Amaral Margarida D
Department of Chemistry and Biochemistry, Faculty of Sciences, University of Lisbon, and Centre of Human Genetics, National Institute of Health Dr. Ricardo Jorge, Lisbon, Portugal.
Pediatr Pulmonol. 2005 Jun;39(6):479-91. doi: 10.1002/ppul.20168.
Biosynthesis of the cystic fibrosis transmembrane conductance regulator (CFTR), like other proteins aimed at the cell surface, involves transport through a series of membranous compartments, the first of which is the endoplasmic reticulum (ER), where CFTR encounters the appropriate environment for folding, oligomerization, maturation, and export from the ER. After exiting the ER, CFTR has to traffic through complex pathways until it reaches the cell surface. Although not yet fully understood, the fine details of these pathways are starting to emerge, partially through identification of an increasing number of CFTR-interacting proteins (CIPs) and the clarification of their roles in CFTR trafficking and function. These aspects of CFTR biogenesis/degradation and by membrane traffic and CIPs are discussed in this review. Following this description of complex pathways and multiple checkpoints to which CFTR is subjected in the cell, the basic question remains of how much CFTR has to overcome these barriers and be functionally expressed at the plasma membrane to avoid CF. This question is also discussed here.
囊性纤维化跨膜传导调节因子(CFTR)的生物合成,与其他靶向细胞表面的蛋白质一样,涉及通过一系列膜性区室的转运,其中第一个区室是内质网(ER),CFTR在内质网中遇到适合其折叠、寡聚化、成熟以及从内质网输出的环境。从内质网出来后,CFTR必须通过复杂的途径运输,直至到达细胞表面。尽管这些途径的详细细节尚未完全明了,但部分通过鉴定越来越多的CFTR相互作用蛋白(CIPs)以及阐明它们在CFTR转运和功能中的作用,这些细节正逐渐显现。本综述讨论了CFTR生物合成/降解以及通过膜运输和CIPs的这些方面。在描述了CFTR在细胞中所经历的复杂途径和多个检查点之后,基本问题仍然是CFTR需要克服多少这些障碍并在质膜上功能性表达以避免囊性纤维化。本文也讨论了这个问题。