Title | Phenotype | Contact | |||||||||
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B10ScSn.BXSB-(D1Mit33-D1Mit223) Chr Y<BXSB/MpJ>/BjmjrH | ANA, 75% mortality, enhanced autoantibody titre, severe glomerulonephritis. | Contact | |||||||||
B6(C)-Npr3<Kylb>/H |
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Homozygotes have an small and elongated body, kyphosis and long bones. | Contact | ||||||||
B6(Cg)-Clec9a<tm1.1Crs>/H |
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The CD8+ve family of dendritic cells lack expression of DNGR-1 (CLEC9) and are impaired in the cross-priming of T-cells. | Contact | ||||||||
B6(Cg)-Grik4<tm1.1(cre)Slab>/H |
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Cre mouse with restricted expression in subregions of the hippocampus, mainly in CA3 and absent in CA1. No obvious phenotype in the absence of a target allele | Contact | ||||||||
B6(Cg)-Klra5<tm1.1Cgbr>/H |
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Lack of expression of Ly49E. Expression of b-geo. No other known phenotype at present. | Contact | ||||||||
B6.129-Abcc8<tm1.1Fmas>/LaakFmasH |
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Homozygous mice develop mild glucose intolerance with age due to a reduction in insulin content in the pancreatic beta-cell. Heterozygous mice are far less affected. Unlike in humans, there is no clear hyperinsulinism in the neonatal period. | Contact | ||||||||
B6.129-Anpep<tm1Afk>/AfkH |
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No overt phenotype is seen in mice homozygous for Anpep<tm1aAfk>. However, a delay in mammary development was detected. Similar knock-outs for Anpep have shown a deficiency in tumour vascularisation. This was not assessed for this mutated allele. Heterozygotes had no detectable phenotype. See PMID:22983824. | Contact | ||||||||
B6.129-Cited2<tm2Bha>/H |
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Cre-mediated recombination throughout the entire epiblast of early embryos recapitulates the complete loss of function phenotype of Cited2, which include cardiac malformations, adrenal agenesis, fusion of cranial ganglia, abnormal cardiac neural crest migration, excencephaly and left right patterning defects. | Contact | ||||||||
B6.129-Flrt2<tm1Rob>/RobH |
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Mouse embryos deficient in Flrt2 display defects in heart morphogenesis, in particular, defects in the integrity of the epicardium and disturbances to the architecture of the underlying basement membrane accompanied by a pronounced reduction in thickness of the ventricular myocardium. A small proportion of homozygous mutants survive gestation (<3%). Heterozygous mice have no overt phenotype. | Contact | ||||||||
B6.129-Krt36<tm1Hpt>/H |
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Hyperkeratosis of scales (tail) and filiform papillae (tongue). The analyses are not yet complete but if present, the phenotype is very weak in heterozygotes. An obvious hyperkeratosis is however apparent in homozygous mutant animals. | Contact | ||||||||
B6.129-Mrc2<tm1Cmi>/H |
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Homozygous Endo180DeltaEx2-6/Endo180DeltaEx2-6 mice are phenotypically normal (at the gross level), healthy and fertile. | Contact | ||||||||
B6.129-Nrxn2<tm1Sud>/H |
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Mice homozygous for a knock-out allele show a 30-40% decrease in body weight and their inhibitory postsynaptic currents (IPSCs) are decreased in cortical slice cultures. Further phenotyping data to be published shortly. | Contact | ||||||||
B6.129-Prdm1<tm1.1Liz>/RobH |
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No overt phenotype. Mice with targeted exon 1A deletion show that Prdm1 expression has been eliminated in LPS-stimulated B cells and plasma cell differentiation has been blocked. Embryonic development is not disrupted, and embryos with this deletion show modestly reduced Prdm1 expression levels. | Contact | ||||||||
B6.129-Prdm1<tm1.1Liz>/RobH |
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No overt phenotype. Mice with targeted exon 1A deletion show that Prdm1 expression has been eliminated in LPS-stimulated B cells and plasma cell differentiation has been blocked. Embryonic development is not disrupted, and embryos with this deletion show modestly reduced Prdm1 expression levels. | Contact | ||||||||
B6.129-Prdm1<tm2.1Liz>/RobH |
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No overt phenotype. Mice with targeted exon 1B deletion have slightly decreased expression in the yolk sac but show no other noticeable effects in embryo or adult tissues. | Contact | ||||||||
B6.129-Prdm1<tm3.1Liz>/RobH |
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Homozygotes are lethal and die around E10.5 due to placental defects. Heterozygotes have no overt phenotype. | Contact | ||||||||
B6.129-Prdm1<tm4.1Liz>/RobH |
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Homozygotes and heterozygotes show no overt phenotype. | Contact | ||||||||
B6.129-Prdm4<tm2.1Liz>/RobH |
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Mice with targeted deletion of the zinc finger domain have no phenotype. Heterozygotes also have no overt phenotype. | Contact | ||||||||
B6.129-S100A10<tm1Jnw>/H |
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None. | Contact | ||||||||
B6.129-Scn10a<tm2(cre)Jnw>/H |
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No phenotype in heterozygotes. Some pain deficits in homozygotes. | Contact |