Vps34- kinase-dead

Tool Details

*FOR RESEARCH USE ONLY (for other uses, please contact the licensing team)

• Tool name: Vps34- kinase-dead
• Research fields: Cancer
• Tool sub type: Mouse
• Model: Knock-In
• Genetic background: Knock-in mice in which the endogenous PIK3C3/vps34 PI3K gene is mutated so that it now encodes a vps34 protein with the D761A mutation in the ATP binding site, converting it to a kinase-dead vps34 protein which is expressed at the same level as wild-type vps34. These mice have been backcrossed onto the B6 background.
• Phenotype: Homozygous mice show prenatal partial lethality at early embryonic stages between embryonic day (E) 6.5 and 8.5 (see PMID 29180704 for details). Heterozygous mice are healthy and display a robustly enhanced insulin sensitivity and glucose tolerance as well as a partial protection against high-fat-diet-induced liver steatosis. (see PMID 29180704 for details).
• Production details: Knock-in mice in which the endogenous PIK3C3/vps34 PI3K gene is mutated so that it now encodes a vps34 protein with the D761A mutation in the ATP binding site, converting it to a kinase-dead vps34 protein which is expressed at the same level as wild-type vps34. These mice have been backcrossed onto the B6 background.
• Additional notes: Homozygous mice show prenatal partial lethality at early embryonic stages between embryonic day (E) 6.5 and 8.5 (see PMID 29180704 for details). Heterozygous mice are healthy and display a robustly enhanced insulin sensitivity and glucose tolerance as well as a partial protection against high-fat-diet-induced liver steatosis. (see PMID 29180704 for details).

Handling

• Shipping conditions: Embryo/Spermatoza- Dry Ice

Target Details

• Target: PIK3C3

References

• Bilanges et al. 2017. Nat Commun. 8(1):1804. PMID: 29180704.