Curated Information
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Curated Information Page
PubMed Id: 14611643 
Vitari AC, et al. (2004) WNK1, the kinase mutated in an inherited high-blood-pressure syndrome, is a novel PKB (protein kinase B)/Akt substrate. Biochem J 378, 257-68 14611643
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, 2012,40:D261-70). To learn more about the scope of PhosphoSitePlus®, click here.
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T60-p - WNK1 (human)
Orthologous residues
WNK1 (human): T60‑p, WNK1 iso4 (human): T60‑p, WNK1 (mouse): T58‑p, WNK1 iso3 (mouse): T58‑p, WNK1 (rat): T58‑p
Characterization
 Methods used to characterize site in vivo mutation of modification site, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  'stem, embryonic', 293 (epithelial)
 Cellular systems studied:  cell lines, primary cells
 Species studied:  human, mouse
 Enzymes shown to modify site in vitro
Type Enzyme
KINASE MSK1 (human)
KINASE Akt1 (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE Akt1 (human) activation of upstream enzyme, inhibition of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
IGF-1 increase
LY294002 IGF-1 inhibit treatment-induced increase
wortmannin IGF-1 inhibit treatment-induced increase
rapamycin IGF-1 no effect upon treatment-induced increase
phorbol ester increase
PD184352 phorbol ester no effect upon treatment-induced increase
forskolin increase
H-89 forskolin inhibit treatment-induced increase


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