PTPRK: Human tyrosine receptor phosphatase kappa (PTPRkappa)
PDB Code: 2C7S
PTPRκ belongs together with PTPRμ, PTPRρ and PTPRλ to the R2A/IIb subfamily of receptor protein tyrosine phosphatases. The protein encoded by this gene is a member of the protein tyrosine phosphatase (PTP) family. PTPRκ possesses an extracellular region, a single transmembrane region, and two tandem catalytic domains. The extracellular region contains a meprin-A5 antigen-PTP mu (MAM) domain, an Ig-like domain and four fibronectin type III-like repeats. The purified extracellular domain of PTPRκ functions as a substrate for adhesion by cells expressing PTPRκ and induces aggregation of coated synthetic beads.
PTPRκ is widely expressed with high expression detected in spleen, prostate and ovary brain, lung, skeletal muscle, heart, placenta, liver, kidney, and intestine. In the brain expression was found in cortical, olfactory, hippocampal, hypothalamic, amygdaloid and visual structures. Expression of PTPRκ is stimulated by TGF-beta and is induced by high cell density. PTPRκ has been shown to stimulate cell motility and neurite outgrowth and PTPRκ is required for both the anti-proliferative and the pro-migratory effects of TGF-beta suggesting a role in regulation, maintenance and restitution of cell adhesions. These functions might be regulated through dephosphorylaion of beta- and gamma-catenin at adherens junctions.
Expression of PTPRκ is absent or down-regulated in more than 20% of melanoma cell lines and in some un-manipulated melanoma biopsies. Furthermore, the human PTPRκ gene lies in a region frequently deleted in hematological neoplasms, melanomas, ovary carcinomas, and many other solid tumors and a peptide derived from mutated PTPRκ has been shown to be immunogenic melanoma-specific .
However, PTPRκ plays a dual role as tumor suppressor and tumor-promoter in mammary epithelial cells. RNA interference (RNAi) experiments showed that down-regulation of PTPRκ results in acceleration of cell cycle progression, enhancement of the cellular response to epidermal growth factor (EGF), and abrogates TGF-beta-mediated antimitogenesis whereas over expression of PTPR k results in inhibition of basal and EGF- induced proliferation and ERbB receptor signalling in cancer cells.
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