Anti-PI 3 Kinase catalytic subunit alpha/PIK3CA Antibody Picoband® Fluoro647 Conjugated

Phosphatidylinositol-4,5-bisphosphate 3-kinase, also called PIK3CA, is composed of an 85 kDa regulatory subunit and a 110 kDa catalytic subunit. PIK3CA gene is mapped to 3q26.32. The protein encoded by this gene represents the catalytic subunit, which uses ATP to phosphorylate phosphatidylinositols (PtdIns), PtdIns4P andPtdIns (4,5) P2. Recent evidence has shown that the PIK3CA gene is mutated in a range of human cancers. It has been found to be oncogenic and has been implicated in cervical cancers. PIK3CA mutations in breast cancer may be a predictive marker to guide the selection of patients who would benefit from mTOR inhibitor therapy. In addition to that, the presence of PIK3CA mutation may predict response to aspirin therapy for colorectal cancer, indicating power and promise of Molecular Pathological Epidemiology (MPE) approach as well as a complex interaction within the tumor microenvironment in this phenomenon.

Phosphatidylinositol 4,5-bisphosphate 3-kinase catalytic subunit alpha isoform; PI3-kinase subunit alpha; PI3K-alpha; PI3Kalpha; PtdIns-3-kinase subunit alpha;2.7.1.153; Phosphatidylinositol 4,5-bisphosphate 3-kinase 110 kDa catalytic subunit alpha; PtdIns-3-kinase subunit p110-alpha; p110alpha; Phosphoinositide-3-kinase catalytic alpha polypeptide; Serine/threonine protein kinase PIK3CA;2.7.11.1; PIK3CA

Phosphoinositide-3-kinase (PI3K) that phosphorylates PtdIns (Phosphatidylinositol), PtdIns4P (Phosphatidylinositol 4- phosphate) and PtdIns (4,5) P2 (Phosphatidylinositol 4,5- bisphosphate) to generate phosphatidylinositol 3,4,5-trisphosphate (PIP3) . PIP3 plays a key role by recruiting PH domain-containing proteins to the membrane, including AKT1 and PDPK1, activating signaling cascades involved in cell growth, survival, proliferation, motility and morphology. Participates in cellular signaling in response to various growth factors. Involved in the activation of AKT1 upon stimulation by receptor tyrosine kinases ligands such as EGF, insulin, IGF1, VEGFA and PDGF. Involved in signaling via insulin-receptor substrate (IRS) proteins. Essential in endothelial cell migration during vascular development through VEGFA signaling, possibly by regulating RhoA activity. Required for lymphatic vasculature development, possibly by binding to RAS and by activation by EGF and FGF2, but not by PDGF. Regulates invadopodia formation in breast cancer cells through the PDPK1- AKT1 pathway. Participates in cardiomyogenesis in embryonic stem cells through a AKT1 pathway. Participates in vasculogenesis in embryonic stem cells through PDK1 and protein kinase C pathway. Has also serine-protein kinase activity: phosphorylates PIK3R1 (p85alpha regulatory subunit), EIF4EBP1 and HRAS. .

1.Hiles I, Otsu M, Volinia S, Fry M, Gout I, Dhand R et al. (August 1992) . Phosphatidylinositol 3-kinase: structure and expression of the 110 kd catalytic subunit. Cell 70 (3) : 419–29. 2.Ma Y, Wei S, Lin Y, Lung J, Chang T, Whang-Peng J et al. (May 2000) . PIK3CA as an oncogene in cervical cancer. Oncogene 19 (23) : 2739–44. 3.Weigelt, B., Warne, P. H., Downward, J. PIK3CA mutation, but not PTEN loss of function, determines the sensitivity of breast cancer cells to mTOR inhibitory drugs. Oncogene 30: 3222-3233, 2011.