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Study show that RAS at the Golgi is selectively activated by apoptogenic stimuli and antagonizes cell survival by suppressing ERK activity through the induction of PTPRkappa, which targets CRAF for dephosphorylation. RAS oncogenic potential is strictly dependent on its sublocalization, with Golgi complex-located RAS antagonizing tumor development.
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PTPRK was identified as a direct target of miR-1260b, and PTPRK expression was inversely correlated with miR-1260b in non-small cell lung cancer cell lines and clinical tissues
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Study found a significant association between PTPRK genetic variants and the risk and age at onset of Alzheimer's disease in two independent samples, and provided initial evidence of several genetic variants in PTPRK influencing the risk of cancer and cholesterol levels.
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The present study identified RSPO fusion transcripts, including three novel transcripts, in one-third of colorectal Traditional serrated adenoma (TSA) and showed that PTPRK-RSPO3 fusions were the predominant cause of RSPO overexpression in colorectal TSA.
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PTPRK plays dual roles in coordinating angiogenesis. It plays a positive role in cell proliferation, adhesion and tubule formation, but suppresses cell migration, in particular, the FGF-promoted migration.
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PTPRK-RSPO3 fusions and RNF43 mutations were found to be characteristic genetic features of traditional serrated adenomas (TSAs).
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By regulating phosphorylation of SRC, RPTPkappa promotes the pathogenic action of rheumatoid arthritis fibroblast-like synoviocytes, mediating cross-activation of growth factor and inflammatory cytokine signalling by TGFbeta in RA FLS.
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Notch and TGF-beta act in concert to stimulate induction of PTPRK, which suppresses EGFR activation in human keratinocytes.
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Findings strongly indicate that the tyrosine phosphorylation of CD133, which is dephosphorylated by PTPRK, regulates AKT signaling and has a critical role in colon cancer progression.
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PTPRK underexpression leads to STAT3 activation and contributes to nasal NK/T-cell lymphoma pathogenesis
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PTPRK showed lower mRNA expression in duodenal mucose of celiac disease patients.
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High expression of PTPRK is associated with prostate cancer.
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Tumor derived mutations of protein tyrosine phosphatase receptor type k affect its function and alter sensitivity to chemotherapeutics in glioma.
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PTPRK is a negative regulator of adhesion, invasion, migration, and proliferation of breast cancer cells.
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PTPkappa was scissored by the processed form of proprotein convertase 5, and galectin-3 binding protein which is over-produced in colon cancer cells and tissues.
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These data describe a novel mechanism of cross-talk between EGFR and TGF-beta pathways, in which RPTP-kappa functions to integrate growth-promoting and growth-inhibiting signaling pathways.
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Our results suggest that GnT-V could decrease human hepatoma SMMC-7721 cell adhesion and promote cell proliferation partially through RPTPkappa.
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RPTP-kappa is a key regulator of EGFR tyrosine phosphorylation and function in human keratinocytes
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the crystal structure of catalytically active, monomeric D1 domain of RPTPkappa at 1.9 A. RPTPkappa is monomeric in solution and crystal structure.
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EGF receptor is activated in human keratinocytes by oxidative inhibition of receptor-type protein-tyrosine phosphatase kappa by ultraviolet irradiation
