- increased circulating triglyceride level / MGI
- increased circulating cholesterol level / MGI
- hyperglycemia / MGI
- increased circulating LDL cholesterol level / MGI
- alopecia / MGI
- abnormal liver physiology / MGI
- abnormal adrenal gland morphology / MGI
- scaly skin / MGI
- thick skin / MGI
- increased circulating HDL cholesterol level / MGI
- hepatic steatosis / MGI
- decreased circulating triglyceride level / MGI
- increased cholesterol level / MGI
- increased circulating VLDL cholesterol level / MGI
- atherosclerotic lesions / MGI
- homeostasis/metabolism phenotype / MGI
- increased liver cholesterol level / MGI
- abnormal microglial cell morphology / MGI
- abnormal circulating cholesterol level / MGI
- decreased circulating HDL cholesterol level / MGI
- abnormal triglyceride level / MGI
- abnormal CNS glial cell morphology / MGI
- hyperactivity / MGI
- abnormal spatial learning / MGI
- increased circulating insulin level / MGI
- abnormal astrocyte morphology / MGI
- amyloid beta deposits / MGI
- increased circulating VLDL triglyceride level / MGI
- impaired glucose tolerance / MGI
- abnormal fat pad morphology / MGI
- increased susceptibility to atherosclerosis / MGI
- increased susceptibility to weight gain / MGI
- increased percent body fat/body weight / MGI
- abnormal spatial working memory / MGI
- increased circulating tumor necrosis factor level / MGI
- decreased circulating interleukin-10 level / MGI
- increased circulating interleukin-6 level / MGI
- increased circulating interleukin-1 beta level / MGI
- increased liver triglyceride level / MGI
- increased grip strength / MGI
- decreased susceptibility to weight gain / MGI
- abnormal hippocampus morphology / MGI
- obese / MGI
- increased circulating free fatty acid level / MGI
- liver inflammation / MGI
- abnormal glucose homeostasis / MGI
- decreased circulating corticosterone level / MGI
- increased circulating alanine transaminase level / MGI
- increased liver weight / MGI
- liver fibrosis / MGI
- oxidative stress / MGI
- maternal effect / MGI
- increased hepatocyte apoptosis / MGI
- decreased lean body mass / MGI
- abnormal arteriole morphology / MGI
- abnormal retinal pigment epithelium morphology / MGI
- abnormal Bruch membrane morphology / MGI
- abnormal circulating amino acid level / MGI
- insulin resistance / MGI
- increased circulating glucose level / MGI
- abnormal choriocapillaris morphology / MGI
- abnormal short term spatial reference memory / MGI
- abnormal synaptic bouton morphology / MGI
- photoreceptor outer segment degeneration / MGI
- abnormal synapse morphology / MGI
- abnormal circulating LDL cholesterol level / MGI
- abnormal lipid homeostasis / MGI
- abnormal cholesterol homeostasis / MGI
- abnormal circulating protein level / MGI
B6.Cg-Ldlrtm1Her Tg(APOB*Q2153L)#Boren/Kctt
Status | Available to order |
EMMA ID | EM:09689 |
International strain name | B6.Cg-Ldlrtm1Her Tg(APOB*Q2153L)#Boren/Kctt |
Alternative name | B6.C57BL/6XSJL-Tg(huB100tm).129S7-Ldlrtm1Her |
Strain type | Targeted Mutant Strains : Knock-out |
Allele/Transgene symbol | Ldlrtm1Her, |
Gene/Transgene symbol | Ldlr |
Information from provider
Provider | Jan Borén |
Provider affiliation | Molecular and Clinical Medicine, University of Gothenburg |
Additional owner | Göran Hansson, Daniel Ketelhuth and Alexandra Bäcklund, The Cardiovascular Medicine Unit, Department of Medicine, Karolinska Institutet, Stockholm, Sweden |
Genetic information | These mice carry the full-length human APOB100 gene, in which codon 2153 has been converted from leucine to glutamine to prevent the formation of ApoB48, generating only ApoB100. They are also deficient in LDLr and have an increased level of LDL-cholesterol, VLDL-cholesterol, and low HDL relative to wild-type mice and develop spontaneous atherosclerosis. |
Phenotypic information | Homozygous:Mice have hypercholesterolemia and develop spontaneous atherosclerotic lesions. Females have an earlier onset with lesions at 18 weeks compared with males (onset at 26 weeks). Mice are healthy and have no visible effect with a normal life span.Heterozygous:Mice have mild hypercholesterolemia but do not develop spontaneous atherosclerotic lesions. Mice are healthy and have no visible effect with a normal life span. |
Breeding history | Mice were received at 4 generations backcrossed to C57BL/6J. The mice were then crossed a further 6 generations to C57BL/6J, purchased from JAX Mice in USA. |
References |
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Homozygous fertile | yes |
Homozygous viable | yes |
Homozygous matings required | no |
Immunocompromised | no |
Information from EMMA
Archiving centre | Karolinska Institutet, Stockholm, Sweden |
Animals used for archiving | homozygous C57BL/6J |
Disease and phenotype information
Orphanet associated rare diseases, based on orthologous gene matching
- Homozygous familial hypercholesterolemia / Orphanet_391665
MGI phenotypes (allele matching)
Literature references
- Inhibition of T cell response to native low-density lipoprotein reduces atherosclerosis.;Hermansson Andreas, Ketelhuth Daniel F J, Strodthoff Daniela, Wurm Marion, Hansson Emil M, Nicoletti Antonino, Paulsson-Berne Gabrielle, Hansson Göran K, ;2010;The Journal of experimental medicine;207;1081-93; 20439543
- Immunotherapy with tolerogenic apolipoprotein B-100-loaded dendritic cells attenuates atherosclerosis in hypercholesterolemic mice.;Hermansson Andreas, Johansson Daniel K, Ketelhuth Daniel F J, Andersson John, Zhou Xinghua, Hansson Göran K, ;2011;Circulation;123;1083-91; 21357823
- Identification of the low density lipoprotein receptor-binding site in apolipoprotein B100 and the modulation of its binding activity by the carboxyl terminus in familial defective apo-B100.;Boren J, Lee I, Zhu W, Arnold K, Taylor S, Innerarity T L, ;1998;The Journal of clinical investigation;101;1084-93; 9486979
- Liver damage promotes pro-inflammatory T-cell responses against apolipoprotein B-100.;Plochg Bastian F J, Englert Hanna, Rangaswamy Chandini, Konrath Sandra, Malle Mandy, Lampalzer Sibylle, Beisel Claudia, Wollin Salma, Frye Maike, Aberle Jens, Kluwe Johannes, Renné Thomas, Mailer Reiner K, ;2022;Journal of internal medicine;291;648-664; 34914849
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