AI Article Synopsis
- Connexin 43 (Cx43) is a phosphoprotein important for cell survival under stress and ischemic conditions, interacting with K(ATP) channels in a signaling pathway.
- Evidence shows that Kir6.1, a component of K(ATP) channels, specifically interacts with Cx43 when Cx43 is phosphorylated at serine 262 (S262).
- Mutating serine 262 to a phospho-deficient form eliminates this interaction, suggesting a critical role for this phosphorylation in the partnership between Cx43 and Kir6.1 during ischemia/hypoxia preconditioning.
Article Abstract
Connexin 43 (Cx43) is a phosphoprotein expressed in a wide variety of cells. Cx43 and adenosine-triphosphate-sensitive K(+)channels [K(+)(ATP)] are part of same signaling pathway that regulates cell survival during stress and ischemia preconditioning. Molecular mechanism for their coordinated role in ischemia/hypoxia preconditioning is not well known. Using pull down, co-immunoprecipitation assays and co-localization studies we provide evidence, for the first time that Kir6.1, a K(+)(ATP) channel protein component, can interact with Cx43. Further we show that the interaction was phospho-specific such that Cx43 phosphorylated at serine 262 (S262) interacted with Kir6.1 in preference to the unphosphorylated form of Cx43. Introduction of phospho-deficient mutation at serine 262 (S262A) in Cx43 completely abolished the interaction. Our data provide an interesting lead about a possible partnership between Cx43 and Kir6.1, which will help in better understanding their role in ischemia/hypoxia preconditioning.
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| http://dx.doi.org/10.1016/j.yexcr.2012.08.004 | DOI Listing |
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