PRKCH
Entrez ID: 5583
Full name: protein kinase C eta
External links: HGNC UniprotKB Ensembl RefSeq COSMIC
Family: AGC: PKC: PKCh
Chromosomal location: 14q23.1
Substructure location: Gatekeeper: 433 A-loop: 496...519 G-loop: 362...369 αC-helix: 388...394
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PRKCH
Calcium-independent, phospholipid- and diacylglycerol (DAG)-dependent serine/threonine-protein kinase that is involved in the regulation of cell differentiation in keratinocytes and pre-B cell receptor, mediates regulation of epithelial tight junction integrity and foam cell formation, and is requir...
Calcium-independent, phospholipid- and diacylglycerol (DAG)-dependent serine/threonine-protein kinase that is involved in the regulation of cell differentiation in keratinocytes and pre-B cell receptor, mediates regulation of epithelial tight junction integrity and foam cell formation, and is required for glioblastoma proliferation and apoptosis prevention in MCF-7 cells. In keratinocytes, binds and activates the tyrosine kinase FYN, which in turn blocks epidermal growth factor receptor (EGFR) signaling and leads to keratinocyte growth arrest and differentiation. Associates with the cyclin CCNE1-CDK2-CDKN1B complex and inhibits CDK2 kinase activity, leading to RB1 dephosphorylation and thereby G1 arrest in keratinocytes. In association with RALA activates actin depolymerization, which is necessary for keratinocyte differentiation. In the pre-B cell receptor signaling, functions downstream of BLNK by up-regulating IRF4, which in turn activates L chain gene rearrangement. Regulates epithelial tight junctions (TJs) by phosphorylating occludin (OCLN) on threonine residues, which is necessary for the assembly and maintenance of TJs. In association with PLD2 and via TLR4 signaling, is involved in lipopolysaccharide (LPS)-induced RGS2 down-regulation and foam cell formation. Upon PMA stimulation, mediates glioblastoma cell proliferation by activating the mTOR pathway, the PI3K/AKT pathway and the ERK1-dependent phosphorylation of ELK1. Involved in the protection of glioblastoma cells from irradiation-induced apoptosis by preventing caspase-9 activation. In camptothecin-treated MCF-7 cells, regulates NF-kappa-B upstream signaling by activating IKBKB, and confers protection against DNA damage-induced apoptosis. Promotes oncogenic functions of ATF2 in the nucleus while blocking its apoptotic function at mitochondria. Phosphorylates ATF2 which promotes its nuclear retention and transcriptional activity and negatively regulates its mitochondrial localization.
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GO - Biological processes (BP):
intracellular signal transduction, negative regulation of glial cell apoptotic process, peptidyl-serine phosphorylation, platelet activation, positive regulation of B cell receptor signaling pathway, positive regulation of glial cell proliferation, positive regulation of keratinocyte differentiation...
intracellular signal transduction, negative regulation of glial cell apoptotic process, peptidyl-serine phosphorylation, platelet activation, positive regulation of B cell receptor signaling pathway, positive regulation of glial cell proliferation, positive regulation of keratinocyte differentiation, positive regulation of macrophage derived foam cell differentiation, positive regulation of NF-kappaB transcription factor activity, positive regulation of protein localization to plasma membrane, protein phosphorylation, regulation of bicellular tight junction assembly, signal transduction
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GO - Molecular function (MF):
ATP binding, calcium-dependent protein kinase C activity, enzyme binding, metal ion binding, protein kinase C activity, protein serine/threonine kinase activity...
ATP binding, calcium-dependent protein kinase C activity, enzyme binding, metal ion binding, protein kinase C activity, protein serine/threonine kinase activity
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GO - Cellular component (CC):
cytosol, extracellular exosome, plasma membrane, cytoplasm...
cytosol, extracellular exosome, plasma membrane, cytoplasm
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protein kinase C eta
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Kaplan plot for PRKCH in
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*NOTE: the Kaplan plots were collected from OncoLnc