Vps34- kinase-dead

Contributors

Inventor Institute
Bart Vanhaesebroeck Ludwig Institute for Cancer Research
Cat. #: 158399
Research Fields: Cancer
Target: PIK3C3
Model: Knock-In
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).
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.
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).
Shipping conditions: Embryo/Spermatoza- Dry Ice
References:

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

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