B6J.B6NTac-Pik3c2btm1.1Arte/H
| Status | Available to order |
| EMMA ID | EM:13249 |
| International strain name | B6J.B6NTac-Pik3c2btm1.1Arte/H |
| Alternative name | PI3K-C2b kinase dead |
| Strain type | Targeted Mutant Strains : Point mutation |
| Allele/Transgene symbol | Pik3c2btm1.1Arte, |
| Gene/Transgene symbol | Pik3c2b |
Information from provider
| Provider | Bart Vanhaesebroeck |
| Provider affiliation | University College London |
| Genetic information | Knock-in mice in which the endogenous Pik3c2b (PIK3C2B/PI3K-C2 beta) gene is mutated so that it now encodes a PIK3C2B protein with the D1212A mutation in the ATP binding site, converting it to a kinase-dead PIK3C2B protein which is expressed at the same level as wild-type PIK3C2B. These mice have been backcrossed onto the C57BL/6 background. |
| Phenotypic information | Homozygous:Mice are phenotypically normal. Mice display enhanced insulin sensitivity and glucose tolerance, as well protection against high fat diet-induced liver steatosis (see Alliouachene S. et al., 2015, PubMed ID: 26655903).Heterozygous:Mice are phenotypically normal. |
| Breeding history | Backcrossed onto C57BL/6J for more than 10 generations. |
| References |
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| Homozygous fertile | yes |
| Homozygous viable | yes |
| Homozygous matings required | no |
| Immunocompromised | no |
Information from EMMA
| Archiving centre | Mary Lyon Centre at MRC Harwell, Oxford, United Kingdom |
Literature references
- Inactivation of the Class II PI3K-C2β Potentiates Insulin Signaling and Sensitivity.;Alliouachene Samira, Bilanges Benoit, Chicanne Gaëtan, Anderson Karen E, Pearce Wayne, Ali Khaled, Valet Colin, Posor York, Low Pei Ching, Chaussade Claire, Scudamore Cheryl L, Salamon Rachel S, Backer Jonathan M, Stephens Len, Hawkins Phill T, Payrastre Bernard, Vanhaesebroeck Bart, ;2015;Cell reports;13;1881-94; 26655903