PI3K-C2b kinase-dead

Contributors

Inventor Institute
Bart Vanhaesebroeck Ludwig Institute for Cancer Research
Cat. #: 158398
Research Fields: Cancer
Target: PIK3C2B
Model: Knock-In
Phenotype: Homozygous mice are phenotypically normaland born at a normal Mendelian ratio, with no impact on organismal growth. Mice display enhanced insulin sensitivity and glucose tolerance, as well as protection against high-fat-diet-induced liver steatosis. (see PMID 26655903 for details). Heterozygous mice are phenotypically normal.
Genetic background: Knock-in mice in which the endogenous PIK3C2B/PI3K-C2beta PI3K gene is mutated so that it now encodes a PI3K-C2beta protein with the D1212A mutation in the ATP binding site, converting it to a kinase-dead PI3K-C2beta protein which is expressed at the same level as wild-type PI3K-C2beta. These mice have been backcrossed onto the B6 background.
Production details: Knock-in mice in which the endogenous PIK3C2B/PI3K-C2beta PI3K gene is mutated so that it now encodes a PI3K-C2beta protein with the D1212A mutation in the ATP binding site, converting it to a kinase-dead PI3K-C2beta protein which is expressed at the same level as wild-type PI3K-C2beta. These mice have been backcrossed onto the B6 background.
Additional notes: Homozygous mice are phenotypically normaland born at a normal Mendelian ratio, with no impact on organismal growth. Mice display enhanced insulin sensitivity and glucose tolerance, as well as protection against high-fat-diet-induced liver steatosis. (see PMID 26655903 for details). Heterozygous mice are phenotypically normal.
Shipping conditions: Embryo/Spermatoza- Dry Ice
References:

Alliouachene et al. 2015. Cell Rep. 13(9):1881-94. PMID: 26655903.

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