| Title | Phenotype | Contact | |||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| B6.C3H;B6-Crh<m1H> |
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Heterozygous Crh<m1H> are obese, exhibit muscle wasting, thin skin, hair loss, elevated plasma and urinary corticosterone, hyperglycaemia, hyperinsulinaemia, hypercholesterolemia, hypertryglyceridemia and hyperleptinaemia. They also have low bone mineral density, hypercalcemia, hypercalciuria and decreased concentrations of plasma PTH and osteocalcin. Heterozygotes can be visibly distinguished from wild types at about 5-6 weeks of age by their short, skinny tails and scruffy coat. They also have thin skin and their hair starts to thin as they age. | Contact | ||||||||||||
| B6.CAnNCrl(C3)-Dync1i2<m1H>/EmcfH | Currently being tested, trend towards slight locomotor deficit, nothing significant so far. | Contact | |||||||||||||
| B6.CAnNCrl(C3H)-Dync1li1<m1Emcf>/H |
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Mouse not completely assessed but so far homozygotes have behavioural and neurological changes. | Contact | ||||||||||||
| B6.Cg-Cited2<L247P>/H |
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Although the amino acid change occurs in a highly conserved residue, the mutant is homozygous viable and fertile, with no detectable phenotype. In trans to the Knock-out allele, it is viable and phenotypically normal. | Contact | ||||||||||||
| B6.Cg-Ddx5<tm1.1Arte> Gt(ROSA)26Sor<tm9(cre/ESR1)Arte>/H |
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Mouse strain has no detectable phenotype in the absence of activated Cre. Tamoxifen treatment induces p68 knockout in multiple tissues; this results in hypoplastic bone marrow and alterations in tissue organisation in the large intestine of a high proportion of mice. However, we have only been able to perform short term experiments. These mice would be ideal for the generation of tissue-specific p68 knockout models. | 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-Mrc2<tm1Cmi>Tg(CAG-EGFP)1Osb/CmiH |
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Homozygous transgenic mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. All of the tissues, with the exception of erythrocytes and hair, appear green under excitation light. | Contact | ||||||||||||
| B6.Cg-Ndrg1<str>/H |
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Mice at first develop normally but around the age of 5-6 weeks develop a peripheral demyelinating neuropathy resulting in weakness of the hind limbs. This manifests as clasping hind legs when suspended by tail, marked tremour, inability to maintain normal posture. Signs progress rapidly at first, stabilize after 20 weeks. | Contact | ||||||||||||
| B6.Cg-Sfrp2<I153N>/H |
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No overt Phenotype. Full description available from Europhenome. | Contact | ||||||||||||
| B6.Cg-Syce1<tm1Hgu>/H |
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Mice homozygous for this mutation in this background can not progress to diplotene stages of meiosis and show a failure of synapsis. Heterozygous mice show close to normal fertility. | Contact | ||||||||||||
| B6.Cg-Syce2<Gt(FHCRC-GT-S8-7E1)Sor>/H |
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Mice homozygous for this mutation in this background can not progress to diplotene stages of meiosis and show a failure of synapsis. Heterozygous mice show close to normal fertility. | Contact | ||||||||||||
| B6.Cg-Tg(ACTFLPe)9205Dym/H |
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No overt phenotype. | Contact | ||||||||||||
| B6.Cg-Tg(IL3,CSF2)C42Pnc/H |
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No overt phenotype. | Contact | ||||||||||||
| B6.Cg-Tg(PRNP-DNAJB2_ia)52aMec/MecH |
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No overt phenotype noted. | Contact | ||||||||||||
| B6.Cg-Tg(PRNP-DNAJB2_ia)61aMec/MecH |
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No overt phenotype. | Contact | ||||||||||||
| B6.Cg-Tg(RP3-340H11)29Kel/H |
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Mild hyperglycaemia in neonates, mildly impaired glucose tolerance post weaning. | Contact | ||||||||||||
| B6.Cg-Tg(Slc16a1-Luc)50Rttr/H |
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When expressed in pancreatic beta cells it renders insulin secretion sensitive to pyruvate and prevents the normal inhibition of insulin secretion induced by exercise, replicating the key features of Exercise-Induced Hyperinsulinism. | Contact | ||||||||||||
| B6.Cg-Tyr<c-Brd> Mir155<tm1.1Brd>/H |
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No visible phenotype is associated with this mutation but the mice do exhibit reduced lung airway remodelling & deficient B-cell, T-cell & dendritic cell function. This mutation is on a C57BL/6<c-/c-> background and is albino in appearance. The BIC mice (EMMA ID EM:02231) have been backcrossed at least 5 times to C57BL/6, thus making them suitable for bone marrow transplantation, without rejection, to any C57BL/6 mice, regardless of coat color. | Contact | ||||||||||||
| B6129S8-Tc(Hsa21)1TybEmcf/H |
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This strain displays learning abnormalities, reduced long-term potentiation in the hippocampus, heart and brain developmental defects, craniofacial dysmorphology (this strain models human Down syndrome). | Contact | ||||||||||||
| B6;129-Anxa6<tm1Moss> |
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Homozygotes have altered mechanical and intracellular calcium signalling in cardiomyocytes. They display altered regulation of mitochondrial morphogenesis. Western blot studies indicate that no detectable protein is produced. Original chimaeric mouse was crossed to C57BL/6 then strain has been maintained by sib crossing for 20 generations. | Contact |
