Curated Information
Javascript is not enabled on this browser. This site will not work properly without Javascript.
PhosphoSitePlus Homepage Cell Signaling Technology
HomeAbout PhosphoSiteUsing PhosphoSiteCuration ProcessContact
NIH-logos NIGMS Logo NIAAA Logo NCI Logo NIH Logo
Curated Information Page
PubMed Id: 16537462 
Erxleben C, et al. (2006) Cyclosporin and Timothy syndrome increase mode 2 gating of CaV1.2 calcium channels through aberrant phosphorylation of S6 helices. Proc Natl Acad Sci U S A 103, 3932-7 16537462
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.
Click on the protein name to open the protein page, and on the RSD number to open the site page.
Download Sites

S439-p - CACNA1C (rabbit)
Orthologous residues
CACNA1C (human): S409‑p, CACNA1C iso12 (human): S409‑p, CACNA1C (mouse): S409‑p, CACNA1C iso5 (mouse): S439‑p, CACNA1C (rat): S439‑p, CACNA1C (rabbit): S439‑p, CACNA1C iso4 (rabbit): S409‑p, CACNA1C (guinea pig): S438‑p
 Enzymes shown to modify site in vitro
Type Enzyme

S1517-p - CACNA1C (rabbit)
Orthologous residues
CACNA1C (human): S1535‑p, CACNA1C iso12 (human): S1487‑p, CACNA1C (mouse): S1487‑p, CACNA1C iso5 (mouse): S1517‑p, CACNA1C (rat): S1516‑p, CACNA1C (rabbit): S1517‑p, CACNA1C iso4 (rabbit): S1512‑p, CACNA1C (guinea pig): S1516‑p
 Methods used to characterize site in vivo mutation of modification site
 Relevant cell lines - cell types - tissues:  293 (epithelial)
 Cellular systems studied:  cell lines
 Species studied:  human
 Enzymes shown to modify site in vitro
Type Enzyme
Downstream Regulation
 Effect of modification (function):  activity, induced
 Comments:  critical for "mode 2" gating of the channel

Home  |  Curator Login With enhanced literature mining using Linguamatics I2E I2E Logo Produced by 3rd Millennium  |  Design by Digizyme
©2003-2013 Cell Signaling Technology, Inc.