Curated Information
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Curated Information Page
PubMed Id: 16174865 
Yan W, Suaud L, Kleyman TR, Rubenstein RC (2006) Differential modulation of a polymorphism in the COOH terminus of the alpha-subunit of the human epithelial sodium channel by protein kinase Cdelta. Am J Physiol Renal Physiol 290, F279-88 16174865
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.
Information from this record has been curated, but not yet edited in PhosphoSitePlus® and may be incomplete.
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T663-p - ENaC-alpha (human)
Orthologous residues
ENaC‑alpha (human): T663‑p, ENaC‑alpha (mouse): A692‑p, ENaC‑alpha (rat): A692‑p
 Methods used to characterize site in vivo mutation of modification site, western blotting
 Relevant cell lines - cell types - tissues:  oocyte
 Cellular systems studied:  primary cells
 Species studied:  frog
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
phorbol ester decrease Phorbol ester caused decrease in expression of T663 and A663 in oocytes.
calphostin C decrease Calphostiin C decreases T663 expression, but not A663.
Downstream Regulation
 Comments:  PKC delta may affect rate of biosynthesis or delivery of T663 to the plasma membrane, but not by direct phosphorylation of T663.

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