Feng L, Subbaraya I, Yamamoto N, Baehr W, Kraus-Friedmann N
Department of Integrative Biology, University of Texas-Houston School of Medicine, USA.
FEBS Lett. 1996 Oct 14;395(1):77-81. doi: 10.1016/0014-5793(96)01011-3.
Glucagon and beta-adrenergic agents increase cAMP levels and stimulate Ca2+ influx in liver cells. There is no consensus as to the mechanism by which these hormones stimulate the influx of Ca2+. Using mouse retinal rod CNGCalpha cDNA probes, we cloned rat liver and skeletal muscle, and human hepatic CNGCalpha subunit sequences showing 97-100% identity with the human rod channel. In order to assess channel activity, the effect of cyclic nucleotides on free intracellular Ca2+ levels of isolated hepatocytes was measured. Dibutyryl-cAMP was more effective in increasing free Ca2+ levels than dibutyryl-cGMP. These data indicate that the CNGCalpha subunit is expressed in both the liver and skeletal muscle possibly mediating hormonal effects on ion fluxes.
胰高血糖素和β-肾上腺素能药物可提高环磷酸腺苷(cAMP)水平,并刺激肝细胞中的钙离子(Ca2+)内流。关于这些激素刺激Ca2+内流的机制尚无定论。我们使用小鼠视网膜视杆细胞环核苷酸门控阳离子通道α亚基(CNGCalpha)的互补DNA(cDNA)探针,克隆了大鼠肝脏和骨骼肌以及人类肝脏的CNGCalpha亚基序列,这些序列与人类视杆细胞通道的一致性为97%-100%。为了评估通道活性,我们测量了环核苷酸对分离肝细胞内游离Ca2+水平的影响。二丁酰-cAMP在提高游离Ca2+水平方面比二丁酰-cGMP更有效。这些数据表明,CNGCalpha亚基在肝脏和骨骼肌中均有表达,可能介导激素对离子通量的影响。