Curated Information
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Curated Information Page
PubMed Id: 12637502 
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.
Cameron SJ, et al. (2003) Regulation of epidermal growth factor-induced connexin 43 gap junction communication by big mitogen-activated protein kinase1/ERK5 but not ERK1/2 kinase activation. J Biol Chem 278, 18682-8 12637502
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S255-p - Cx43 (rat)
Orthologous residues
Cx43 (human): S255‑p, Cx43 (mouse): S255‑p, Cx43 (rat): S255‑p, Cx43 (rabbit): S255‑p, Cx43 (hamster): N255‑p
Characterization
 Methods used to characterize site in vivo electrophoretic mobility shift, mutation of modification site
 Relevant cell lines - cell types - tissues:  293 (epithelial) [Cx43 (rat)], 293 (epithelial) [MEK5 (human)]
 Cellular systems studied:  cell lines
 Species studied:  human
 Comments:  constitutively active MEK5 activate endogenous ERK5 which phosphorylates CX43 on S254.
 Enzymes shown to modify site in vitro
Type Enzyme
KINASE ERK5 (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE ERK5 (human) genetic transfer of dominant-negative enzyme


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