PKCA Antibodies

Target Information

a classical protein kinase C (PKC) downstream of many receptors. Classical PKCs are calcium-dependent enzymes that are activated by phosphatidylserine, diacylglycerol and phorbol esters. Contains a pseudo-substrate autoinhibitory domain that binds to the catalytic domain preventing its activation in the absence of cofactors or activators. Involved in positive and negative regulation of cell proliferation, apoptosis, differentiation, migration and adhesion, tumorigenesis, cardiac hypertrophy, angiogenesis, platelet function and inflammation. Involved in cell proliferation and cell growth arrest by positive and negative regulation of the cell cycle. Can promote cell growth by phosphorylating and activating RAF1, which mediates the activation of the MAPK/ERK signaling cascade. Exhibits anti-apoptotic function in glioma cells and protects them from apoptosis by suppressing the p53-mediated activation of IGFBP3, and in leukemia cells mediates anti-apoptotic action by phosphorylating BCL2. After wounding, translocates from focal contacts to lamellipodia and participates in the modulation of desmosomal adhesion. Associated with increases in cellular polarization and motility. During chemokine-induced CD4(+) T cell migration, phosphorylates CDC42-guanine exchange factor DOCK8 resulting in its dissociation from LRCH1 and the activation of GTPase CDC42. Is highly expressed in a number of cancer cells where it can act as a tumor promoter and is implicated in malignant phenotypes of several tumors such as gliomas and breast cancers. Negatively regulates myocardial contractility and positively regulates angiogenesis, platelet aggregation and thrombus formation in arteries. Regulates cardiomyocyte function by phosphorylating cardiac troponin T (TNNT2), which induces significant reduction in actomyosin ATPase activity, myofilament calcium sensitivity and myocardial contractility. In angiogenesis, is required for full endothelial cell migration, adhesion to vitronectin (VTN), and vascular endothelial growth factor A (VEGFA)-dependent regulation of kinase activation and vascular tube formation. Involved in the stabilization of VEGFA mRNA at post-transcriptional level, and the regulation of calcium-induced platelet aggregation. During response to lipopolysaccharides (LPS), may regulate selective LPS-induced macrophage functions involved in host defense and inflammation. But in some inflammatory responses, may negatively regulate NF-kappa-B-induced genes, through IL1A-dependent induction of NF-kappa-B inhibitor alpha (NFKBIA/IKBA). Phosphorylates KIT, leading to inhibition of KIT activity. Phosphorylates ATF2 which promotes cooperation between ATF2 and JUN, activating transcription. Belongs to the AGC Ser/Thr protein kinase family, PKC subfamily. Note: This description may include information from UniProtKB.

Alternate Names