a single autosomal recessive gene confers susceptibility to subacute O3-induced inflammation.(ABSTRACT TRUNCATED AT 250 WORDS)"	Am J Physiol	1993	Jan	"Kleeberger SR, Levitt RC, Zhang LY."	8430812	6 - 8 weeks	both		Number of PMNs in BAL (x10^3)	10	2	26	3	1	18		20	1	1		7	15	1
Number of lavageable polymorphonuclear leukocytes in bronchoalveolar lavage returns from BXH RI strains 6 hours after :	subacute (48h) exposure to 0.30 ppm ozone	Susceptibility to ozone-induced inflammation. I. Genetic control of the response to subacute exposure.	"We demonstrated previously that C57BL/6J (B6) inbred mice are susceptible and C3H/HeJ (C3) mice are resistant to airway inflammation that is induced by acute (3 h) exposure to 2 parts per million (ppm) ozone (O3). In the present study we tested the hypothesis that B6 and C3 mice are also differentially susceptible to the airway inflammatory responses to subacute (72 h) exposure to environmentally relevant concentrations of O3 (0.12 and 0.30 ppm). Male mice (20-25 g, 5-7 wk) were exposed continuously to 0.12 ppm O3, 0.30 ppm O3, or filtered air (control). Pulmonary inflammation was assessed after 24, 48, and 72 h by differential cell count and total protein in bronchoalveolar lavage (BAL) returns. Exposure to 0.12 ppm O3 caused significant influx of alveolar macrophages, polymorphonuclear leukocytes (PMNs), lymphocytes, and total BAL protein in both strains, but no differences in the magnitude of the responses were found between B6 and C3 mice. In contrast to the effect of 0.12 ppm O3, exposure to 0.30 ppm O3 elicited significantly greater numbers of inflammatory cells and BAL protein concentration in B6 mice relative to C3 mice. The phenotypes of the B6 and C3 mice were termed susceptible and resistant, respectively. To further evaluate the potential genetic contribution to the inflammatory response to 0.30 ppm O3, the F1, F2, and backcross progeny from B6 and C3 progenitors were examined. The ratios of susceptible and resistant phenotypes of these progeny support the hypothesis that a single autosomal recessive gene confers susceptibility to subacute O3-induced inflammation.(ABSTRACT TRUNCATED AT 250 WORDS)"	Am J Physiol	1993	Jan	"Kleeberger SR, Levitt RC, Zhang LY."	8430812	6 - 8 weeks	both		Number of PMNs in BAL (x10^3)	10	2	3	15	2	2		13	1	3		2	11	1
Phenotypes and Genotypes of Parental (C57BL/6J and C3H/HeJ) and of BXH RI Strains	Lesion scores	"Genetic evidence for a common pathway mediating oxidative stress, inflammatory gene induction, and aortic fatty streak formation in mice."	"In a previous survey of inbred mouse strains on an atherogenic diet, we observed that the susceptibility to aortic atherosclerotic lesion formation was associated with the accumulation of lipid peroxidation products, induction of inflammatory genes, and the activation of NF-kB-like transcription factors (Liao, F., A. Andalibi, F. C. deBeer, A. M. Fogelman, and A.J. Lusis. 1993. J. Clin. Invest. 91:2572-2579). We hypothesized that the inflammation-related processes were stimulated by oxidized lipids, since injection of minimally oxidized LDL (MM-LDL) activated the same set of genes. We now report that the induction of inflammatory genes and activation of NF-kB-like transcription factors cosegregate with aortic atherosclerotic lesion formation in BXH recombinant inbred strains derived from parental C57BL/6J (susceptible) and C3H/HeJ (resistant) mice. In addition, the accumulation of hepatic conjugated dienes exhibited a significant correlation with inflammatory gene activation. These results provide strong evidence for the role of inflammatory mediators inducible by oxidative stress in atherogenesis. They also suggest that a major gene contributing to aortic lesion development in this mouse model, designated Ath-1, may control either the accumulation of lipid peroxides in tissues or the cellular responses to such lipid peroxides."	J Clin Invest	1994	Aug	"Liao F, Andalibi A, Qiao JH, Allayee H, Fogelman AM, Lusis AJ."	8040344	4 - 6 months	female	3 - 9 animals	mm^3/section	"13,749"	673		"2,496"	473	563	665	"24,365"	250	"1,831"	"7,374"		"3,406"	"13,080"
Phenotypes and Genotypes of Parental (C57BL/6J and C3H/HeJ) and of BXH RI Strains	SAA units	"Genetic evidence for a common pathway mediating oxidative stress, inflammatory gene induction, and aortic fatty streak formation in mice."	"In a previous survey of inbred mouse strains on an atherogenic diet, we observed that the susceptibility to aortic atherosclerotic lesion formation was associated with the accumulation of lipid peroxidation products, induction of inflammatory genes, and the activation of NF-kB-like transcription factors (Liao, F., A. Andalibi, F. C. deBeer, A. M. Fogelman, and A.J. Lusis. 1993. J. Clin. Invest. 91:2572-2579). We hypothesized that the inflammation-related processes were stimulated by oxidized lipids, since injection of minimally oxidized LDL (MM-LDL) activated the same set of genes. We now report that the induction of inflammatory genes and activation of NF-kB-like transcription factors cosegregate with aortic atherosclerotic lesion formation in BXH recombinant inbred strains derived from parental C57BL/6J (susceptible) and C3H/HeJ (resistant) mice. In addition, the accumulation of hepatic conjugated dienes exhibited a significant correlation with inflammatory gene activation. These results provide strong evidence for the role of inflammatory mediators inducible by oxidative stress in atherogenesis. They also suggest that a major gene contributing to aortic lesion development in this mouse model, designated Ath-1, may control either the accumulation of lipid peroxides in tissues or the cellular responses to such lipid peroxides."	J Clin Invest	1994	Aug	"Liao F, Andalibi A, Qiao JH, Allayee H, Fogelman AM, Lusis AJ."	8040344	4 - 6 months	female	3 - 9 animals	Densitometric units of particular mRNAs normalized to those of 18S rRNA mRNA	15.7	3.4		6	5.3	5.4	3	8.5	1.9	3.8	12		5.5	7.4
Phenotypes and Genotypes of Parental (C57BL/6J and C3H/HeJ) and of BXH RI Strains	HO units	"Genetic evidence for a common pathway mediating oxidative stress, inflammatory gene induction, and aortic fatty streak formation in mice."	"In a previous survey of inbred mouse strains on an atherogenic diet, we observed that the susceptibility to aortic atherosclerotic lesion formation was associated with the accumulation of lipid peroxidation products, induction of inflammatory genes, and the activation of NF-kB-like transcription factors (Liao, F., A. Andalibi, F. C. deBeer, A. M. Fogelman, and A.J. Lusis. 1993. J. Clin. Invest. 91:2572-2579). We hypothesized that the inflammation-related processes were stimulated by oxidized lipids, since injection of minimally oxidized LDL (MM-LDL) activated the same set of genes. We now report that the induction of inflammatory genes and activation of NF-kB-like transcription factors cosegregate with aortic atherosclerotic lesion formation in BXH recombinant inbred strains derived from parental C57BL/6J (susceptible) and C3H/HeJ (resistant) mice. In addition, the accumulation of hepatic conjugated dienes exhibited a significant correlation with inflammatory gene activation. These results provide strong evidence for the role of inflammatory mediators inducible by oxidative stress in atherogenesis. They also suggest that a major gene contributing to aortic lesion development in this mouse model, designated Ath-1, may control either the accumulation of lipid peroxides in tissues or the cellular responses to such lipid peroxides."	J Clin Invest	1994	Aug	"Liao F, Andalibi A, Qiao JH, Allayee H, Fogelman AM, Lusis AJ."	8040344	4 - 6 months	female	3 - 9 animals	Densitometric units of particular mRNAs normalized to those of 18S rRNA mRNA	3.2	1.5		2	0.9	3	1.5	5.3	0.4	2.2	5.9		1.1	1.4
Phenotypes and Genotypes of Parental (C57BL/6J and C3H/HeJ) and of BXH RI Strains	apo A-IV units	"Genetic evidence for a common pathway mediating oxidative stress, inflammatory gene induction, and aortic fatty streak formation in mice."	"In a previous survey of inbred mouse strains on an atherogenic diet, we observed that the susceptibility to aortic atherosclerotic lesion formation was associated with the accumulation of lipid peroxidation products, induction of inflammatory genes, and the activation of NF-kB-like transcription factors (Liao, F., A. Andalibi, F. C. deBeer, A. M. Fogelman, and A.J. Lusis. 1993. J. Clin. Invest. 91:2572-2579). We hypothesized that the inflammation-related processes were stimulated by oxidized lipids, since injection of minimally oxidized LDL (MM-LDL) activated the same set of genes. We now report that the induction of inflammatory genes and activation of NF-kB-like transcription factors cosegregate with aortic atherosclerotic lesion formation in BXH recombinant inbred strains derived from parental C57BL/6J (susceptible) and C3H/HeJ (resistant) mice. In addition, the accumulation of hepatic conjugated dienes exhibited a significant correlation with inflammatory gene activation. These results provide strong evidence for the role of inflammatory mediators inducible by oxidative stress in atherogenesis. They also suggest that a major gene contributing to aortic lesion development in this mouse model, designated Ath-1, may control either the accumulation of lipid peroxides in tissues or the cellular responses to such lipid peroxides."	J Clin Invest	1994	Aug	"Liao F, Andalibi A, Qiao JH, Allayee H, Fogelman AM, Lusis AJ."	8040344	4 - 6 months	female	3 - 9 animals	Densitometric units of particular mRNAs normalized to those of 18S rRNA mRNA				2.7	3.8	7.8	5	7	5.8	4.2	3.9		4	3.9
Phenotypes and Genotypes of Parental (C57BL/6J and C3H/HeJ) and of BXH RI Strains	Nf-kB-like	"Genetic evidence for a common pathway mediating oxidative stress, inflammatory gene induction, and aortic fatty streak formation in mice."	"In a previous survey of inbred mouse strains on an atherogenic diet, we observed that the susceptibility to aortic atherosclerotic lesion formation was associated with the accumulation of lipid peroxidation products, induction of inflammatory genes, and the activation of NF-kB-like transcription factors (Liao, F., A. Andalibi, F. C. deBeer, A. M. Fogelman, and A.J. Lusis. 1993. J. Clin. Invest. 91:2572-2579). We hypothesized that the inflammation-related processes were stimulated by oxidized lipids, since injection of minimally oxidized LDL (MM-LDL) activated the same set of genes. We now report that the induction of inflammatory genes and activation of NF-kB-like transcription factors cosegregate with aortic atherosclerotic lesion formation in BXH recombinant inbred strains derived from parental C57BL/6J (susceptible) and C3H/HeJ (resistant) mice. In addition, the accumulation of hepatic conjugated dienes exhibited a significant correlation with inflammatory gene activation. These results provide strong evidence for the role of inflammatory mediators inducible by oxidative stress in atherogenesis. They also suggest that a major gene contributing to aortic lesion development in this mouse model, designated Ath-1, may control either the accumulation of lipid peroxides in tissues or the cellular responses to such lipid peroxides."	J Clin Invest	1994	Aug	"Liao F, Andalibi A, Qiao JH, Allayee H, Fogelman AM, Lusis AJ."	8040344	4 - 6 months	female	3 - 9 animals	Denitometric units of shifted radioactive-labeled olgonucleotide bands on mobility shift assays	840	20		126	47	23	232	786	20	59	1425		76	286
Phenotypes and Genotypes of Parental (C57BL/6J and C3H/HeJ) and of BXH RI Strains	Conjugated dienes	"Genetic evidence for a common pathway mediating oxidative stress, inflammatory gene induction, and aortic fatty streak formation in mice."	"In a previous survey of inbred mouse strains on an atherogenic diet, we observed that the susceptibility to aortic atherosclerotic lesion formation was associated with the accumulation of lipid peroxidation products, induction of inflammatory genes, and the activation of NF-kB-like transcription factors (Liao, F., A. Andalibi, F. C. deBeer, A. M. Fogelman, and A.J. Lusis. 1993. J. Clin. Invest. 91:2572-2579). We hypothesized that the inflammation-related processes were stimulated by oxidized lipids, since injection of minimally oxidized LDL (MM-LDL) activated the same set of genes. We now report that the induction of inflammatory genes and activation of NF-kB-like transcription factors cosegregate with aortic atherosclerotic lesion formation in BXH recombinant inbred strains derived from parental C57BL/6J (susceptible) and C3H/HeJ (resistant) mice. In addition, the accumulation of hepatic conjugated dienes exhibited a significant correlation with inflammatory gene activation. These results provide strong evidence for the role of inflammatory mediators inducible by oxidative stress in atherogenesis. They also suggest that a major gene contributing to aortic lesion development in this mouse model, designated Ath-1, may control either the accumulation of lipid peroxides in tissues or the cellular responses to such lipid peroxides."	J Clin Invest	1994	Aug	"Liao F, Andalibi A, Qiao JH, Allayee H, Fogelman AM, Lusis AJ."	8040344	4 - 6 months	female	3 - 9 animals	Conjugated dienes in the liver tissue (mmol/g net weight)	1250	564		1148	1166	1075	829	1431	682	680	1954		280	654
Phenotypes and Genotypes of Parental (C57BL/6J and C3H/HeJ) and of BXH RI Strains	Lps allele	"Genetic evidence for a common pathway mediating oxidative stress, inflammatory gene induction, and aortic fatty streak formation in mice."	"In a previous survey of inbred mouse strains on an atherogenic diet, we observed that the susceptibility to aortic atherosclerotic lesion formation was associated with the accumulation of lipid peroxidation products, induction of inflammatory genes, and the activation of NF-kB-like transcription factors (Liao, F., A. Andalibi, F. C. deBeer, A. M. Fogelman, and A.J. Lusis. 1993. J. Clin. Invest. 91:2572-2579). We hypothesized that the inflammation-related processes were stimulated by oxidized lipids, since injection of minimally oxidized LDL (MM-LDL) activated the same set of genes. We now report that the induction of inflammatory genes and activation of NF-kB-like transcription factors cosegregate with aortic atherosclerotic lesion formation in BXH recombinant inbred strains derived from parental C57BL/6J (susceptible) and C3H/HeJ (resistant) mice. In addition, the accumulation of hepatic conjugated dienes exhibited a significant correlation with inflammatory gene activation. These results provide strong evidence for the role of inflammatory mediators inducible by oxidative stress in atherogenesis. They also suggest that a major gene contributing to aortic lesion development in this mouse model, designated Ath-1, may control either the accumulation of lipid peroxides in tissues or the cellular responses to such lipid peroxides."	J Clin Invest	1994	Aug	"Liao F, Andalibi A, Qiao JH, Allayee H, Fogelman AM, Lusis AJ."	8040344	4 - 6 months	female	3 - 9 animals	B = inherited from C57BL/6J; H = inherited from C3H/HeJ	B	H		H	H	H	H	H	H	B	B		B	B
SDP of MMTV proviral loci in the BXH RI strain set	"Mtv-1, 7"	Segregation patterns of endogenous mouse mammary tumor viruses in five recombinant inbred strain sets.	"We identified mouse mammary tumor proviral loci in the AKR/J, C3H/HeJ, C57BL/6J, C57L/J, DBA/2J, and SWR/J inbred mouse strains and determined their segregation patterns in the AKXD, AKXL, BXD, BXH, and SWXL recombinant inbred strain sets. Two new Mtv loci, Mtv-29 and Mtv-30, were identified. Mtv-30 was genetically mapped to chromosome 12. Additionally, two previously identified Mtv loci, Mtv-14 and Mtv-23, were genetically mapped to chromosome 4 and chromosome 6, respectively."	J Virol	1990	Sept	"Lee BK, Eicher EM."	2166832				B = C57BL/6J; H =C3H/HeJ			H	H	H	H	B	H	B	H	H	H	H	H
SDP of MMTV proviral loci in the BXH RI strain set	"Mtv6, 16"	Segregation patterns of endogenous mouse mammary tumor viruses in five recombinant inbred strain sets.	"We identified mouse mammary tumor proviral loci in the AKR/J, C3H/HeJ, C57BL/6J, C57L/J, DBA/2J, and SWR/J inbred mouse strains and determined their segregation patterns in the AKXD, AKXL, BXD, BXH, and SWXL recombinant inbred strain sets. Two new Mtv loci, Mtv-29 and Mtv-30, were identified. Mtv-30 was genetically mapped to chromosome 12. Additionally, two previously identified Mtv loci, Mtv-14 and Mtv-23, were genetically mapped to chromosome 4 and chromosome 6, respectively."	J Virol	1990	Sept	"Lee BK, Eicher EM."	2166832				B = C57BL/6J; H =C3H/HeJ			B	B	H	H	B	H	B	B	H	H	B	H
SDP of MMTV proviral loci in the BXH RI strain set	"Mtv9, 12"	Segregation patterns of endogenous mouse mammary tumor viruses in five recombinant inbred strain sets.	"We identified mouse mammary tumor proviral loci in the AKR/J, C3H/HeJ, C57BL/6J, C57L/J, DBA/2J, and SWR/J inbred mouse strains and determined their segregation patterns in the AKXD, AKXL, BXD, BXH, and SWXL recombinant inbred strain sets. Two new Mtv loci, Mtv-29 and Mtv-30, were identified. Mtv-30 was genetically mapped to chromosome 12. Additionally, two previously identified Mtv loci, Mtv-14 and Mtv-23, were genetically mapped to chromosome 4 and chromosome 6, respectively."	J Virol	1990	Sept	"Lee BK, Eicher EM."	2166832				B = C57BL/6J; H =C3H/HeJ			B	B	B	B	H	B	H	H	B	H	H	H
SDP of MMTV proviral loci in the BXH RI strain set	"Mtv11, 14"	Segregation patterns of endogenous mouse mammary tumor viruses in five recombinant inbred strain sets.	"We identified mouse mammary tumor proviral loci in the AKR/J, C3H/HeJ, C57BL/6J, C57L/J, DBA/2J, and SWR/J inbred mouse strains and determined their segregation patterns in the AKXD, AKXL, BXD, BXH, and SWXL recombinant inbred strain sets. Two new Mtv loci, Mtv-29 and Mtv-30, were identified. Mtv-30 was genetically mapped to chromosome 12. Additionally, two previously identified Mtv loci, Mtv-14 and Mtv-23, were genetically mapped to chromosome 4 and chromosome 6, respectively."	J Virol	1990	Sept	"Lee BK, Eicher EM."	2166832				B = C57BL/6J; H =C3H/HeJ			H	B	H	B	B	B	B	B	H	H	H	H
SDP of MMTV proviral loci in the BXH RI strain set	"Mtv14, 4"	Segregation patterns of endogenous mouse mammary tumor viruses in five recombinant inbred strain sets.	"We identified mouse mammary tumor proviral loci in the AKR/J, C3H/HeJ, C57BL/6J, C57L/J, DBA/2J, and SWR/J inbred mouse strains and determined their segregation patterns in the AKXD, AKXL, BXD, BXH, and SWXL recombinant inbred strain sets. Two new Mtv loci, Mtv-29 and Mtv-30, were identified. Mtv-30 was genetically mapped to chromosome 12. Additionally, two previously identified Mtv loci, Mtv-14 and Mtv-23, were genetically mapped to chromosome 4 and chromosome 6, respectively."	J Virol	1990	Sept	"Lee BK, Eicher EM."	2166832				B = C57BL/6J; H =C3H/HeJ			B	B	B	H	H	H	B	B	H	H	B	B
SDP of MMTV proviral loci in the BXH RI strain set	"Mtv17, 4"	Segregation patterns of endogenous mouse mammary tumor viruses in five recombinant inbred strain sets.	"We identified mouse mammary tumor proviral loci in the AKR/J, C3H/HeJ, C57BL/6J, C57L/J, DBA/2J, and SWR/J inbred mouse strains and determined their segregation patterns in the AKXD, AKXL, BXD, BXH, and SWXL recombinant inbred strain sets. Two new Mtv loci, Mtv-29 and Mtv-30, were identified. Mtv-30 was genetically mapped to chromosome 12. Additionally, two previously identified Mtv loci, Mtv-14 and Mtv-23, were genetically mapped to chromosome 4 and chromosome 6, respectively."	J Virol	1990	Sept	"Lee BK, Eicher EM."	2166832				B = C57BL/6J; H =C3H/HeJ			B	H	B	H	H	H	B	H	B	H	H	B
"Inheritance of EcoRV apoB gene polymorphism, LDL size polymorphism, and other chromosome 12 markers"	LDL size	Genetic heterogeneity of plasma lipoproteins in the mouse: control of low density lipoprotein particle sizes by genetic factors.	"In order to assess the genetic control of sizes and concentrations of mouse plasma low density (LDL) and high density lipoproteins (HDL), we used gel permeation fast protein liquid chromatography (FPLC) and nondenaturing gradient polyacrylamide gel electrophoresis to measure the particle sizes of LDL and HDL. Using chromatography we also quantified LDL-cholesterol and HDL-cholesterol concentrations in plasma and used them as indexes of plasma concentrations of the respective particles among 10 inbred strains (AKR/J, BALB/cByJ, C3H/HeJ, C57BL/6J, C57BL/6ByJ, C57L/J, DBA/1LacJ, 129/J, NZB/BINJ, SWR/J) and three sets of recombinant inbred (RI) strains (AKXL/TyJ, BXH/TyJ, CXB/ByJ) of mice. HDL had a dichotomous distribution among the 10 inbred strains. One group had large HDL particle sizes and high HDL-cholesterol concentrations. Another group had smaller HDL particles and lower HDL-cholesterol concentrations, and HDL sizes and HDL-cholesterol concentrations were significantly correlated. In the RI strains, HDL sizes and HDL-cholesterol cholesterol concentrations clearly segregated with one or another of the progenitor strains, and RI strain distributions showed a strong linkage to the apolipoprotein (apo) A-II gene (Apoa-2). In contrast, LDL-cholesterol concentrations and particle sizes on FPLC did not show dichotomous distributions among the 10 inbred strains. In RI strains, the configuration of the LDL FPLC profiles and LDL-cholesterol concentrations did resemble one or another of the progenitors in the majority of cases, but LDLs of several RI strains resembled neither progenitor strain in profile configuration, and LDL-cholesterol concentrations were both greater and smaller than those of progenitor strains. However, LDL particle diameters (as judged by peaks of LDL-cholesterol profiles) did segregate with progenitors in 29/33 (88%) of RI strains suggesting that a major gene may affect LDL size. In attempting to identify a major LDL-size determining gene, we compared apoB gene restriction fragment length polymorphisms (RFLPs) to the distributions of peak LDL sizes in RI strains. Concordance rates of peak LDL sizes to apoB gene polymorphisms were 18/22 (82%) for the EcoRV RFLP, 5/7 (71%) for HindIII RFLP, and 23/29 (79%) for both (range of P values 0.90-0.95). Thus we could not unequivocally implicate the apoB gene in determining the size of LDL particles. In summary, the genetic control of LDL sizes is more complicated than is the case for HDL; however, the differences in LDL size among these strains of mice may be controlled by a major, as yet unidentified, gene."	 J Lipid Res	1990	Mar	"Jiao S, Cole TG, Kitchens RT, Pfleger B, Schonfeld G."	1971301	8 - 10 weeks	female		B = C57BL/6J; H =C3H/HeJ			B	B	H	H	H	B	H				H	B
"Inheritance of EcoRV apoB gene polymorphism, LDL size polymorphism, and other chromosome 12 markers"	Rnr - 12	Genetic heterogeneity of plasma lipoproteins in the mouse: control of low density lipoprotein particle sizes by genetic factors.	"In order to assess the genetic control of sizes and concentrations of mouse plasma low density (LDL) and high density lipoproteins (HDL), we used gel permeation fast protein liquid chromatography (FPLC) and nondenaturing gradient polyacrylamide gel electrophoresis to measure the particle sizes of LDL and HDL. Using chromatography we also quantified LDL-cholesterol and HDL-cholesterol concentrations in plasma and used them as indexes of plasma concentrations of the respective particles among 10 inbred strains (AKR/J, BALB/cByJ, C3H/HeJ, C57BL/6J, C57BL/6ByJ, C57L/J, DBA/1LacJ, 129/J, NZB/BINJ, SWR/J) and three sets of recombinant inbred (RI) strains (AKXL/TyJ, BXH/TyJ, CXB/ByJ) of mice. HDL had a dichotomous distribution among the 10 inbred strains. One group had large HDL particle sizes and high HDL-cholesterol concentrations. Another group had smaller HDL particles and lower HDL-cholesterol concentrations, and HDL sizes and HDL-cholesterol concentrations were significantly correlated. In the RI strains, HDL sizes and HDL-cholesterol cholesterol concentrations clearly segregated with one or another of the progenitor strains, and RI strain distributions showed a strong linkage to the apolipoprotein (apo) A-II gene (Apoa-2). In contrast, LDL-cholesterol concentrations and particle sizes on FPLC did not show dichotomous distributions among the 10 inbred strains. In RI strains, the configuration of the LDL FPLC profiles and LDL-cholesterol concentrations did resemble one or another of the progenitors in the majority of cases, but LDLs of several RI strains resembled neither progenitor strain in profile configuration, and LDL-cholesterol concentrations were both greater and smaller than those of progenitor strains. However, LDL particle diameters (as judged by peaks of LDL-cholesterol profiles) did segregate with progenitors in 29/33 (88%) of RI strains suggesting that a major gene may affect LDL size. In attempting to identify a major LDL-size determining gene, we compared apoB gene restriction fragment length polymorphisms (RFLPs) to the distributions of peak LDL sizes in RI strains. Concordance rates of peak LDL sizes to apoB gene polymorphisms were 18/22 (82%) for the EcoRV RFLP, 5/7 (71%) for HindIII RFLP, and 23/29 (79%) for both (range of P values 0.90-0.95). Thus we could not unequivocally implicate the apoB gene in determining the size of LDL particles. In summary, the genetic control of LDL sizes is more complicated than is the case for HDL; however, the differences in LDL size among these strains of mice may be controlled by a major, as yet unidentified, gene."	 J Lipid Res	1990	Mar	"Jiao S, Cole TG, Kitchens RT, Pfleger B, Schonfeld G."	1971301	8 - 10 weeks	female		B = C57BL/6J; H =C3H/HeJ			B	B	B	H	H	B	H				H	H
"Inheritance of EcoRV apoB gene polymorphism, LDL size polymorphism, and other chromosome 12 markers"	Apob	Genetic heterogeneity of plasma lipoproteins in the mouse: control of low density lipoprotein particle sizes by genetic factors.	"In order to assess the genetic control of sizes and concentrations of mouse plasma low density (LDL) and high density lipoproteins (HDL), we used gel permeation fast protein liquid chromatography (FPLC) and nondenaturing gradient polyacrylamide gel electrophoresis to measure the particle sizes of LDL and HDL. Using chromatography we also quantified LDL-cholesterol and HDL-cholesterol concentrations in plasma and used them as indexes of plasma concentrations of the respective particles among 10 inbred strains (AKR/J, BALB/cByJ, C3H/HeJ, C57BL/6J, C57BL/6ByJ, C57L/J, DBA/1LacJ, 129/J, NZB/BINJ, SWR/J) and three sets of recombinant inbred (RI) strains (AKXL/TyJ, BXH/TyJ, CXB/ByJ) of mice. HDL had a dichotomous distribution among the 10 inbred strains. One group had large HDL particle sizes and high HDL-cholesterol concentrations. Another group had smaller HDL particles and lower HDL-cholesterol concentrations, and HDL sizes and HDL-cholesterol concentrations were significantly correlated. In the RI strains, HDL sizes and HDL-cholesterol cholesterol concentrations clearly segregated with one or another of the progenitor strains, and RI strain distributions showed a strong linkage to the apolipoprotein (apo) A-II gene (Apoa-2). In contrast, LDL-cholesterol concentrations and particle sizes on FPLC did not show dichotomous distributions among the 10 inbred strains. In RI strains, the configuration of the LDL FPLC profiles and LDL-cholesterol concentrations did resemble one or another of the progenitors in the majority of cases, but LDLs of several RI strains resembled neither progenitor strain in profile configuration, and LDL-cholesterol concentrations were both greater and smaller than those of progenitor strains. However, LDL particle diameters (as judged by peaks of LDL-cholesterol profiles) did segregate with progenitors in 29/33 (88%) of RI strains suggesting that a major gene may affect LDL size. In attempting to identify a major LDL-size determining gene, we compared apoB gene restriction fragment length polymorphisms (RFLPs) to the distributions of peak LDL sizes in RI strains. Concordance rates of peak LDL sizes to apoB gene polymorphisms were 18/22 (82%) for the EcoRV RFLP, 5/7 (71%) for HindIII RFLP, and 23/29 (79%) for both (range of P values 0.90-0.95). Thus we could not unequivocally implicate the apoB gene in determining the size of LDL particles. In summary, the genetic control of LDL sizes is more complicated than is the case for HDL; however, the differences in LDL size among these strains of mice may be controlled by a major, as yet unidentified, gene."	 J Lipid Res	1990	Mar	"Jiao S, Cole TG, Kitchens RT, Pfleger B, Schonfeld G."	1971301	8 - 10 weeks	female		B = C57BL/6J; H =C3H/HeJ			B	B	B	H	H	B	H				H	H
"Inheritance of EcoRV apoB gene polymorphism, LDL size polymorphism, and other chromosome 12 markers"	D12 Nyu2	Genetic heterogeneity of plasma lipoproteins in the mouse: control of low density lipoprotein particle sizes by genetic factors.	"In order to assess the genetic control of sizes and concentrations of mouse plasma low density (LDL) and high density lipoproteins (HDL), we used gel permeation fast protein liquid chromatography (FPLC) and nondenaturing gradient polyacrylamide gel electrophoresis to measure the particle sizes of LDL and HDL. Using chromatography we also quantified LDL-cholesterol and HDL-cholesterol concentrations in plasma and used them as indexes of plasma concentrations of the respective particles among 10 inbred strains (AKR/J, BALB/cByJ, C3H/HeJ, C57BL/6J, C57BL/6ByJ, C57L/J, DBA/1LacJ, 129/J, NZB/BINJ, SWR/J) and three sets of recombinant inbred (RI) strains (AKXL/TyJ, BXH/TyJ, CXB/ByJ) of mice. HDL had a dichotomous distribution among the 10 inbred strains. One group had large HDL particle sizes and high HDL-cholesterol concentrations. Another group had smaller HDL particles and lower HDL-cholesterol concentrations, and HDL sizes and HDL-cholesterol concentrations were significantly correlated. In the RI strains, HDL sizes and HDL-cholesterol cholesterol concentrations clearly segregated with one or another of the progenitor strains, and RI strain distributions showed a strong linkage to the apolipoprotein (apo) A-II gene (Apoa-2). In contrast, LDL-cholesterol concentrations and particle sizes on FPLC did not show dichotomous distributions among the 10 inbred strains. In RI strains, the configuration of the LDL FPLC profiles and LDL-cholesterol concentrations did resemble one or another of the progenitors in the majority of cases, but LDLs of several RI strains resembled neither progenitor strain in profile configuration, and LDL-cholesterol concentrations were both greater and smaller than those of progenitor strains. However, LDL particle diameters (as judged by peaks of LDL-cholesterol profiles) did segregate with progenitors in 29/33 (88%) of RI strains suggesting that a major gene may affect LDL size. In attempting to identify a major LDL-size determining gene, we compared apoB gene restriction fragment length polymorphisms (RFLPs) to the distributions of peak LDL sizes in RI strains. Concordance rates of peak LDL sizes to apoB gene polymorphisms were 18/22 (82%) for the EcoRV RFLP, 5/7 (71%) for HindIII RFLP, and 23/29 (79%) for both (range of P values 0.90-0.95). Thus we could not unequivocally implicate the apoB gene in determining the size of LDL particles. In summary, the genetic control of LDL sizes is more complicated than is the case for HDL; however, the differences in LDL size among these strains of mice may be controlled by a major, as yet unidentified, gene."	 J Lipid Res	1990	Mar	"Jiao S, Cole TG, Kitchens RT, Pfleger B, Schonfeld G."	1971301	8 - 10 weeks	female		B = C57BL/6J; H =C3H/HeJ			B	B	B	H	H	B	H				H	H
"Inheritance of EcoRV apoB gene polymorphism, LDL size polymorphism, and other chromosome 12 markers"	Ly- 18	Genetic heterogeneity of plasma lipoproteins in the mouse: control of low density lipoprotein particle sizes by genetic factors.	"In order to assess the genetic control of sizes and concentrations of mouse plasma low density (LDL) and high density lipoproteins (HDL), we used gel permeation fast protein liquid chromatography (FPLC) and nondenaturing gradient polyacrylamide gel electrophoresis to measure the particle sizes of LDL and HDL. Using chromatography we also quantified LDL-cholesterol and HDL-cholesterol concentrations in plasma and used them as indexes of plasma concentrations of the respective particles among 10 inbred strains (AKR/J, BALB/cByJ, C3H/HeJ, C57BL/6J, C57BL/6ByJ, C57L/J, DBA/1LacJ, 129/J, NZB/BINJ, SWR/J) and three sets of recombinant inbred (RI) strains (AKXL/TyJ, BXH/TyJ, CXB/ByJ) of mice. HDL had a dichotomous distribution among the 10 inbred strains. One group had large HDL particle sizes and high HDL-cholesterol concentrations. Another group had smaller HDL particles and lower HDL-cholesterol concentrations, and HDL sizes and HDL-cholesterol concentrations were significantly correlated. In the RI strains, HDL sizes and HDL-cholesterol cholesterol concentrations clearly segregated with one or another of the progenitor strains, and RI strain distributions showed a strong linkage to the apolipoprotein (apo) A-II gene (Apoa-2). In contrast, LDL-cholesterol concentrations and particle sizes on FPLC did not show dichotomous distributions among the 10 inbred strains. In RI strains, the configuration of the LDL FPLC profiles and LDL-cholesterol concentrations did resemble one or another of the progenitors in the majority of cases, but LDLs of several RI strains resembled neither progenitor strain in profile configuration, and LDL-cholesterol concentrations were both greater and smaller than those of progenitor strains. However, LDL particle diameters (as judged by peaks of LDL-cholesterol profiles) did segregate with progenitors in 29/33 (88%) of RI strains suggesting that a major gene may affect LDL size. In attempting to identify a major LDL-size determining gene, we compared apoB gene restriction fragment length polymorphisms (RFLPs) to the distributions of peak LDL sizes in RI strains. Concordance rates of peak LDL sizes to apoB gene polymorphisms were 18/22 (82%) for the EcoRV RFLP, 5/7 (71%) for HindIII RFLP, and 23/29 (79%) for both (range of P values 0.90-0.95). Thus we could not unequivocally implicate the apoB gene in determining the size of LDL particles. In summary, the genetic control of LDL sizes is more complicated than is the case for HDL; however, the differences in LDL size among these strains of mice may be controlled by a major, as yet unidentified, gene."	 J Lipid Res	1990	Mar	"Jiao S, Cole TG, Kitchens RT, Pfleger B, Schonfeld G."	1971301	8 - 10 weeks	female		B = C57BL/6J; H =C3H/HeJ			B	B	B	B	H	B	H				H	H
Mitogenic and adjuvant responses to LPS in BXH recombinant inbred strains	Mitogenic Response: No LPS	The response of recombinant inbred strains of mice to bacterial lipopolysaccharides.	"Fourteen recombinant inbred strains of mice have been produced by the inbreeding of the F2 generation of a cross between C57BL/6J and C3H/HeJ progenitor mice. The responses of these BXH strains to bacterial lipopolysaccharides (LPS) have been characterized. Four BXH strains are high LPS responders and nine strains are low LPS responders. One BXH strain shows intermediate responsiveness which may reflect residual heterozygosity. F1 hybrid mice from low x high responder strains were intermediate in their response to LPS suggesting additive genetic control. The LPS responses in backcross mice from the F1 x low LPS responders showed segregation consistent with LPS responsiveness being determined by a single gene. In 13/14 BXH strains, there was concordant inheritance of LPS responsiveness and the major urinary protein locus Mup-1b. The association of the expression of the Mup-1 alleles with LPS responsiveness in the BXH strains suggests that the defective LPS response gene in C3H/HeJ mice is located on chromosome 4."	J Immunol	1977	June	"Watson J, Riblet R, Taylor BA."	325138	6 - 12 weeks	both		cpm x10^-3	4.7	4.4	1.1	1.1	3.7	3.3	2.2	1.2	3.7	3.3	2.2	2.8	3.9	3.5
Mitogenic and adjuvant responses to LPS in BXH recombinant inbred strains	Mitogenic Response:  5 micrograms	The response of recombinant inbred strains of mice to bacterial lipopolysaccharides.	"Fourteen recombinant inbred strains of mice have been produced by the inbreeding of the F2 generation of a cross between C57BL/6J and C3H/HeJ progenitor mice. The responses of these BXH strains to bacterial lipopolysaccharides (LPS) have been characterized. Four BXH strains are high LPS responders and nine strains are low LPS responders. One BXH strain shows intermediate responsiveness which may reflect residual heterozygosity. F1 hybrid mice from low x high responder strains were intermediate in their response to LPS suggesting additive genetic control. The LPS responses in backcross mice from the F1 x low LPS responders showed segregation consistent with LPS responsiveness being determined by a single gene. In 13/14 BXH strains, there was concordant inheritance of LPS responsiveness and the major urinary protein locus Mup-1b. The association of the expression of the Mup-1 alleles with LPS responsiveness in the BXH strains suggests that the defective LPS response gene in C3H/HeJ mice is located on chromosome 4."	J Immunol	1977	June	"Watson J, Riblet R, Taylor BA."	325138	6 - 12 weeks	both		cpm x10^-3	17.8	4.7	2.8	2.2	5.7	4.1	2.3	1.5	4	7.2	22	4.8	21.1	11.7
Mitogenic and adjuvant responses to LPS in BXH recombinant inbred strains	Mitogenic Response: 25 micrograms	The response of recombinant inbred strains of mice to bacterial lipopolysaccharides.	"Fourteen recombinant inbred strains of mice have been produced by the inbreeding of the F2 generation of a cross between C57BL/6J and C3H/HeJ progenitor mice. The responses of these BXH strains to bacterial lipopolysaccharides (LPS) have been characterized. Four BXH strains are high LPS responders and nine strains are low LPS responders. One BXH strain shows intermediate responsiveness which may reflect residual heterozygosity. F1 hybrid mice from low x high responder strains were intermediate in their response to LPS suggesting additive genetic control. The LPS responses in backcross mice from the F1 x low LPS responders showed segregation consistent with LPS responsiveness being determined by a single gene. In 13/14 BXH strains, there was concordant inheritance of LPS responsiveness and the major urinary protein locus Mup-1b. The association of the expression of the Mup-1 alleles with LPS responsiveness in the BXH strains suggests that the defective LPS response gene in C3H/HeJ mice is located on chromosome 4."	J Immunol	1977	June	"Watson J, Riblet R, Taylor BA."	325138	6 - 12 weeks	both		cpm x10^-3	51.5	5.6	5.1	3.1	8.3	4.5	3	2.5	5.3	8.1	43.1	5.6	46.6	44.5
Mitogenic and adjuvant responses to LPS in BXH recombinant inbred strains	Serum Titers	The response of recombinant inbred strains of mice to bacterial lipopolysaccharides.	"Fourteen recombinant inbred strains of mice have been produced by the inbreeding of the F2 generation of a cross between C57BL/6J and C3H/HeJ progenitor mice. The responses of these BXH strains to bacterial lipopolysaccharides (LPS) have been characterized. Four BXH strains are high LPS responders and nine strains are low LPS responders. One BXH strain shows intermediate responsiveness which may reflect residual heterozygosity. F1 hybrid mice from low x high responder strains were intermediate in their response to LPS suggesting additive genetic control. The LPS responses in backcross mice from the F1 x low LPS responders showed segregation consistent with LPS responsiveness being determined by a single gene. In 13/14 BXH strains, there was concordant inheritance of LPS responsiveness and the major urinary protein locus Mup-1b. The association of the expression of the Mup-1 alleles with LPS responsiveness in the BXH strains suggests that the defective LPS response gene in C3H/HeJ mice is located on chromosome 4."	J Immunol	1977	June	"Watson J, Riblet R, Taylor BA."	325138	6 - 12 weeks	both		"The first number represents the titer if the prebleed serum, and the second represents the titer 7 days after immunization.  the seurm are presented as a reciprocal of the endpoint dilution.  The initial dilution was always 1/10"	<10 / 10	<10 / 1280	<10/ 10	<10 / 20	20-Oct	<10 / 40	Oct-80	<10/ 10	<10/ 10	Oct-80	10/ 320	<10/ 10	10/ 1280	10/ 320
Mitogenic and adjuvant responses to LPS in BXH recombinant inbred strains	LPS Response 	The response of recombinant inbred strains of mice to bacterial lipopolysaccharides.	"Fourteen recombinant inbred strains of mice have been produced by the inbreeding of the F2 generation of a cross between C57BL/6J and C3H/HeJ progenitor mice. The responses of these BXH strains to bacterial lipopolysaccharides (LPS) have been characterized. Four BXH strains are high LPS responders and nine strains are low LPS responders. One BXH strain shows intermediate responsiveness which may reflect residual heterozygosity. F1 hybrid mice from low x high responder strains were intermediate in their response to LPS suggesting additive genetic control. The LPS responses in backcross mice from the F1 x low LPS responders showed segregation consistent with LPS responsiveness being determined by a single gene. In 13/14 BXH strains, there was concordant inheritance of LPS responsiveness and the major urinary protein locus Mup-1b. The association of the expression of the Mup-1 alleles with LPS responsiveness in the BXH strains suggests that the defective LPS response gene in C3H/HeJ mice is located on chromosome 4."	J Immunol	1977	June	"Watson J, Riblet R, Taylor BA."	325138	6 - 12 weeks	both		High/ Low	high	low	low	low	low	low	low	low	low	low	high	low	high	high
Mitogenic and adjuvant responses to LPS in BXH recombinant inbred strains	Generations Tested	The response of recombinant inbred strains of mice to bacterial lipopolysaccharides.	"Fourteen recombinant inbred strains of mice have been produced by the inbreeding of the F2 generation of a cross between C57BL/6J and C3H/HeJ progenitor mice. The responses of these BXH strains to bacterial lipopolysaccharides (LPS) have been characterized. Four BXH strains are high LPS responders and nine strains are low LPS responders. One BXH strain shows intermediate responsiveness which may reflect residual heterozygosity. F1 hybrid mice from low x high responder strains were intermediate in their response to LPS suggesting additive genetic control. The LPS responses in backcross mice from the F1 x low LPS responders showed segregation consistent with LPS responsiveness being determined by a single gene. In 13/14 BXH strains, there was concordant inheritance of LPS responsiveness and the major urinary protein locus Mup-1b. The association of the expression of the Mup-1 alleles with LPS responsiveness in the BXH strains suggests that the defective LPS response gene in C3H/HeJ mice is located on chromosome 4."	J Immunol	1977	June	"Watson J, Riblet R, Taylor BA."	325138	6 - 12 weeks	both					"F14, F23"	"F16, F23"	"F15, F20"	"F15, F22"	F15	"F12, F19"	"F14, F23, F26"	"F15, F19BC4F4, F19BC4F5"	"F15, F23, 28, F29"	F14	"F15, F22, F28"	"F15, F22, F28"
Mitogenic and adjuvant responses to LPS in BXH recombinant inbred strains	H - 2	The response of recombinant inbred strains of mice to bacterial lipopolysaccharides.	"Fourteen recombinant inbred strains of mice have been produced by the inbreeding of the F2 generation of a cross between C57BL/6J and C3H/HeJ progenitor mice. The responses of these BXH strains to bacterial lipopolysaccharides (LPS) have been characterized. Four BXH strains are high LPS responders and nine strains are low LPS responders. One BXH strain shows intermediate responsiveness which may reflect residual heterozygosity. F1 hybrid mice from low x high responder strains were intermediate in their response to LPS suggesting additive genetic control. The LPS responses in backcross mice from the F1 x low LPS responders showed segregation consistent with LPS responsiveness being determined by a single gene. In 13/14 BXH strains, there was concordant inheritance of LPS responsiveness and the major urinary protein locus Mup-1b. The association of the expression of the Mup-1 alleles with LPS responsiveness in the BXH strains suggests that the defective LPS response gene in C3H/HeJ mice is located on chromosome 4."	J Immunol	1977	June	"Watson J, Riblet R, Taylor BA."	325138	6 - 12 weeks	both					k	k	b	k	k	b	b	b	b	k	k	b
Mitogenic and adjuvant responses to LPS in BXH recombinant inbred strains	Ig - 1	The response of recombinant inbred strains of mice to bacterial lipopolysaccharides.	"Fourteen recombinant inbred strains of mice have been produced by the inbreeding of the F2 generation of a cross between C57BL/6J and C3H/HeJ progenitor mice. The responses of these BXH strains to bacterial lipopolysaccharides (LPS) have been characterized. Four BXH strains are high LPS responders and nine strains are low LPS responders. One BXH strain shows intermediate responsiveness which may reflect residual heterozygosity. F1 hybrid mice from low x high responder strains were intermediate in their response to LPS suggesting additive genetic control. The LPS responses in backcross mice from the F1 x low LPS responders showed segregation consistent with LPS responsiveness being determined by a single gene. In 13/14 BXH strains, there was concordant inheritance of LPS responsiveness and the major urinary protein locus Mup-1b. The association of the expression of the Mup-1 alleles with LPS responsiveness in the BXH strains suggests that the defective LPS response gene in C3H/HeJ mice is located on chromosome 4."	J Immunol	1977	June	"Watson J, Riblet R, Taylor BA."	325138	6 - 12 weeks	both					a	b	a	a	a	b	a	b	b	a	b	a
Mitogenic and adjuvant responses to LPS in BXH recombinant inbred strains	Mup - 1	The response of recombinant inbred strains of mice to bacterial lipopolysaccharides.	"Fourteen recombinant inbred strains of mice have been produced by the inbreeding of the F2 generation of a cross between C57BL/6J and C3H/HeJ progenitor mice. The responses of these BXH strains to bacterial lipopolysaccharides (LPS) have been characterized. Four BXH strains are high LPS responders and nine strains are low LPS responders. One BXH strain shows intermediate responsiveness which may reflect residual heterozygosity. F1 hybrid mice from low x high responder strains were intermediate in their response to LPS suggesting additive genetic control. The LPS responses in backcross mice from the F1 x low LPS responders showed segregation consistent with LPS responsiveness being determined by a single gene. In 13/14 BXH strains, there was concordant inheritance of LPS responsiveness and the major urinary protein locus Mup-1b. The association of the expression of the Mup-1 alleles with LPS responsiveness in the BXH strains suggests that the defective LPS response gene in C3H/HeJ mice is located on chromosome 4."	J Immunol	1977	June	"Watson J, Riblet R, Taylor BA."	325138	6 - 12 weeks	both					a	a	a	a	a	a	a	b	b	a	a	b
Mitogenic and adjuvant responses to LPS in BXH recombinant inbred strains	LPS (Responder/ Nonresponder)	The response of recombinant inbred strains of mice to bacterial lipopolysaccharides.	"Fourteen recombinant inbred strains of mice have been produced by the inbreeding of the F2 generation of a cross between C57BL/6J and C3H/HeJ progenitor mice. The responses of these BXH strains to bacterial lipopolysaccharides (LPS) have been characterized. Four BXH strains are high LPS responders and nine strains are low LPS responders. One BXH strain shows intermediate responsiveness which may reflect residual heterozygosity. F1 hybrid mice from low x high responder strains were intermediate in their response to LPS suggesting additive genetic control. The LPS responses in backcross mice from the F1 x low LPS responders showed segregation consistent with LPS responsiveness being determined by a single gene. In 13/14 BXH strains, there was concordant inheritance of LPS responsiveness and the major urinary protein locus Mup-1b. The association of the expression of the Mup-1 alleles with LPS responsiveness in the BXH strains suggests that the defective LPS response gene in C3H/HeJ mice is located on chromosome 4."	J Immunol	1977	June	"Watson J, Riblet R, Taylor BA."	325138	6 - 12 weeks	both		Responder/ nonresponder			NR	NR	NR	NR	NR	NR	NR	R	R	NR	NR	R
Phenotypes and Genotypes of Parental (C57BL/ 6J and C3H/ HeJ) and of BXH Ri strains	Lesion scores	"Genetic evidence for a common pathway mediating oxidative stress, inflammatory gene induction, and aortic fatty streak formation in mice."	"In a previous survey of inbred mouse strains on an atherogenic diet, we observed that the susceptibility to aortic atherosclerotic lesion formation was associated with the accumulation of lipid peroxidation products, induction of inflammatory genes, and the activation of NF-kB-like transcription factors (Liao, F., A. Andalibi, F. C. deBeer, A. M. Fogelman, and A.J. Lusis. 1993. J. Clin. Invest. 91:2572-2579). We hypothesized that the inflammation-related processes were stimulated by oxidized lipids, since injection of minimally oxidized LDL (MM-LDL) activated the same set of genes. We now report that the induction of inflammatory genes and activation of NF-kB-like transcription factors cosegregate with aortic atherosclerotic lesion formation in BXH recombinant inbred strains derived from parental C57BL/6J (susceptible) and C3H/HeJ (resistant) mice. In addition, the accumulation of hepatic conjugated dienes exhibited a significant correlation with inflammatory gene activation. These results provide strong evidence for the role of inflammatory mediators inducible by oxidative stress in atherogenesis. They also suggest that a major gene contributing to aortic lesion development in this mouse model, designated Ath-1, may control either the accumulation of lipid peroxides in tissues or the cellular responses to such lipid peroxides."	J Clin Invest	1994	Aug	"Liao F, Andalibi A, Qiao JH, Allayee H, Fogelman AM, Lusis AJ."	8040344	4 - 6 months	both		um^2/ section	"13,749"	673		"2,496"	473	563	665	"24,365"	250	"1,831"	"7,724"		"3,406"	"13,080"
Phenotypes and Genotypes of Parental (C57BL/ 6J and C3H/ HeJ) and of BXH Ri strains	SAA units	"Genetic evidence for a common pathway mediating oxidative stress, inflammatory gene induction, and aortic fatty streak formation in mice."	"In a previous survey of inbred mouse strains on an atherogenic diet, we observed that the susceptibility to aortic atherosclerotic lesion formation was associated with the accumulation of lipid peroxidation products, induction of inflammatory genes, and the activation of NF-kB-like transcription factors (Liao, F., A. Andalibi, F. C. deBeer, A. M. Fogelman, and A.J. Lusis. 1993. J. Clin. Invest. 91:2572-2579). We hypothesized that the inflammation-related processes were stimulated by oxidized lipids, since injection of minimally oxidized LDL (MM-LDL) activated the same set of genes. We now report that the induction of inflammatory genes and activation of NF-kB-like transcription factors cosegregate with aortic atherosclerotic lesion formation in BXH recombinant inbred strains derived from parental C57BL/6J (susceptible) and C3H/HeJ (resistant) mice. In addition, the accumulation of hepatic conjugated dienes exhibited a significant correlation with inflammatory gene activation. These results provide strong evidence for the role of inflammatory mediators inducible by oxidative stress in atherogenesis. They also suggest that a major gene contributing to aortic lesion development in this mouse model, designated Ath-1, may control either the accumulation of lipid peroxides in tissues or the cellular responses to such lipid peroxides."	J Clin Invest	1994	Aug	"Liao F, Andalibi A, Qiao JH, Allayee H, Fogelman AM, Lusis AJ."	8040344	4 - 6 months	both			15.7	3.4		6	5.3	5.4	3	8.5	1.9	3.8	12		5.5	7.4
Phenotypes and Genotypes of Parental (C57BL/ 6J and C3H/ HeJ) and of BXH Ri strains	HO units	"Genetic evidence for a common pathway mediating oxidative stress, inflammatory gene induction, and aortic fatty streak formation in mice."	"In a previous survey of inbred mouse strains on an atherogenic diet, we observed that the susceptibility to aortic atherosclerotic lesion formation was associated with the accumulation of lipid peroxidation products, induction of inflammatory genes, and the activation of NF-kB-like transcription factors (Liao, F., A. Andalibi, F. C. deBeer, A. M. Fogelman, and A.J. Lusis. 1993. J. Clin. Invest. 91:2572-2579). We hypothesized that the inflammation-related processes were stimulated by oxidized lipids, since injection of minimally oxidized LDL (MM-LDL) activated the same set of genes. We now report that the induction of inflammatory genes and activation of NF-kB-like transcription factors cosegregate with aortic atherosclerotic lesion formation in BXH recombinant inbred strains derived from parental C57BL/6J (susceptible) and C3H/HeJ (resistant) mice. In addition, the accumulation of hepatic conjugated dienes exhibited a significant correlation with inflammatory gene activation. These results provide strong evidence for the role of inflammatory mediators inducible by oxidative stress in atherogenesis. They also suggest that a major gene contributing to aortic lesion development in this mouse model, designated Ath-1, may control either the accumulation of lipid peroxides in tissues or the cellular responses to such lipid peroxides."	J Clin Invest	1994	Aug	"Liao F, Andalibi A, Qiao JH, Allayee H, Fogelman AM, Lusis AJ."	8040344	4 - 6 months	both			3.2	1.5		2	0.9	3	1.5	5.3	0.4	2.2	5.9		1.1	1.4
Phenotypes and Genotypes of Parental (C57BL/ 6J and C3H/ HeJ) and of BXH Ri strains	apo A- IV units	"Genetic evidence for a common pathway mediating oxidative stress, inflammatory gene induction, and aortic fatty streak formation in mice."	"In a previous survey of inbred mouse strains on an atherogenic diet, we observed that the susceptibility to aortic atherosclerotic lesion formation was associated with the accumulation of lipid peroxidation products, induction of inflammatory genes, and the activation of NF-kB-like transcription factors (Liao, F., A. Andalibi, F. C. deBeer, A. M. Fogelman, and A.J. Lusis. 1993. J. Clin. Invest. 91:2572-2579). We hypothesized that the inflammation-related processes were stimulated by oxidized lipids, since injection of minimally oxidized LDL (MM-LDL) activated the same set of genes. We now report that the induction of inflammatory genes and activation of NF-kB-like transcription factors cosegregate with aortic atherosclerotic lesion formation in BXH recombinant inbred strains derived from parental C57BL/6J (susceptible) and C3H/HeJ (resistant) mice. In addition, the accumulation of hepatic conjugated dienes exhibited a significant correlation with inflammatory gene activation. These results provide strong evidence for the role of inflammatory mediators inducible by oxidative stress in atherogenesis. They also suggest that a major gene contributing to aortic lesion development in this mouse model, designated Ath-1, may control either the accumulation of lipid peroxides in tissues or the cellular responses to such lipid peroxides."	J Clin Invest	1994	Aug	"Liao F, Andalibi A, Qiao JH, Allayee H, Fogelman AM, Lusis AJ."	8040344	4 - 6 months	both		ND = not determined	ND	ND		2.7	3.8	7.8	5	7	5.8	4.2	3.9		4	3.9
Phenotypes and Genotypes of Parental (C57BL/ 6J and C3H/ HeJ) and of BXH Ri strains	NF - kb - like	"Genetic evidence for a common pathway mediating oxidative stress, inflammatory gene induction, and aortic fatty streak formation in mice."	"In a previous survey of inbred mouse strains on an atherogenic diet, we observed that the susceptibility to aortic atherosclerotic lesion formation was associated with the accumulation of lipid peroxidation products, induction of inflammatory genes, and the activation of NF-kB-like transcription factors (Liao, F., A. Andalibi, F. C. deBeer, A. M. Fogelman, and A.J. Lusis. 1993. J. Clin. Invest. 91:2572-2579). We hypothesized that the inflammation-related processes were stimulated by oxidized lipids, since injection of minimally oxidized LDL (MM-LDL) activated the same set of genes. We now report that the induction of inflammatory genes and activation of NF-kB-like transcription factors cosegregate with aortic atherosclerotic lesion formation in BXH recombinant inbred strains derived from parental C57BL/6J (susceptible) and C3H/HeJ (resistant) mice. In addition, the accumulation of hepatic conjugated dienes exhibited a significant correlation with inflammatory gene activation. These results provide strong evidence for the role of inflammatory mediators inducible by oxidative stress in atherogenesis. They also suggest that a major gene contributing to aortic lesion development in this mouse model, designated Ath-1, may control either the accumulation of lipid peroxides in tissues or the cellular responses to such lipid peroxides."	J Clin Invest	1994	Aug	"Liao F, Andalibi A, Qiao JH, Allayee H, Fogelman AM, Lusis AJ."	8040344	4 - 6 months	both			840	20		126	47	23	232	786	20	59	1425		76	286
Phenotypes and Genotypes of Parental (C57BL/ 6J and C3H/ HeJ) and of BXH Ri strains	Conjugated dienes	"Genetic evidence for a common pathway mediating oxidative stress, inflammatory gene induction, and aortic fatty streak formation in mice."	"In a previous survey of inbred mouse strains on an atherogenic diet, we observed that the susceptibility to aortic atherosclerotic lesion formation was associated with the accumulation of lipid peroxidation products, induction of inflammatory genes, and the activation of NF-kB-like transcription factors (Liao, F., A. Andalibi, F. C. deBeer, A. M. Fogelman, and A.J. Lusis. 1993. J. Clin. Invest. 91:2572-2579). We hypothesized that the inflammation-related processes were stimulated by oxidized lipids, since injection of minimally oxidized LDL (MM-LDL) activated the same set of genes. We now report that the induction of inflammatory genes and activation of NF-kB-like transcription factors cosegregate with aortic atherosclerotic lesion formation in BXH recombinant inbred strains derived from parental C57BL/6J (susceptible) and C3H/HeJ (resistant) mice. In addition, the accumulation of hepatic conjugated dienes exhibited a significant correlation with inflammatory gene activation. These results provide strong evidence for the role of inflammatory mediators inducible by oxidative stress in atherogenesis. They also suggest that a major gene contributing to aortic lesion development in this mouse model, designated Ath-1, may control either the accumulation of lipid peroxides in tissues or the cellular responses to such lipid peroxides."	J Clin Invest	1994	Aug	"Liao F, Andalibi A, Qiao JH, Allayee H, Fogelman AM, Lusis AJ."	8040344	4 - 6 months	both		umol/ g wet weight	1250	564		1148	1166	1075	829	1431	682	680	1954		560	654
Phenotypes and Genotypes of Parental (C57BL/ 6J and C3H/ HeJ) and of BXH Ri strains	LPS allele	"Genetic evidence for a common pathway mediating oxidative stress, inflammatory gene induction, and aortic fatty streak formation in mice."	"In a previous survey of inbred mouse strains on an atherogenic diet, we observed that the susceptibility to aortic atherosclerotic lesion formation was associated with the accumulation of lipid peroxidation products, induction of inflammatory genes, and the activation of NF-kB-like transcription factors (Liao, F., A. Andalibi, F. C. deBeer, A. M. Fogelman, and A.J. Lusis. 1993. J. Clin. Invest. 91:2572-2579). We hypothesized that the inflammation-related processes were stimulated by oxidized lipids, since injection of minimally oxidized LDL (MM-LDL) activated the same set of genes. We now report that the induction of inflammatory genes and activation of NF-kB-like transcription factors cosegregate with aortic atherosclerotic lesion formation in BXH recombinant inbred strains derived from parental C57BL/6J (susceptible) and C3H/HeJ (resistant) mice. In addition, the accumulation of hepatic conjugated dienes exhibited a significant correlation with inflammatory gene activation. These results provide strong evidence for the role of inflammatory mediators inducible by oxidative stress in atherogenesis. They also suggest that a major gene contributing to aortic lesion development in this mouse model, designated Ath-1, may control either the accumulation of lipid peroxides in tissues or the cellular responses to such lipid peroxides."	J Clin Invest	1994	Aug	"Liao F, Andalibi A, Qiao JH, Allayee H, Fogelman AM, Lusis AJ."	8040344	4 - 6 months	both		B = C57BL/6J; H =C3H/HeJ	B	H		H	H	H	H	H	H	B	B		B	B
"Inheritance of EcoRV apoB gene polymorphism, LDL size polymorphism, and other chromosome 12 markers"	LDL size	Genetic heterogeneity of plasma lipoproteins in the mouse: control of low density lipoprotein particle sizes by genetic factors.	"In order to assess the genetic control of sizes and concentrations of mouse plasma low density (LDL) and high density lipoproteins (HDL), we used gel permeation fast protein liquid chromatography (FPLC) and nondenaturing gradient polyacrylamide gel electrophoresis to measure the particle sizes of LDL and HDL. Using chromatography we also quantified LDL-cholesterol and HDL-cholesterol concentrations in plasma and used them as indexes of plasma concentrations of the respective particles among 10 inbred strains (AKR/J, BALB/cByJ, C3H/HeJ, C57BL/6J, C57BL/6ByJ, C57L/J, DBA/1LacJ, 129/J, NZB/BINJ, SWR/J) and three sets of recombinant inbred (RI) strains (AKXL/TyJ, BXH/TyJ, CXB/ByJ) of mice. HDL had a dichotomous distribution among the 10 inbred strains. One group had large HDL particle sizes and high HDL-cholesterol concentrations. Another group had smaller HDL particles and lower HDL-cholesterol concentrations, and HDL sizes and HDL-cholesterol concentrations were significantly correlated. In the RI strains, HDL sizes and HDL-cholesterol cholesterol concentrations clearly segregated with one or another of the progenitor strains, and RI strain distributions showed a strong linkage to the apolipoprotein (apo) A-II gene (Apoa-2). In contrast, LDL-cholesterol concentrations and particle sizes on FPLC did not show dichotomous distributions among the 10 inbred strains. In RI strains, the configuration of the LDL FPLC profiles and LDL-cholesterol concentrations did resemble one or another of the progenitors in the majority of cases, but LDLs of several RI strains resembled neither progenitor strain in profile configuration, and LDL-cholesterol concentrations were both greater and smaller than those of progenitor strains. However, LDL particle diameters (as judged by peaks of LDL-cholesterol profiles) did segregate with progenitors in 29/33 (88%) of RI strains suggesting that a major gene may affect LDL size. In attempting to identify a major LDL-size determining gene, we compared apoB gene restriction fragment length polymorphisms (RFLPs) to the distributions of peak LDL sizes in RI strains. Concordance rates of peak LDL sizes to apoB gene polymorphisms were 18/22 (82%) for the EcoRV RFLP, 5/7 (71%) for HindIII RFLP, and 23/29 (79%) for both (range of P values 0.90-0.95). Thus we could not unequivocally implicate the apoB gene in determining the size of LDL particles. In summary, the genetic control of LDL sizes is more complicated than is the case for HDL; however, the differences in LDL size among these strains of mice may be controlled by a major, as yet unidentified, gene."	J Lipid Res	1990	Mar	"Jiao S, Cole TG, Kitchens RT, Pfleger B, Schonfeld G."	1971301	8 - 10 weeks	female		B = C57BL/6J; H =C3H/HeJ			B	B	H	H	H	B	H	intermediate LDL size of progenitors			H	H
"Inheritance of EcoRV apoB gene polymorphism, LDL size polymorphism, and other chromosome 12 markers"	Rnr - 12	Genetic heterogeneity of plasma lipoproteins in the mouse: control of low density lipoprotein particle sizes by genetic factors.	"In order to assess the genetic control of sizes and concentrations of mouse plasma low density (LDL) and high density lipoproteins (HDL), we used gel permeation fast protein liquid chromatography (FPLC) and nondenaturing gradient polyacrylamide gel electrophoresis to measure the particle sizes of LDL and HDL. Using chromatography we also quantified LDL-cholesterol and HDL-cholesterol concentrations in plasma and used them as indexes of plasma concentrations of the respective particles among 10 inbred strains (AKR/J, BALB/cByJ, C3H/HeJ, C57BL/6J, C57BL/6ByJ, C57L/J, DBA/1LacJ, 129/J, NZB/BINJ, SWR/J) and three sets of recombinant inbred (RI) strains (AKXL/TyJ, BXH/TyJ, CXB/ByJ) of mice. HDL had a dichotomous distribution among the 10 inbred strains. One group had large HDL particle sizes and high HDL-cholesterol concentrations. Another group had smaller HDL particles and lower HDL-cholesterol concentrations, and HDL sizes and HDL-cholesterol concentrations were significantly correlated. In the RI strains, HDL sizes and HDL-cholesterol cholesterol concentrations clearly segregated with one or another of the progenitor strains, and RI strain distributions showed a strong linkage to the apolipoprotein (apo) A-II gene (Apoa-2). In contrast, LDL-cholesterol concentrations and particle sizes on FPLC did not show dichotomous distributions among the 10 inbred strains. In RI strains, the configuration of the LDL FPLC profiles and LDL-cholesterol concentrations did resemble one or another of the progenitors in the majority of cases, but LDLs of several RI strains resembled neither progenitor strain in profile configuration, and LDL-cholesterol concentrations were both greater and smaller than those of progenitor strains. However, LDL particle diameters (as judged by peaks of LDL-cholesterol profiles) did segregate with progenitors in 29/33 (88%) of RI strains suggesting that a major gene may affect LDL size. In attempting t