PTK6
Non-receptor tyrosine-protein kinase implicated in the regulation of a variety of signaling pathways that control the differentiation and maintenance of normal epithelia, as well as tumor growth. Function seems to be context dependent and differ depending on cell type, as well as its intracellular l...
Non-receptor tyrosine-protein kinase implicated in the regulation of a variety of signaling pathways that control the differentiation and maintenance of normal epithelia, as well as tumor growth. Function seems to be context dependent and differ depending on cell type, as well as its intracellular localization. A number of potential nuclear and cytoplasmic substrates have been identified. These include the RNA-binding proteins: KHDRBS1/SAM68, KHDRBS2/SLM1, KHDRBS3/SLM2 and SFPQ/PSF; transcription factors: STAT3 and STAT5A/B and a variety of signaling molecules: ARHGAP35/p190RhoGAP, PXN/paxillin, BTK/ATK, STAP2/BKS. Associates also with a variety of proteins that are likely upstream of PTK6 in various signaling pathways, or for which PTK6 may play an adapter-like role. These proteins include ADAM15, EGFR, ERBB2, ERBB3 and IRS4. In normal or non-tumorigenic tissues, PTK6 promotes cellular differentiation and apoptosis. In tumors PTK6 contributes to cancer progression by sensitizing cells to mitogenic signals and enhancing proliferation, anchorage-independent survival and migration/invasion. Association with EGFR, ERBB2, ERBB3 may contribute to mammary tumor development and growth through enhancement of EGF-induced signaling via BTK/AKT and PI3 kinase. Contributes to migration and proliferation by contributing to EGF-mediated phosphorylation of ARHGAP35/p190RhoGAP, which promotes association with RASA1/p120RasGAP, inactivating RhoA while activating RAS. EGF stimulation resulted in phosphorylation of PNX/Paxillin by PTK6 and activation of RAC1 via CRK/CrKII, thereby promoting migration and invasion. PTK6 activates STAT3 and STAT5B to promote proliferation. Nuclear PTK6 may be important for regulating growth in normal epithelia, while cytoplasmic PTK6 might activate oncogenic signaling pathways.
View more >>
GO - Biological processes (BP):
cell differentiation, cell migration, cellular response to retinoic acid, ERBB2 signaling pathway, intestinal epithelial cell differentiation, negative regulation of growth, negative regulation of protein tyrosine kinase activity, negative regulation of signal transduction, peptidyl-tyrosine autopho...
cell differentiation, cell migration, cellular response to retinoic acid, ERBB2 signaling pathway, intestinal epithelial cell differentiation, negative regulation of growth, negative regulation of protein tyrosine kinase activity, negative regulation of signal transduction, peptidyl-tyrosine autophosphorylation, positive regulation of cell cycle, positive regulation of epidermal growth factor receptor signaling pathway, positive regulation of neuron projection development, positive regulation of tyrosine phosphorylation of STAT protein, protein autophosphorylation, protein phosphorylation, regulation of cell population proliferation, transmembrane receptor protein tyrosine kinase signaling pathway, tyrosine phosphorylation of STAT protein
View more >>
GO - Molecular function (MF):
ATP binding, identical protein binding, non-membrane spanning protein tyrosine kinase activity, protein tyrosine kinase activity, signaling receptor binding...
ATP binding, identical protein binding, non-membrane spanning protein tyrosine kinase activity, protein tyrosine kinase activity, signaling receptor binding
View more >>
GO - Cellular component (CC):
cytosol, nuclear body, nucleoplasm, nucleus, extrinsic component of cytoplasmic side of plasma membrane, plasma membrane, cytoplasm, ruffle...
cytosol, nuclear body, nucleoplasm, nucleus, extrinsic component of cytoplasmic side of plasma membrane, plasma membrane, cytoplasm, ruffle
View more >>