Regulation of cardiac gap junctions by protein phosphatases

Abstract Sufficient connexin-mediated intercellular coupling is critical to maintain gap junctional communication for proper cardiac function. Alterations in connexin phosphorylation state, particularly dephosphorylation of connexin 43 (Cx43), may impact cell coupling and conduction in disease state...

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Bibliographic Details
Published in:Journal of molecular and cellular cardiology 2017-06, Vol.107, p.52-57
Main Authors: Hood, Ashleigh R, Ai, Xun, Pogwizd, Steven M
Format: Article
Language:English
Subjects:
Animals
Cardiovascular
Cell Communication - genetics
Connexin 43
Connexin 43 - genetics
Connexin 43 - metabolism
Gap junction
Gap Junctions - genetics
Gap Junctions - metabolism
Gap Junctions - pathology
Heart - physiology
Humans
Phosphatase
Phosphoprotein Phosphatases - genetics
Phosphorylation
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Summary:Abstract Sufficient connexin-mediated intercellular coupling is critical to maintain gap junctional communication for proper cardiac function. Alterations in connexin phosphorylation state, particularly dephosphorylation of connexin 43 (Cx43), may impact cell coupling and conduction in disease states. Cx43 dephosphorylation may be carried out by protein phosphatase activity. Here, we present an overview of the key phosphatases known to interact with Cx43 or modulators of Cx43, as well as some possible therapeutic targets to regulate phosphatase activity in the heart.
ISSN:0022-2828
1095-8584
DOI:10.1016/j.yjmcc.2017.05.002