Schreiber R, Pavenstädt H, Greger R, Kunzelmann K
Department of Physiology and Pharmacology, University of Queensland, St. Lucia, Brisbane, Australia.
FEBS Lett. 2000 Jun 23;475(3):291-5. doi: 10.1016/s0014-5793(00)01689-6.
The cystic fibrosis transmembrane conductance regulator (CFTR) is essential for epithelial electrolyte transport and has been shown to be a regulator of epithelial Na(+), K(+), and Cl(-) channels. CFTR also enhances osmotic water permeability when activated by cAMP. This was detected initially in Xenopus oocytes and is also present in human airway epithelial cells, however, the mechanisms remain obscure. Here, we show that CFTR activates aquaporin 3 expressed endogenously and exogenously in oocytes of Xenopus laevis. The interaction requires stimulation of wild type CFTR by cAMP and an intact first nucleotide binding domain as demonstrated for other CFTR-protein interactions.
囊性纤维化跨膜传导调节因子（CFTR）对于上皮细胞电解质转运至关重要，并且已被证明是上皮细胞钠（Na⁺）、钾（K⁺）和氯（Cl⁻）通道的调节因子。当被环磷酸腺苷（cAMP）激活时，CFTR还会增强渗透水通透性。这最初是在非洲爪蟾卵母细胞中检测到的，在人气道上皮细胞中也存在，然而，其机制仍不清楚。在这里，我们表明CFTR可激活非洲爪蟾卵母细胞中内源性和外源性表达的水通道蛋白3。这种相互作用需要cAMP对野生型CFTR的刺激以及完整的第一个核苷酸结合结构域，这与其他CFTR-蛋白质相互作用所证明的情况相同。
