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首页> 外文期刊>Cell communication & adhesion >Regulation of Gap Junction Coupling Through the Neuronal Connexin Cx35 by Nitric Oxide and cGMP
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Regulation of Gap Junction Coupling Through the Neuronal Connexin Cx35 by Nitric Oxide and cGMP

机译：一氧化氮和cGMP通过神经元连接蛋白Cx35调节间隙连接的耦合。

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摘要

Gap-junctional coupling among neurons is subject to regulation by a number of neurotrans-mitters 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, PICG phosphorylated Cx35 at three sites: Serl 10, Ser276, and Ser289. A mutational analysis indicated that phosphorylation on Serl 10 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.
机译：神经元之间的间隙连接偶联受包括一氧化氮在内的许多神经递质的调节。我们研究了NO调节表达Cx35（在整个中枢神经系统的神经元中表达的连接蛋白）的细胞中偶联的机制。没有供体导致稳定转染Cx35的HeLa细胞有效解偶联。 Bay 21-4272（鸟苷酸环化酶的激活剂）模仿了这种效果。药理分析表明，NO诱导的解偶联涉及PKG依赖性和PKG依赖性途径。 PKA参与了这两种途径，这表明依赖PKG的解偶联可能是间接的。在体外，PICG在三个位点磷酸化Cx35：Serl 10，Ser276和Ser289。突变分析表明，之前显示也被PKA磷酸化的Serl 10和Ser276上的磷酸化对调节有重要影响。 Ser289磷酸化的作用非常有限。我们得出结论，NO可以通过Cx35调节偶联，并且该调节在HeLa细胞中是间接的。

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