Regulation of gap junction coupling through the neuronal connexin Cx35 by nitric oxide and cGMP

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Abstract

Gap-junctional coupling among neurons is subject to regulation by a number of neurotransmitters including nitric oxide. We studied the mechanisms by which NO regulates coupling in cells expressing Cx35, a connexin expressed in neurons throughout the central nervous system. NO donors caused potent uncoupling of HeLa cells stably transfected with Cx35. This effect was mimicked by Bay 21-4272, an activator of guanylyl cyclase. A pharmacological analysis indicated that NO-induced uncoupling involved both PKG-dependent and PKG-independent pathways. PKA was involved in both pathways, suggesting that PKG-dependent uncoupling may be indirect. In vitro, PKG phosphorylated Cx35 at three sites: Ser110, Ser276, and Ser289. A mutational analysis indicated that phosphorylation on Ser110 and Ser276, sites previously shown also to be phosphorylated by PKA, had a significant influence on regulation. Ser289 phosphorylation had very limited effects. We conclude that NO can regulate coupling through Cx35 and that regulation is indirect in HeLa cells. Copyright © Taylor & Francis Group, LLC.

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Patel, L. S., Mitchell, C. K., Dubinsky, W. P., & O’Brien, J. (2006). Regulation of gap junction coupling through the neuronal connexin Cx35 by nitric oxide and cGMP. Cell Communication and Adhesion, 13(1–2), 41–54. https://doi.org/10.1080/15419060600631474

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