| Title | Phenotype | Contact | |
|---|---|---|---|
| B6.Cg-Tg(IL3,CSF2)C42Pnc/H | No overt phenotype. | Contact | |
| B6.Cg-Tg(PRNP-DNAJB2_ia)52aMec/MecH | No overt phenotype noted. | Contact | |
| B6.Cg-Tg(PRNP-DNAJB2_ia)61aMec/MecH | No overt phenotype. | Contact | |
| B6.Cg-Tg(RP3-340H11)29Kel/H | Mild hyperglycaemia in neonates, mildly impaired glucose tolerance post weaning. | Contact | |
| B6.Cg-Tg(Slc16a1-Luc)50Rttr/H | 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 | 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 | 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> | 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 | |
| B6;129-Apoe<tm1Bres> Lgals3<tm1Ftl>/CljH | No overt phenotype reported. | Contact | |
| B6;129-Brca1<tm1Aash>/Aash | No visible phenotype. | Contact | |
| B6;129-Ccr9<tm1Dgen>/H | MGI report that homozygotes have impaired coordination. | Contact | |
| B6;129-Flrt2<tm1c(EUCOMM)Wtsi>/RobH | Both heterozygotes and homozygotes have no overt phenotype. | Contact | |
| B6;129-Fshr<tm1Mha>/H | Homozygous males are fertile, but testis weight is reduced (~50% of normal). Homozygous females are infertile, ovulation does not occur. Heterozygous males are indistinguishable from wild type. | Contact | |
| B6;129-Gt(ROSA)26Sor<tm1(CAG-Venus/GMNN,Cherry/CDT1)Jkn>/JknH | The Fucci system was developed by fusing red- and green-emitting fluorescent proteins to the E3 ligase substrates, Cdt1 and Geminin. These fluorescent probes make it possible to distinguish between cells in the G1 or S/G2/M phases of the cell cycle in live cells/tissue (Sakaue-Sawano al 2008). Fucci2a is a bicistronic version of Fucci2 allowing Cre-mediated tissue-specific expression in mice (Mort, R et al 2014). | Contact | |
| B6;129-Khdrbs3<tm1Dell>/DellH | These mice do not express T-STAR protein by Western blotting | Contact | |
| B6;129-Nek6<tm1Dgen>/H | No visible phenotype. | Contact | |
| B6;129-P2ry12<tm1Dgen>/H | None | Contact | |
| B6;129-Ptprc<tm1Holm>/H | Defective lymphocyte development, more severe in T lineage, severe combined immunodeficiency. | Contact | |
| B6;129-Reg2<tm1Lchr>/H | Viable, normal breeding pattern, no obvious phenotype. | Contact | |
| B6;129-Scn10a<tm3(cre/ERT2)Jnw>/H | None observed (heterozygous Nav1.8-CreERT2 can express enough Cre to delete the floxed fragment, but it does not affect the expression of Nav1.8 in Nav1.8 positive neurons in DRG). | Contact |
