Cat. #158396
PI3K-C2a kinase-dead
Cat. #: 158396
Sub-type: Mouse
Availability: 8-10 weeks
Model: Knock-In
This fee is applicable only for non-profit organisations. If you are a for-profit organisation or a researcher working on commercially-sponsored academic research, you will need to contact our licensing team for a commercial use license.
Contributor
Inventor: Bart Vanhaesebroeck
Institute: Ludwig Institute for Cancer Research
Tool Details
*FOR RESEARCH USE ONLY (for other uses, please contact the licensing team)
- Tool name: PI3K-C2a kinase-dead
- Research fields: Cancer
- Tool sub type: Mouse
- Model: Knock-In
- Genetic background: The genomic DNA encoding the ATP-binding DFG motif in the gene encoding PI3K-C2a (Pik3c2a) is mutated to encode the AFG sequence, resulting in the production of a kinase-dead PI3K-C2a protein.
- Phenotype: Homozygote mice are lethal between embryonic day 10.5 & 11.5. Heterozygous PI3K-C2a KI mice were viable and fertile, with no significant histopathological findings. However, male heterozygous mice showed early onset leptin resistance, with a defect in leptin signalling in the hypothalamus,correlating with a mild, age-dependent obesity, insulin resistance and glucose intolerance. Insulin signalling was unaffected in insulin target tissues of PI3K-C2a KI mice, in contrast to previous reports in which downregulation of PI3K-C2a in cell lines was shown to dampen insulin signalling. Interestingly, no metabolic phenotypes were detected in female PI3K-C2a KI mice at any age.
- Production details: The genomic DNA encoding the ATP-binding DFG motif in the gene encoding PI3K-C2Îą (Pik3c2a) is mutated to encode the AFG sequence, resulting in the production of a kinase-dead PI3K-C2Îą protein.
- Additional notes: Homozygote mice are lethal between embryonic day 10.5 & 11.5. Heterozygous PI3K-C2Îą KI mice were viable and fertile, with no significant histopathological findings. However, male heterozygous mice showed early onset leptin resistance, with a defect in leptin signalling in the hypothalamus,correlating with a mild, age-dependent obesity, insulin resistance and glucose intolerance. Insulin signalling was unaffected in insulin target tissues of PI3K-C2Îą KI mice, in contrast to previous reports in which downregulation of PI3K-C2Îą in cell lines was shown to dampen insulin signalling. Interestingly, no metabolic phenotypes were detected in female PI3K-C2Îą KI mice at any age.
Handling
- Shipping conditions: Embryo/Spermatoza- Dry Ice
Target Details
- Target: PIK3C2A
References
- Alliouachene et al. 2016. Diabetologia. 59(7):1503-1512. PMID: 27138914.
