PI3K-C2a kinase-dead

Contributors

Inventor Institute
Bart Vanhaesebroeck Ludwig Institute for Cancer Research
Cat. #: 158396
Research Fields: Cancer
Target: PIK3C2A
Model: Knock-In
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.
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.
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.
Shipping conditions: Embryo/Spermatoza- Dry Ice
References:

Alliouachene et al. 2016. Diabetologia. 59(7):1503-1512. PMID: 27138914.

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