Takagi H, et al. (2010) Activation of PKN mediates survival of cardiac myocytes in the heart during ischemia/reperfusion. Circ Res 107, 642-9 20595653

This page summarizes selected information from the record referenced above and curated into PhosphoSitePlus®, a comprehensive online resource for the study of protein post-translational modifications (NAR, 2015, 43:D512-20). To learn more about the scope of PhosphoSitePlus®, click here.

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S45-p - CRYAB (mouse) ▲

Modsite: FSTATSLsPFYLRPP SwissProt Entrez-Gene Orthologous residues CRYAB (human): S45‑p, CRYAB (mouse): S45‑p, CRYAB (rat): S45‑p, CRYAB (rabbit): S45‑p, CRYAB (pig): S45‑p, CRYAB (cow): S45‑p Characterization Methods used to characterize site in vivo:  phospho-antibody, western blotting Relevant cell lines - cell types - tissues:  heart [PKN1 (mouse), transgenic], myocyte-heart [PKN1 (mouse), transgenic] Cellular systems studied:  primary cells Species studied:  mouse Upstream Regulation Potential in vivo enzymes for site:  Type Enzyme Evidence Notes KINASE PKN1 (mouse) genetic transfer of constitutively active upstream enzyme, genetic transfer of dominant-negative enzyme, phospho-antibody Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes PKN1 (mouse) increase transgenic mice expressing constitutively active PKN; translocates from cytosolic ot cytoskelatal fraction

S59-p - CRYAB (mouse) ▲

Modsite: PSFLRAPsWIDtGLS SwissProt Entrez-Gene Orthologous residues CRYAB (human): S59‑p, CRYAB (mouse): S59‑p, CRYAB (rat): S59‑p, CRYAB (rabbit): S59‑p, CRYAB (pig): S59‑p, CRYAB (cow): S59‑p Characterization Methods used to characterize site in vivo:  phospho-antibody, western blotting Relevant cell lines - cell types - tissues:  heart [PKN1 (mouse), transgenic], myocyte-heart [PKN1 (mouse), transgenic] Cellular systems studied:  primary cells Species studied:  mouse Upstream Regulation Potential in vivo enzymes for site:  Type Enzyme Evidence Notes KINASE PKN1 (mouse) genetic transfer of constitutively active upstream enzyme, genetic transfer of dominant-negative enzyme, phospho-antibody Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes PKN1 (mouse) increase transgenic mice expressing constitutively active PKN; translocates from cytosolic ot cytoskelatal fraction

T778-p - PKN1 (mouse) ▲

Modsite: GyGDRtstFCGtPEF SwissProt Entrez-Gene Orthologous residues PKN1 (human): T774‑p, PKN1 iso2 (human): T780‑p, PKN1 (mouse): T778‑p, PKN1 (rat): T778‑p Characterization Methods used to characterize site in vivo:  phospho-antibody, western blotting Relevant cell lines - cell types - tissues:  heart [PKN1 (mouse), transgenic], myocyte-heart [PKN1 (mouse), transgenic] Cellular systems studied:  primary cells Species studied:  mouse Upstream Regulation Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes ischemia increase ischemia/reperfusion increase PKN1 (mouse) increase constitutively active PKN mice H2O2 increase