GENERATION OF CAMP-ACTIVATED CHLORIDE CURRENTS BY EXPRESSION OF CFTR
GENERATION OF CAMP-ACTIVATED CHLORIDE CURRENTS BY EXPRESSION OF CFTR
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DOI：
10.1126/science.1704151
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发表时间：
1991-02-08
期刊：
影响因子：
56.9
通讯作者：
WELSH, MJ
中科院分区：
文献类型：
--
作者：
ANDERSON, MP;RICH, DP;WELSH, MJ
囊性纤维化跨膜电导调节因子 (CFTR) 的突变会导致囊性纤维化。 为了评估其功能，CFTR 在 HeLa、中国仓鼠卵巢 (CHO) 和 NIH 3T3 成纤维细胞中表达，并通过荧光显微镜测定和全细胞膜片钳技术评估阴离子通透性。 腺苷 3',5'-单磷酸 (cAMP) 会增加表达 CFTR 的细胞中的阴离子通透性和氯电流，但不会增加表达突变型 CFTR (DELTA-F508) 的细胞或未转染的细胞。 对这些观察结果的最简单解释是 CFTR 本身就是 cAMP 激活的氯离子通道。 另一种解释是，CFTR 直接或间接调节氯离子通道，要求这些细胞具有内源性隐性氯离子通道，只有在 CFTR 存在的情况下，cAMP 才会刺激这些通道。
Mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) cause cystic fibrosis. In order to evaluate its function, CFTR was expressed in HeLa, Chinese hamster ovary (CHO), and NIH 3T3 fibroblast cells, and anion permeability was assessed with a fluorescence microscopic assay and the whole-cell patch-clamp technique. Adenosine 3',5'-monophosphate (cAMP) increased anion permeability and chloride currents in cells expressing CFTR, but not in cells expressing a mutant CFTR (DELTA-F508) or in nontransfected cells. The simplest interpretation of these observations is that CFTR is itself a cAMP-activated chloride channel. The alternative interpretation, that CFTR directly or indirectly regulates chloride channels, requires that these cells have endogenous cryptic, chloride channels that are stimulated by cAMP only in the presence of CFTR.