Curated Information
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Curated Information Page
PubMed Id: 20595653 
This page summarizes selected information from the article referenced above and curated into PhosphoSitePlus®, a comprehensive online resource for the study of protein post-translational modifications (NAR, 2012,40:D261-70). To learn more about the scope of PhosphoSitePlus®, click here.
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
Only sites from this record are displayed on this page. Click on the protein name to open the protein page, and on the RSD number to open the site page. For the complete dataset, click the download button, on the right.
Download Sites

S45-p - CRYAB (mouse) ▲
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) ▲
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) ▲
Orthologous residues
PKN1 (human): T774‑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


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