Gunaratne A, Thai BL, Di Guglielmo GM (2013) Atypical protein kinase C phosphorylates Par6 and facilitates transforming growth factor β-induced epithelial-to-mesenchymal transition. Mol Cell Biol 33, 874-86 23249950

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S345-p - PARD6A (human) ▲

Modsite: RGDGSGFsL______ SwissProt Entrez-Gene Orthologous residues PARD6A (human): S345‑p, PARD6A iso2 (human): S344‑p, PARD6A (mouse): S345‑p, PARD6A (rat): S345‑p Characterization Methods used to characterize site in vivo:  immunoprecipitation, mutation of modification site, phospho-antibody, western blotting Disease tissue studied:  lung cancer, non-small cell lung cancer, non-small cell lung adenocarcinoma Relevant cell lines - cell types - tissues:  A549 (pulmonary), HEK293T (epithelial), NCI-H1299 (pulmonary) Cellular systems studied:  cell lines Species studied:  human Upstream Regulation Potential in vivo enzymes for site:  Type Enzyme Evidence Notes KINASE PKCZ (human) activation of upstream enzyme, transfection of wild-type enzyme, siRNA inhibition of enzyme, co-immunoprecipitation, transfection of inactive enzyme, phospho-antibody KINASE PKCI (human) activation of upstream enzyme, transfection of wild-type enzyme, siRNA inhibition of enzyme, co-immunoprecipitation, transfection of inactive enzyme, phospho-antibody Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes TGFBR1 (human) increase siRNA decrease PKCI-siRNA inhibits SMURF1 (human) decrease Downstream Regulation Effect of modification (function):  protein degradation Effect of modification (process):  cell motility, induced, cytoskeletal reorganization Comments:  phosphorylation necessary to induce Epithelial to mesenchymal transition (EMT) and RhoA degradation, TGFß induced E-cadherin loss, stress fiber formation Associated Diseases Diseases Alterations Comments non-small cell lung cancer increased