EC Number   |
General Information |
Reference |
|---|
   2.7.1.154 | evolution |
PI3K enzyme sequence comparisons |
761194 |
| 2.7.1.154 | evolution |
three enzymes belong to the class II subfamily, PI3K-C2alpha, beta, and gamma |
739678 |
| 2.7.1.154 | malfunction |
agonist-induced 3-phosphorylated phosphoinositide production and cellular activation are normal in PI3KC2alpha-deficient platelets. PI3KC2alpha deficiency exacerbates bleeding and impairs thrombosis. Phenotype of Pik3c2alpha-/- mice. PI3KC2alpha deficiency alters platelet and megakaryocyte internal membrane structures, overview. PI3KC2alpha deficiency causes unstable platelet thrombi and enhances shear-dependent platelet adhesion |
739146 |
| 2.7.1.154 | malfunction |
different deficiency types of PI3KC2alpha can cause different phenotypes, including stunted growth, decreased survival, renal abnormalities, embryonic lethality, decreased retinal angiogenesis, impaired revascularization following ischemic injury, and impaired platelet function during thrombosis. Mouse models of PI3KC2alpha deficiency. While homozygosity for kinase-dead PI3KC2alpha is embryonic lethal, heterozygous PI3KC2alpha KI mice are viable and fertile, with no significant histopathological findings. Male heterozygous mice show early onset leptin resistance, with a defect in leptin signaling in the hypothalamus, correlating with a mild, age-dependent obesity, insulin resistance, and glucose intolerance |
761670 |
| 2.7.1.154 | malfunction |
downregulation of PI3K-C2beta in breast cancer cell lines reduces colony formation, induces cell cycle arrest and inhibits tumor growth, in particular in an estrogen-dependent in vivo xenograft. PI3K-C2beta inhibits breast cancer cell invasion in vitro and breast cancer metastasis in vivo |
739216 |
| 2.7.1.154 | malfunction |
downregulation of PI3KC2beta results the inhibition of early stage neuroblastoma formation. Serum-dependent lamellipodia formation has been significantly reduced in cells lacking PI3KC2beta. Selective inhibition of PI3KC2beta with ceramide has been shown to diminish PI3KC2beta-dependent lamellipodia formation, reducing ovarian cancer cell mobility. Blocking of PI3KC2? pathway results in the impairment of SKOV3 cell migration. Depletion of PI3KC2beta can increase resistance of cells to chemotherapeutics |
761670 |
| 2.7.1.154 | malfunction |
effects of LY294002, sevoflurane (SEVO) and isoflurane (ISO) on KCl-elicited PI3KC2alpha mediated vasoconstriction in rat aortic smooth muscle, overview. PI3K inhibitor LY294002 inhibits PI3K-C2alpha membrane translocation in response to KCl. SEVO and ISO inhibit KCl-stimulated MLC phosphorylation, PI3K-C2alpha and Rock-II, but not PI3K p85, membrane translocation in a concentration-dependent manner in rat aorta |
760780 |
| 2.7.1.154 | malfunction |
global deficiency of PI3KC2gamma causes a phenotype of hyperlipidemia, adiposity, and insulin resistance |
761670 |
| 2.7.1.154 | malfunction |
heterozygous kinase-dead inactivating mutation of PI3KC2gamma causes a phenotype of decreased circulating insulin levels, increased glucose tolerance, and protection against steatosis. Inhibition of PI3KC2beta significantly reduced ovarian cancer metastasis in mice |
761670 |
| 2.7.1.154 | malfunction |
inhibition of MEK/ERK activation as well as downregulation of PI3K-C2beta does not affect cell proliferation while specifically inhibiting cell invasion |
739678 |
