Faculty of Sciences, Biosystems and Integrative Sciences Institute, University of Lisboa Lisbon, Portugal.
Department of Cell Biology, University of Pittsburgh School of MedicinePittsburgh, PA, USA; Children's Hospital of Pittsburgh of UPMC, University of Pittsburgh School of MedicinePittsburgh, PA, USA.
Front Chem. 2016 Jan 20;4:1. doi: 10.3389/fchem.2016.00001. eCollection 2016.
Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) is a member of the ATP binding cassette (ABC) transporter superfamily that functions as a cAMP-activated chloride ion channel in fluid-transporting epithelia. There is abundant evidence that CFTR activity (i.e., channel opening and closing) is regulated by protein kinases and phosphatases via phosphorylation and dephosphorylation. Here, we review recent evidence for the role of protein kinases in regulation of CFTR delivery to and retention in the plasma membrane. We review this information in a broader context of regulation of other transporters by protein kinases because the overall functional output of transporters involves the integrated control of both their number at the plasma membrane and their specific activity. While many details of the regulation of intracellular distribution of CFTR and other transporters remain to be elucidated, we hope that this review will motivate research providing new insights into how protein kinases control membrane transport to impact health and disease.
囊性纤维化跨膜电导调节因子（CFTR）是 ATP 结合盒（ABC）转运体超家族的成员，在液体转运上皮细胞中作为 cAMP 激活的氯离子通道发挥作用。有大量证据表明，CFTR 活性（即通道的开启和关闭）通过蛋白激酶和磷酸酶的磷酸化和去磷酸化来调节。在这里，我们回顾了蛋白激酶在调节 CFTR 向质膜转运和保留中的作用的最新证据。我们在蛋白激酶调节其他转运体的更广泛背景下回顾这些信息，因为转运体的整体功能输出涉及对其在质膜上的数量和特定活性的综合控制。虽然 CFTR 和其他转运体的细胞内分布的调节的许多细节仍有待阐明，但我们希望本综述将激发研究，提供新的见解，了解蛋白激酶如何控制膜运输以影响健康和疾病。
