Raber G, Waldegger S, Herzer T, Gulbins E, Murer H, Busch A E, Lang F
Institute of Physiology, Eberhard-Karls-Universität Tübingen, Germany.
Biochem Biophys Res Commun. 1995 Feb 6;207(1):195-201. doi: 10.1006/bbrc.1995.1172.
In Xenopus oocytes expressing slowly activating IsK channels superfusion with the nitroso-donor S-Nitroso-Cysteine (SNOC) resulted in an increase of IsK, which was greatly enhanced when the amino acid-exchanger rBAT was coexpressed. The effects of SNOC on IsK could not be prevented by the guanylate cyclase inhibitor LY-83,583 and the cGMP kinase inhibitor H8, but was abolished in the presence of staurosporine. SNOC also increased the currents induced by the expression of protein mutants lacking intracellular sites, previously described to be involved in IsK regulation by oxidation and phosphorylation. These data suggest that the NO-donor SNOC regulates IsK indirectly via a cGMP independent, but staurosporine sensitive, pathway.
在表达缓慢激活的IsK通道的非洲爪蟾卵母细胞中，用亚硝基供体S-亚硝基半胱氨酸（SNOC）进行灌流会导致IsK增加，当共表达氨基酸交换体rBAT时，这种增加会大大增强。鸟苷酸环化酶抑制剂LY-83,583和cGMP激酶抑制剂H8无法阻止SNOC对IsK的影响，但在存在星形孢菌素的情况下这种影响会被消除。SNOC还增加了由缺乏细胞内位点的蛋白质突变体表达所诱导的电流，这些位点先前被描述为参与通过氧化和磷酸化对IsK的调节。这些数据表明，NO供体SNOC通过一条不依赖cGMP但对星形孢菌素敏感的途径间接调节IsK。
