Curated Information

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Curated Information Page

PubMed Id: 16174865

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.

Information from this record has been curated, but not yet edited in PhosphoSitePlus^® and may be incomplete.

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

T663-p - ENaC-alpha (human)

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Orthologous residues

ENaC‑alpha (human): T663‑p, ENaC‑alpha (mouse): A692‑p, ENaC‑alpha (rat): A692‑p

Characterization

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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