#158398

PI3K-C2b kinase-dead

Cat. #158398

PI3K-C2b kinase-dead

Cat. #: 158398

Sub-type: Mouse

Availability: 6-8 weeks

Model: Knock-In

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Contributor

Inventor: Bart Vanhaesebroeck

Institute: Ludwig Institute for Cancer Research

Tool Details
Handling
Target Details
References

Tool Details

*FOR RESEARCH USE ONLY

  • Tool name: PI3K-C2b kinase-dead
  • Tool sub type: Mouse
  • Model: Knock-In
  • 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.
  • 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.
  • 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.

Handling

  • Shipping conditions: Embryo/Spermatoza- Dry Ice

Target Details

  • Target: PIK3C2B

References

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