Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.


Sci. STKE, 5 July 2005
Vol. 2005, Issue 291, p. pe33
[DOI: 10.1126/stke.2912005pe33]


c-Src: Bridging the Gap Between Phosphorylation- and Acidification-Induced Gap Junction Channel Closure

Alan F. Lau*

Natural Products and Cancer Biology Program, Cancer Research Center, University of Hawaii at Manoa, Honolulu, HI 96813, USA.

Abstract: Gap junctions are a unique type of intercellular junction that mediate the direct exchange of small molecules between neighboring cells and play critical roles in the normal function of numerous organs. Mutations in the connexin proteins that make up gap junctions have been implicated in numerous human skin and neurosensory disorders. The ability of gap junctions to transmit molecules between cells is regulated by intracellular pH, the phosphorylation state of connexin, and the interaction of connexin with other cellular proteins. This Perspective focuses on the novel and complex events initiated by intracellular acidification resulting from tissue ischemia or hypoxia that lead to the interruption of intercellular communication between astrocytes. These events include alterations in connexin43 (Cx43) phosphorylation, disruption of β-actin binding to Cx43, and the induced interaction of Cx43 with the c-Src tyrosine kinase, extracellular signal-regulated kinase 1 and 2, and mitogen-activated protein kinase phosphatase 1.

*Corresponding author. E-mail: aflau{at}

Citation: A. F. Lau, c-Src: Bridging the Gap Between Phosphorylation- and Acidification-Induced Gap Junction Channel Closure. Sci. STKE 2005, pe33 (2005).

Read the Full Text

To Advertise     Find Products

Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882