Description

Strain Information

Type Mutant Stock; Targeted Mutation; Additional information on Genetically Engineered and Mutant Mice. Visit our online Nomenclature tutorial. Mating System Homozygote x Homozygote         (Female x Male)   01-MAR-06 Species laboratory mouse   Donating Investigator Dr. Joachim Herz,   Univ of Texas Southwest Med Ctr Dallas

Appearance
black
Related Genotype: a/a

Description
Mice homozygous for the Vldlr^tm1Her targeted mutation are viable and fertile. They are smaller and leaner than normal wildtype siblings. The high level of expression in muscle and adipose tissue suggests a role in VLDL triacylglycerol delivery. Plasma levels of cholesterol, triacylglycerol, and lipoproteins were normal when mice were fed normal, high-carbohydrate or high fat diets. However, homozygous mice do show a modest decrease in body weight, body mass index, and adipose tissue mass as determined by the weights of epididymal fat pads. Many homozygous pups in the colony at the Jackson Lab have patchy fur (hair loss) at weaning but look normal at about 6 weeks of age. In a segregation analysis crossing homozygous females with normal "C57BL6/2J" mice, offspring that were homozygous for this Vldlr^tm1Her mutation are associated with subretinal neovascularization and were found to have a neovascularization process similar to a type seen in patients with macular degeneration.

Development
This strain was developed in the lab of Dr. Joachim Herz at The University of Texas, Southwestern Medical Center at Dallas. The mutant allele contains a partial deletion of exon 5 of the Vldlr gene. The neo cassette inserted disrupted the reading frame. No protein is detectable by immunoblot analysis. The 129/Sv-derived JH-1 ES cell line was used.

Control Information

	Control
	101045 B6129SF2/J	(approximate)
Considerations for Choosing Controls

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI

- Model with phenotypic similarity to human disease where etiologies are distinct. Human genes are associated with this disease. Orthologs of these genes do not appear in the mouse genotype(s).

Macular Degeneration, Age-Related, 1; ARMD1

- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested. Cerebellar Ataxia, Mental Retardation, and Dysequilibrium Syndrome 1; CAMRQ1   (VLDLR)

View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI

      assigned by genotype

Vldlr^tm1Her/Vldlr^tm1Her

        involves: 129S7/SvEvBrd * C57BL/6J

• adipose tissue phenotype
• decreased epididymal fat pad weight
  • decreased adipose tissue, determined by weights of epididymal fat pads   (MGI Ref ID J:28591)
• growth/size phenotype
• decreased body size   (MGI Ref ID J:28591)
• • decreased body weight
    • weight reduced by 15 to 20% versus littermates   (MGI Ref ID J:28591)
    • decreased body mass index (BMI)   (MGI Ref ID J:28591)
• homeostasis/metabolism phenotype
• *normal* homeostasis/metabolism phenotype
  • normal plasma concentrations of cholesterol, triacylglycerol, lipoproteins, glucose, insulin, and free fatty acids   (MGI Ref ID J:28591)

Vldlr^tm1Her/Vldlr^tm1Her

        involves: 129S7/SvEvBrd * C57BL/6

• vision/eye phenotype
• abnormal ocular fundus morphology
  • at 6 weeks, some depigmented pink spots are observed in the fundus; spots develop into large, irregularly shaped pink areas by 6 months of age   (MGI Ref ID J:114757)
• • choroidal neovascularization   (MGI Ref ID J:114757)
• cardiovascular system phenotype
• pathological neovascularization
  • at 3 weeks, focal areas of neovascular leakage are observed and increase in number with age   (MGI Ref ID J:114757)
  • new vessels originate in the plexiform layer, grow and migrate into the subretinal space   (MGI Ref ID J:114757)
  • choroidal anastomoses occur commonly by 3 months, but are seen as early as 15 days in some animals   (MGI Ref ID J:114757)
• • choroidal neovascularization   (MGI Ref ID J:114757)
• homeostasis/metabolism phenotype
• *normal* homeostasis/metabolism phenotype
  • mice show normal FVIII (Factor 8) and VWF (von Willebrand factor) levels in plasma   (MGI Ref ID J:117317)
• • increased circulating cholesterol level
    • levels are significantly increased (>3-fold) compared to controls   (MGI Ref ID J:117317)
  • increased circulating triglyceride level
    • levels are significantly increased (4-fold) compared to controls   (MGI Ref ID J:117317)

Vldlr^tm1Her/Vldlr^tm1Her

        B6;129S7-Vldlr^tm1Her/J

• vision/eye phenotype
• abnormal retina morphology
  • accumulation of cell debris is observed prior to development of intraretinal neovascularization   (MGI Ref ID J:128315)
  • angiomatous growths are densely distributed throughout retina at 4 weeks   (MGI Ref ID J:132497)
  • at 6 weeks, scattered pink spots progress to large, irregular pink areas by 6 months; leaking spots decrease after 8 months with large rigid vascular tangles still present and leakage is barely detectable by 12 months   (MGI Ref ID J:132497)
  • fibrosis formation is present at 12 months, beginning around 3 months with fibroblast accumulation at lesion site   (MGI Ref ID J:132497)
• • abnormal retinal neuronal layer morphology
    • between 6 and 8 weeks, both outer and inner segments are disrupted in lesion area; migration of RPE cells into lesion area is observed   (MGI Ref ID J:128315)
  • • decreased retinal photoreceptor cell number
      • significant loss of photoreceptors is seen at 6 months, resulting in thinning of outer nuclear layer   (MGI Ref ID J:128315)
      • increased loss is detected at 12 months   (MGI Ref ID J:132497)
    • disorganized retinal inner nuclear layer
      • by 4 weeks   (MGI Ref ID J:128315)
    • retinal outer nuclear layer degeneration
      • destruction of ONL is seen starting at 6 months   (MGI Ref ID J:132497)
    • retinal photoreceptor degeneration
      • observed at 10 months   (MGI Ref ID J:132497)
    • thin retinal outer nuclear layer
      • reduced in thickness by 6 months   (MGI Ref ID J:128315)
      • reduced overall at 12 months; layer is completely diminished by 24 months   (MGI Ref ID J:132497)
  • abnormal retinal pigment epithelium morphology
    • thickening of RPE cells is observed prior to development of intraretinal neovascularization   (MGI Ref ID J:128315)
    • disruption of RPE layer is observed by 6 weeks of age   (MGI Ref ID J:132497)
    • pigment adhesions to neural tissue are seen by 6 weeks, representing pigment epithelium detachment   (MGI Ref ID J:132497)
  • retinal neovascularization
    • new vessels form in outer plexiform layer of retina around 3 weeks of age; vessels migrate into subretinal space by 4 weeks   (MGI Ref ID J:128315)
    • angiography shows leakage in retinas at 6 weeks, mainly in central area of retina near optic nerve, with red blood cells found around the leakage spot; neovascularization is localized to outer nuclear layer and in subretinal space   (MGI Ref ID J:128315)
    • signs of new vessel growth is observed at 14 days in deep capillary bed of outer plexiform layer (OPL) of retina, protruding into avascular zone of outer nuclear layer (ONL)   (MGI Ref ID J:132497)
    • new vessel buds reach subretinal space by P15   (MGI Ref ID J:132497)
    • leakage is first seen at 3 weeks and increases with age, with leaking areas covering most of retinal by 6 weeks   (MGI Ref ID J:132497)
    • clumps of retinal pigmented epithelial cells (RPE) adhere to neovascular tufts in subretinal space; these increase with age   (MGI Ref ID J:132497)
    • subretinal neovascularization (SRN) is seen at 6 weeks of age   (MGI Ref ID J:132497)
    • fibrosis formation is present at 12 months, beginning around 3 months with fibroblast accumulation at lesion site   (MGI Ref ID J:132497)
• choroidal neovascularization
  • CNV membranes develop after 6 months of age with some tissue destruction in INL and ONL   (MGI Ref ID J:132497)
  • some retinal-choroidal anastomoses may be observed at 10 months   (MGI Ref ID J:132497)
• nervous system phenotype
• decreased retinal photoreceptor cell number
  • significant loss of photoreceptors is seen at 6 months, resulting in thinning of outer nuclear layer   (MGI Ref ID J:128315)
  • increased loss is detected at 12 months   (MGI Ref ID J:132497)
• retinal photoreceptor degeneration
  • observed at 10 months   (MGI Ref ID J:132497)
• cardiovascular system phenotype
• choroidal neovascularization
  • CNV membranes develop after 6 months of age with some tissue destruction in INL and ONL   (MGI Ref ID J:132497)
  • some retinal-choroidal anastomoses may be observed at 10 months   (MGI Ref ID J:132497)
• retinal neovascularization
  • new vessels form in outer plexiform layer of retina around 3 weeks of age; vessels migrate into subretinal space by 4 weeks   (MGI Ref ID J:128315)
  • angiography shows leakage in retinas at 6 weeks, mainly in central area of retina near optic nerve, with red blood cells found around the leakage spot; neovascularization is localized to outer nuclear layer and in subretinal space   (MGI Ref ID J:128315)
  • signs of new vessel growth is observed at 14 days in deep capillary bed of outer plexiform layer (OPL) of retina, protruding into avascular zone of outer nuclear layer (ONL)   (MGI Ref ID J:132497)
  • new vessel buds reach subretinal space by P15   (MGI Ref ID J:132497)
  • leakage is first seen at 3 weeks and increases with age, with leaking areas covering most of retinal by 6 weeks   (MGI Ref ID J:132497)
  • clumps of retinal pigmented epithelial cells (RPE) adhere to neovascular tufts in subretinal space; these increase with age   (MGI Ref ID J:132497)
  • subretinal neovascularization (SRN) is seen at 6 weeks of age   (MGI Ref ID J:132497)
  • fibrosis formation is present at 12 months, beginning around 3 months with fibroblast accumulation at lesion site   (MGI Ref ID J:132497)
• pigmentation phenotype
• abnormal retinal pigment epithelium morphology
  • thickening of RPE cells is observed prior to development of intraretinal neovascularization   (MGI Ref ID J:128315)
  • disruption of RPE layer is observed by 6 weeks of age   (MGI Ref ID J:132497)
  • pigment adhesions to neural tissue are seen by 6 weeks, representing pigment epithelium detachment   (MGI Ref ID J:132497)

The following phenotype information may relate to a genetic background differing from this JAX^® Mice strain.

Vldlr^tm1Her/Vldlr^tm1Her

        involves: 129S7/SvEvBrd

• nervous system phenotype
• abnormal brain morphology   (MGI Ref ID J:55691)
• • abnormal brain development
    • cortical layering disrupted, layers not clearly separated and neurons were arranged in a radial fashion   (MGI Ref ID J:55691)
  • • abnormal cerebellar foliation
      • less foliated than wild-type   (MGI Ref ID J:55691)
  • abnormal cerebellum morphology   (MGI Ref ID J:55691)
  • • abnormal cerebellar foliation
      • less foliated than wild-type   (MGI Ref ID J:55691)
    • small cerebellum   (MGI Ref ID J:55691)
• abnormal long term potentiation
  • while synaptic transmission and short term plasticity appeared normal in the CA1 region, LTP induction was impaired   (MGI Ref ID J:79593)
• • reduced long term potentiation   (MGI Ref ID J:79593)
• impaired synaptic plasticity   (MGI Ref ID J:79593)
• behavior/neurological phenotype
• abnormal contextual conditioning behavior
  • contextual fear-conditioned learning deficits   (MGI Ref ID J:79593)
• abnormal cued conditioning behavior
  • cued conditioning was reduced when tested 24 hours following training, however it was normal when tested 1 hour following training   (MGI Ref ID J:79593)
• hyperactivity   (MGI Ref ID J:79593)

View Research Applications

Research Applications

This mouse can be used to support research in many areas including:

Sensorineural Research
Eye Defects

Vldlr^tm1Her related

Cardiovascular Research
Other
      altered fat metabolism

Genes & Alleles

Gene & Allele Information provided by MGI

Allele Symbol		Vldlrtm1Her
Allele Name		targeted mutation 1, Joachim Herz
Allele Type		Targeted (knock-out)
Common Name(s)		VLDLR-;
Mutation Made By		Dr. Joachim Herz,   Univ of Texas Southwest Med Ctr Dallas
Strain of Origin		129S7/SvEvBrd
ES Cell Line Name		JH1
ES Cell Line Strain		129S7/SvEvBrd
Gene Symbol and Name		Vldlr, very low density lipoprotein receptor
Chromosome		19
Gene Common Name(s)		AA408956; AI451093; AW047288; CARMQ1; CHRMQ1; VLDLRCH; expressed sequence AA408956; expressed sequence AI451093; expressed sequence AW047288;
Molecular Note		The insertion of a neomycin selection cassette into exon 5 deleted a portion of the coding sequence and disrupted the reading frame. Immunoblot analysis of heart muscle membranes did not detect protein in homozygous mutant animals. [MGI Ref ID J:28591]

Genotyping

Genotyping Information

Genotyping Protocols

Vldlr^tm1Her, Standard PCR

Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Frykman PK; Brown MS; Yamamoto T; Goldstein JL; Herz J. 1995. Normal plasma lipoproteins and fertility in gene-targeted mice homozygous for a disruption in the gene encoding very low density lipoprotein receptor. Proc Natl Acad Sci U S A 92(18):8453-7. [PubMed: 7667310]  [MGI Ref ID J:28591]

Additional References

Drakew A; Deller T; Heimrich B; Gebhardt C; Del Turco D; Tielsch A; Forster E; Herz J; Frotscher M. 2002. Dentate granule cells in reeler mutants and VLDLR and ApoER2 knockout mice. Exp Neurol 176(1):12-24. [PubMed: 12093079]  [MGI Ref ID J:78001]

Gebhardt C; Del Turco D; Drakew A; Tielsch A; Herz J; Frotscher M; Deller T. 2002. Abnormal positioning of granule cells alters afferent fiber distribution in the mouse fascia dentata: Morphologic evidence from reeler, apolipoprotein E receptor 2-, and very low density lipoprotein receptor knockout mice. J Comp Neurol 445(3):278-92. [PubMed: 11920707]  [MGI Ref ID J:75080]

Heckenlively JR; Hawes NL; Friedlander M; Nusinowitz S; Hurd R; Davisson M; Chang B. 2003. Mouse model of subretinal neovascularization with choroidal anastomosis. Retina 23(4):518-22. [PubMed: 12972764]  [MGI Ref ID J:114757]

Weiss KH; Johanssen C; Tielsch A; Herz J; Deller T; Frotscher M; Forster E. 2003. Malformation of the radial glial scaffold in the dentate gyrus of reeler mice, scrambler mice, and ApoER2/VLDLR-deficient mice. J Comp Neurol 460(1):56-65. [PubMed: 12687696]  [MGI Ref ID J:83151]

Vldlr^tm1Her related

Akopians AL; Babayan AH; Beffert U; Herz J; Basbaum AI; Phelps PE. 2008. Contribution of the Reelin signaling pathways to nociceptive processing. Eur J Neurosci 27(3):523-37. [PubMed: 18279306]  [MGI Ref ID J:132269]

Andrade N; Komnenovic V; Blake SM; Jossin Y; Howell B; Goffinet A; Schneider WJ; Nimpf J. 2007. ApoER2/VLDL receptor and Dab1 in the rostral migratory stream function in postnatal neuronal migration independently of Reelin. Proc Natl Acad Sci U S A 104(20):8508-13. [PubMed: 17494763]  [MGI Ref ID J:121846]

Assadi AH; Zhang G; Beffert U; McNeil RS; Renfro AL; Niu S; Quattrocchi CC; Antalffy BA; Sheldon M; Armstrong DD; Wynshaw-Boris A; Herz J; D'Arcangelo G; Clark GD. 2003. Interaction of reelin signaling and Lis1 in brain development. Nat Genet 35(3):270-6. [PubMed: 14578885]  [MGI Ref ID J:86398]

Barr AM; Fish KN; Markou A. 2007. The reelin receptors VLDLR and ApoER2 regulate sensorimotor gating in mice. Neuropharmacology 52(4):1114-23. [PubMed: 17261317]  [MGI Ref ID J:124495]

Beffert U; Durudas A; Weeber EJ; Stolt PC; Giehl KM; Sweatt JD; Hammer RE; Herz J. 2006. Functional dissection of Reelin signaling by site-directed disruption of Disabled-1 adaptor binding to apolipoprotein E receptor 2: distinct roles in development and synaptic plasticity. J Neurosci 26(7):2041-52. [PubMed: 16481437]  [MGI Ref ID J:105699]

Beffert U; Weeber EJ; Morfini G; Ko J; Brady ST; Tsai LH; Sweatt JD; Herz J. 2004. Reelin and cyclin-dependent kinase 5-dependent signals cooperate in regulating neuronal migration and synaptic transmission. J Neurosci 24(8):1897-906. [PubMed: 14985430]  [MGI Ref ID J:90122]

Blake SM; Strasser V; Andrade N; Duit S; Hofbauer R; Schneider WJ; Nimpf J. 2008. Thrombospondin-1 binds to ApoER2 and VLDL receptor and functions in postnatal neuronal migration. EMBO J 27(22):3069-80. [PubMed: 18946489]  [MGI Ref ID J:143787]

Bock HH; Herz J. 2003. Reelin activates SRC family tyrosine kinases in neurons. Curr Biol 13(1):18-26. [PubMed: 12526740]  [MGI Ref ID J:109819]

Bovenschen N; Mertens K; Hu L; Havekes LM; van Vlijmen BJ. 2005. LDL receptor cooperates with LDL receptor-related protein in regulating plasma levels of coagulation factor VIII in vivo. Blood 106(3):906-12. [PubMed: 15840700]  [MGI Ref ID J:117317]

Bovenschen N; van Dijk KW; Havekes LM; Mertens K; van Vlijmen BJ. 2004. Clearance of coagulation factor VIII in very low-density lipoprotein receptor knockout mice. Br J Haematol 126(5):722-5. [PubMed: 15327526]  [MGI Ref ID J:109394]

Cariboni A; Rakic S; Liapi A; Maggi R; Goffinet A; Parnavelas JG. 2005. Reelin provides an inhibitory signal in the migration of gonadotropin-releasing hormone neurons. Development 132(21):4709-18. [PubMed: 16207762]  [MGI Ref ID J:102848]

Chang B; Hawes NL; Hurd RE; Wang J; Howell D; Davisson MT; Roderick TH; Nusinowitz S; Heckenlively JR. 2005. Mouse models of ocular diseases. Vis Neurosci 22(5):587-93. [PubMed: 16332269]  [MGI Ref ID J:156373]

Chen Y; Hu Y; Lu K; Flannery JG; Ma JX. 2007. Very low density lipoprotein receptor, a negative regulator of the wnt signaling pathway and choroidal neovascularization. J Biol Chem 282(47):34420-8. [PubMed: 17890782]  [MGI Ref ID J:128338]

Deane R; Sagare A; Hamm K; Parisi M; Lane S; Finn MB; Holtzman DM; Zlokovic BV. 2008. apoE isoform-specific disruption of amyloid beta peptide clearance from mouse brain. J Clin Invest 118(12):4002-13. [PubMed: 19033669]  [MGI Ref ID J:144730]

Dierssen M; Arque G; McDonald J; Andreu N; Martinez-Cue C; Florez J; Fillat C. 2011. Behavioral characterization of a mouse model overexpressing DSCR1/ RCAN1. PLoS One 6(2):e17010. [PubMed: 21364922]  [MGI Ref ID J:171071]

Fish KN; Krucker T. 2008. Functional consequences of hippocampal neuronal ectopia in the apolipoprotein E receptor-2 knockout mouse. Neurobiol Dis 32(3):391-401. [PubMed: 18778775]  [MGI Ref ID J:142541]

Gebhardt C; Del Turco D; Drakew A; Tielsch A; Herz J; Frotscher M; Deller T. 2002. Abnormal positioning of granule cells alters afferent fiber distribution in the mouse fascia dentata: Morphologic evidence from reeler, apolipoprotein E receptor 2-, and very low density lipoprotein receptor knockout mice. J Comp Neurol 445(3):278-92. [PubMed: 11920707]  [MGI Ref ID J:75080]

Goudriaan JR; Tacken PJ; Dahlmans VE; Gijbels MJ; van Dijk KW; Havekes LM; Jong MC. 2001. Protection from obesity in mice lacking the VLDL receptor. Arterioscler Thromb Vasc Biol 21(9):1488-93. [PubMed: 11557677]  [MGI Ref ID J:102939]

Hack I; Hellwig S; Junghans D; Brunne B; Bock HH; Zhao S; Frotscher M. 2007. Divergent roles of ApoER2 and Vldlr in the migration of cortical neurons. Development 134(21):3883-91. [PubMed: 17913789]  [MGI Ref ID J:126335]

Hashimoto-Torii K; Torii M; Sarkisian MR; Bartley CM; Shen J; Radtke F; Gridley T; Sestan N; Rakic P. 2008. Interaction between Reelin and Notch signaling regulates neuronal migration in the cerebral cortex. Neuron 60(2):273-84. [PubMed: 18957219]  [MGI Ref ID J:144065]

Heckenlively JR; Hawes NL; Friedlander M; Nusinowitz S; Hurd R; Davisson M; Chang B. 2003. Mouse model of subretinal neovascularization with choroidal anastomosis. Retina 23(4):518-22. [PubMed: 12972764]  [MGI Ref ID J:114757]

Hu L; van der Hoogt CC; Espirito Santo SM; Out R; Kypreos KE; van Vlijmen BJ; Van Berkel TJ; Romijn JA; Havekes LM; van Dijk KW; Rensen PC. 2008. The hepatic uptake of VLDL in lrp-ldlr-/-vldlr-/- mice is regulated by LPL activity and involves proteoglycans and SR-BI. J Lipid Res 49(7):1553-61. [PubMed: 18367731]  [MGI Ref ID J:138462]

Hu W; Jiang A; Liang J; Meng H; Chang B; Gao H; Qiao X. 2008. Expression of VLDLR in the retina and evolution of subretinal neovascularization in the knockout mouse model's retinal angiomatous proliferation. Invest Ophthalmol Vis Sci 49(1):407-15. [PubMed: 18172119]  [MGI Ref ID J:132497]

Hua J; Guerin KI; Chen J; Michan S; Stahl A; Krah NM; Seaward MR; Dennison RJ; Juan AM; Hatton CJ; Sapieha P; Sinclair DA; Smith LE. 2011. Resveratrol inhibits pathologic retinal neovascularization in vldlr-/- mice. Invest Ophthalmol Vis Sci 52(5):2809-16. [PubMed: 21282584]  [MGI Ref ID J:171523]

Jiang A; Hu W; Meng H; Gao H; Qiao X. 2009. Loss of VLDL receptor activates retinal vascular endothelial cells and promotes angiogenesis. Invest Ophthalmol Vis Sci 50(2):844-50. [PubMed: 18936153]  [MGI Ref ID J:146685]

Jossin Y; Gui L; Goffinet AM. 2007. Processing of Reelin by embryonic neurons is important for function in tissue but not in dissociated cultured neurons. J Neurosci 27(16):4243-52. [PubMed: 17442808]  [MGI Ref ID J:121108]

Kruger MT; Zhao S; Chai X; Brunne B; Bouche E; Bock HH; Frotscher M. 2010. Role for Reelin-induced cofilin phosphorylation in the assembly of sympathetic preganglionic neurons in the murine intermediolateral column. Eur J Neurosci 32(10):1611-7. [PubMed: 21039973]  [MGI Ref ID J:169495]

Larouche M; Beffert U; Herz J; Hawkes R. 2008. The reelin receptors apoer2 and vldlr coordinate the patterning of purkinje cell topography in the developing mouse cerebellum. PLoS ONE 3(2):e1653. [PubMed: 18301736]  [MGI Ref ID J:132885]

Leemhuis J; Bouche E; Frotscher M; Henle F; Hein L; Herz J; Meyer DK; Pichler M; Roth G; Schwan C; Bock HH. 2010. Reelin signals through apolipoprotein E receptor 2 and Cdc42 to increase growth cone motility and filopodia formation. J Neurosci 30(44):14759-72. [PubMed: 21048135]  [MGI Ref ID J:166701]

Li C; Huang Z; Kingsley R; Zhou X; Li F; Parke DW 2nd; Cao W. 2007. Biochemical alterations in the retinas of very low-density lipoprotein receptor knockout mice: an animal model of retinal angiomatous proliferation. Arch Ophthalmol 125(6):795-803. [PubMed: 17562991]  [MGI Ref ID J:128315]

McKenzie JA; Fruttiger M; Abraham S; Lange CA; Stone J; Gandhi P; Wang X; Bainbridge J; Moss SE; Greenwood J. 2012. Apelin is required for non-neovascular remodeling in the retina. Am J Pathol 180(1):399-409. [PubMed: 22067912]  [MGI Ref ID J:180164]

Park K; Lee K; Zhang B; Zhou T; He X; Gao G; Murray AR; Ma JX. 2011. Identification of a novel inhibitor of the canonical wnt pathway. Mol Cell Biol 31(14):3038-51. [PubMed: 21576363]  [MGI Ref ID J:174092]

Perman JC; Bostrom P; Lindbom M; Lidberg U; StAhlman M; Hagg D; Lindskog H; Scharin Tang M; Omerovic E; Mattsson Hulten L; Jeppsson A; Petursson P; Herlitz J; Olivecrona G; Strickland DK; Ekroos K; Olofsson SO; Boren J. 2011. The VLDL receptor promotes lipotoxicity and increases mortality in mice following an acute myocardial infarction. J Clin Invest 121(7):2625-40. [PubMed: 21670500]  [MGI Ref ID J:175645]

Rossel M; Loulier K; Feuillet C; Alonso S; Carroll P. 2005. Reelin signaling is necessary for a specific step in the migration of hindbrain efferent neurons. Development 132(6):1175-85. [PubMed: 15703280]  [MGI Ref ID J:97218]

Roubtsova A; Munkonda MN; Awan Z; Marcinkiewicz J; Chamberland A; Lazure C; Cianflone K; Seidah NG; Prat A. 2011. Circulating proprotein convertase subtilisin/kexin 9 (PCSK9) regulates VLDLR protein and triglyceride accumulation in visceral adipose tissue. Arterioscler Thromb Vasc Biol 31(4):785-91. [PubMed: 21273557]  [MGI Ref ID J:184166]

Senturk A; Pfennig S; Weiss A; Burk K; Acker-Palmer A. 2011. Ephrin Bs are essential components of the Reelin pathway to regulate neuronal migration. Nature 472(7343):356-60. [PubMed: 21460838]  [MGI Ref ID J:171375]

Tacken PJ; Teusink B; Jong MC; Harats D; Havekes LM; van Dijk KW; Hofker MH. 2000. LDL receptor deficiency unmasks altered VLDL triglyceride metabolism in VLDL receptor transgenic and knockout mice J Lipid Res 41(12):2055-62. [PubMed: 11108739]  [MGI Ref ID J:66431]

Tao H; Aakula S; Abumrad NN; Hajri T. 2010. Peroxisome proliferator-activated receptor-gamma regulates the expression and function of very-low-density lipoprotein receptor. Am J Physiol Endocrinol Metab 298(1):E68-79. [PubMed: 19861583]  [MGI Ref ID J:170136]

Tao H; Hajri T. 2011. Very low density lipoprotein receptor promotes adipocyte differentiation and mediates the proadipogenic effect of peroxisome proliferator-activated receptor gamma agonists. Biochem Pharmacol 82(12):1950-62. [PubMed: 21924248]  [MGI Ref ID J:178736]

Trommsdorff M; Gotthardt M; Hiesberger T; Shelton J; Stockinger W ; Nimpf J ; Hammer RE ; Richardson JA ; Herz J. 1999. Reeler/Disabled-like disruption of neuronal migration in knockout mice lacking the VLDL receptor and ApoE receptor 2. Cell 97(6):689-701. [PubMed: 10380922]  [MGI Ref ID J:55691]

Trotter JH; Klein M; Jinwal UK; Abisambra JF; Dickey CA; Tharkur J; Masiulis I; Ding J; Locke KG; Rickman CB; Birch DG; Weeber EJ; Herz J. 2011. ApoER2 Function in the Establishment and Maintenance of Retinal Synaptic Connectivity. J Neurosci 31(40):14413-14423. [PubMed: 21976526]  [MGI Ref ID J:177435]

Uchida T; Baba A; Perez-Martinez FJ; Hibi T; Miyata T; Luque JM; Nakajima K; Hattori M. 2009. Downregulation of functional Reelin receptors in projection neurons implies that primary Reelin action occurs at early/premigratory stages. J Neurosci 29(34):10653-62. [PubMed: 19710317]  [MGI Ref ID J:152314]

Weeber EJ; Beffert U; Jones C; Christian JM; Forster E; Sweatt JD; Herz J. 2002. Reelin and ApoE Receptors Cooperate to Enhance Hippocampal Synaptic Plasticity and Learning. J Biol Chem 277(42):39944-52. [PubMed: 12167620]  [MGI Ref ID J:79593]

Weiss KH; Johanssen C; Tielsch A; Herz J; Deller T; Frotscher M; Forster E. 2003. Malformation of the radial glial scaffold in the dentate gyrus of reeler mice, scrambler mice, and ApoER2/VLDLR-deficient mice. J Comp Neurol 460(1):56-65. [PubMed: 12687696]  [MGI Ref ID J:83151]

Xia CH; Lu E; Liu H; Du X; Beutler B; Gong X. 2011. The role of Vldlr in intraretinal angiogenesis in mice. Invest Ophthalmol Vis Sci 52(9):6572-9. [PubMed: 21757581]  [MGI Ref ID J:176337]

Yagyu H; Lutz EP; Kako Y; Marks S; Hu Y; Choi SY; Bensadoun A; Goldberg IJ. 2002. Very low density lipoprotein (VLDL) receptor-deficient mice have reduced lipoprotein lipase activity. Possible causes of hypertriglyceridemia and reduced body mass with VLDL receptor deficiency. J Biol Chem 277(12):10037-43. [PubMed: 11790777]  [MGI Ref ID J:75452]

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Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           A1

Colony Maintenance

Breeding & Husbandry	This strain is maintained by homozygous sibling matings. Expected coat color from breeding:Black
Mating System	Homozygote x Homozygote         (Female x Male)   01-MAR-06
Diet Information	LabDiet® 5K52/5K67

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls

General Supply Notes

• This strain is included in the Eye Mutant Resource within the Mouse Mutant Resource collection.
• Genomic DNA is available for this strain from the Mouse DNA Resource.

Control Information

	Control
	101045 B6129SF2/J	(approximate)
Considerations for Choosing Controls
Control Pricing Information for Genetically Engineered Mutant Strains.

Payment Terms and Conditions

Terms are granted by individual review and stated on the customer invoice(s) and account statement. These transactions are payable in U.S. currency within the granted terms. Payment for services, products, shipping containers, and shipping costs that are rendered are expected within the payment terms indicated on the invoice or stated by contract. Invoices and account balances in arrears of stated terms may result in The Jackson Laboratory pursuing collection activities including but not limited to outside agencies and court filings.

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The Jackson Laboratory's Genotype Promise

The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX^® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX^® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX^® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project.

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Terms of Use

General Terms and Conditions

Contact information

General inquiries regarding Terms of Use

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phone:	207-288-6470
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JAX^® Mice, Products & Services Conditions of Use

"MICE" means mouse strains, their progeny derived by inbreeding or crossbreeding, unmodified derivatives from mouse strains or their progeny supplied by The Jackson Laboratory ("JACKSON"). "PRODUCTS" means biological materials supplied by JACKSON, and their derivatives. "RECIPIENT" means each recipient of MICE, PRODUCTS, or services provided by JACKSON including each institution, its employees and other researchers under its control. MICE or PRODUCTS shall not be: (i) used for any purpose other than the internal research, (ii) sold or otherwise provided to any third party for any use, or (iii) provided to any agent or other third party to provide breeding or other services. Acceptance of MICE or PRODUCTS from JACKSON shall be deemed as agreement by RECIPIENT to these conditions, and departure from these conditions requires JACKSON's prior written authorization.

In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of mice, products or services, JACKSON will, at its option, provide credit or replacement for the mice or product received or the services provided.

No Liability

In no event shall JACKSON, its trustees, directors, officers, employees, and affiliates be liable for any causes of action or damages, including any direct, indirect, special, or consequential damages, arising out of the provision of MICE, PRODUCTS or services, including economic damage or injury to property and lost profits, and including any damage arising from acts or negligence on the part of JACKSON, its agents or employees. Unless prohibited by law, in purchasing or receiving MICE, PRODUCTS or services from JACKSON, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges JACKSON from all such causes of action or damages, and further agrees to defend and indemnify JACKSON from any costs or damages arising out of any third party claims.

MICE and PRODUCTS are to be used in a safe manner and in accordance with all applicable governmental rules and regulations.

The foregoing represents the General Terms and Conditions applicable to JACKSON’s MICE, PRODUCTS or services. In addition, special terms and conditions of sale of certain MICE, PRODUCTS or services may be set forth separately in JACKSON web pages, catalogs, price lists, contracts, and/or other documents, and these special terms and conditions shall also govern the sale of these MICE, PRODUCTS and services by JACKSON, and by its licensees and distributors.

Acceptance of delivery of MICE, PRODUCTS or services shall be deemed agreement to these terms and conditions. No purchase order or other document transmitted by purchaser or recipient that may modify the terms and conditions hereof, shall be in any way binding on JACKSON, and instead the terms and conditions set forth herein, including any special terms and conditions set forth separately, shall govern the sale of MICE, PRODUCTS or services by JACKSON.