Stead Family Department of Pediatrics and the Lung Biology and Cystic Fibrosis Research Center of the Pappajohn Biomedical Institute, University of Iowa, Iowa City, Iowa 52242.
J Biol Chem. 2018 Aug 17;293(33):12960-12961. doi: 10.1074/jbc.H118.004669.
The intestinal consequences of cholera enterotoxin are caused by activation of the cystic fibrosis transmembrane conductance regulator (CFTR) anion channel through the actions of an as-yet-unknown adenylate cyclase. A new study hunts down this elusive enzyme, showing that mouse and human intestinal epithelium functionally and structurally pair adenylate cyclase isoform 6 (AC6) with CFTR. These findings provide important insights into the molecular mechanisms underlying the robust pathological activation of CFTR activity and promise new opportunities to treat cholera.
霍乱肠毒素引起的肠道后果是通过尚未明确的腺苷酸环化酶的作用激活囊性纤维化跨膜电导调节因子（CFTR）阴离子通道引起的。一项新的研究追踪到这种难以捉摸的酶，表明小鼠和人肠上皮细胞在功能和结构上使腺苷酸环化酶同工型 6（AC6）与 CFTR 配对。这些发现为 CFTR 活性的强大病理激活的分子机制提供了重要的见解，并为治疗霍乱提供了新的机会。
