IMPC phenotypes (gene matching)
Vps34-kinase dead
| Status | Available to order |
| EMMA ID | EM:13250 |
| Citation information | RRID:IMSR_EM:13250 Research Resource Identifiers (RRID) are persistent unique ID numbers assigned to help researchers cite key resources (e.g. antibodies, model organisms and software projects) in the biomedical literature to improve transparency and reproducibility in research. See https://www.rrids.org/ for more information. |
| International strain name | Vps34-kinase dead |
| Alternative name | Vps34-kinase dead |
| Strain type | Targeted Mutant Strains : Point mutation |
| Allele/Transgene symbol | Pik3c3tm1.1Arte |
| Gene/Transgene symbol | Pik3c3 |
Information from provider
| Provider | Bart Vanhaesebroeck |
| Provider affiliation | University College London |
| Genetic information | Mutant mice in which the endogenous Pik3c3 (PIK3C3/Vps34 PI3K) gene is mutated so that it now encodes a protein with the D761A mutation in the ATP binding site, converting it to a kinase-dead PIK3C3 (Vps34) protein, which is expressed at the same level as the wild-type. These mice have been backcrossed onto the C57BL/6 background. |
| Phenotypic information | Homozygous:Mice show prenatal partial lethality at early embryonic stages between embryonic day E6.5 and 8.5 (for details see Bilanges B. et al., 2017, PubMed ID: 29180704).Heterozygous:Heterozygous mice are healthy and display a robustly enhanced insulin sensitivity and glucose tolerance as well as partial protection against high fat diet-induced liver steatosis. |
| Breeding history | Backcrossed onto C57BL/6J for more than 10 generations. |
| References |
|
| Homozygous fertile | no |
| Homozygous viable | no |
| Homozygous matings required | no |
| Immunocompromised | not known |
Information from EMMA
| Archiving centre | Mary Lyon Centre at MRC Harwell, Oxford, United Kingdom |
Disease and phenotype information
MGI phenotypes (gene matching)
- decreased cell proliferation / MGI
- absent mesoderm / MGI
- failure of primitive streak formation / MGI
- failure to gastrulate / MGI
- decreased embryo size / MGI
- embryonic growth arrest / MGI
- no abnormal phenotype detected / MGI
- abnormal embryonic epiblast morphology / MGI
- embryonic growth retardation / MGI
- disorganized embryonic tissue / MGI
- cellular phenotype / MGI
- embryonic lethality between implantation and placentation, complete penetrance / MGI
- abnormal visceral endoderm morphology / MGI
Literature references
- Vps34 PI 3-kinase inactivation enhances insulin sensitivity through reprogramming of mitochondrial metabolism.;Bilanges Benoit, Alliouachene Samira, Pearce Wayne, Morelli Daniele, Szabadkai Gyorgy, Chung Yuen-Li, Chicanne Gaëtan, Valet Colin, Hill Julia M, Voshol Peter J, Collinson Lucy, Peddie Christopher, Ali Khaled, Ghazaly Essam, Rajeeve Vinothini, Trichas Georgios, Srinivas Shankar, Chaussade Claire, Salamon Rachel S, Backer Jonathan M, Scudamore Cheryl L, Whitehead Maria A, Keaney Erin P, Murphy Leon O, Semple Robert K, Payrastre Bernard, Tooze Sharon A, Vanhaesebroeck Bart, ;2017;Nature communications;8;1804; 29180704