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本文引用的文献

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A stable ATP binding to the nucleotide binding domain is important for reliable gating cycle in an ABC transporter CFTR.稳定的 ATP 结合到核苷酸结合域对于 ABC 转运体 CFTR 的可靠门控循环很重要。
J Physiol Sci. 2010 Sep;60(5):353-62. doi: 10.1007/s12576-010-0102-2. Epub 2010 Jul 14.
2
Architecture of the cystic fibrosis transmembrane conductance regulator protein and structural changes associated with phosphorylation and nucleotide binding.囊性纤维化跨膜传导调节蛋白的结构以及与磷酸化和核苷酸结合相关的结构变化。
J Struct Biol. 2009 Sep;167(3):242-51. doi: 10.1016/j.jsb.2009.06.004. Epub 2009 Jun 12.
3
Relationship between nucleotide binding and ion channel gating in cystic fibrosis transmembrane conductance regulator.囊性纤维化跨膜传导调节因子中核苷酸结合与离子通道门控之间的关系。
J Physiol. 2009 Jun 15;587(Pt 12):2875-86. doi: 10.1113/jphysiol.2009.170258. Epub 2009 Apr 29.
4
CFTR functions as a bicarbonate channel in pancreatic duct cells.囊性纤维化跨膜传导调节因子在胰腺导管细胞中作为碳酸氢盐通道发挥作用。
J Gen Physiol. 2009 Mar;133(3):315-26. doi: 10.1085/jgp.200810122. Epub 2009 Feb 9.
5
Evolutionary and functional divergence between the cystic fibrosis transmembrane conductance regulator and related ATP-binding cassette transporters.囊性纤维化跨膜传导调节因子与相关ATP结合盒转运蛋白之间的进化和功能差异。
Proc Natl Acad Sci U S A. 2008 Dec 2;105(48):18865-70. doi: 10.1073/pnas.0806306105. Epub 2008 Nov 19.
6
Mechanism of direct bicarbonate transport by the CFTR anion channel.CFTR阴离子通道介导直接碳酸氢根转运的机制。
J Cyst Fibros. 2009 Mar;8(2):115-21. doi: 10.1016/j.jcf.2008.10.004. Epub 2008 Nov 18.
7
Review. ATP hydrolysis-driven gating in cystic fibrosis transmembrane conductance regulator.综述:囊性纤维化跨膜传导调节因子中由ATP水解驱动的门控作用
Philos Trans R Soc Lond B Biol Sci. 2009 Jan 27;364(1514):247-55. doi: 10.1098/rstb.2008.0191.
8
Three-dimensional reconstruction of human cystic fibrosis transmembrane conductance regulator chloride channel revealed an ellipsoidal structure with orifices beneath the putative transmembrane domain.人类囊性纤维化跨膜传导调节因子氯离子通道的三维重建显示,在假定的跨膜结构域下方有孔的椭圆形结构。
J Biol Chem. 2008 Oct 31;283(44):30300-10. doi: 10.1074/jbc.M803185200. Epub 2008 Aug 22.
9
Monomeric CFTR in plasma membranes in live cells revealed by single molecule fluorescence imaging.通过单分子荧光成像揭示活细胞质膜中的单体囊性纤维化跨膜传导调节因子
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10
Atomic model of human cystic fibrosis transmembrane conductance regulator: membrane-spanning domains and coupling interfaces.人类囊性纤维化跨膜传导调节因子的原子模型:跨膜结构域和偶联界面。
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CFTR 通道孔构象的 ATP 水解依赖性不对称性。

ATP hydrolysis-dependent asymmetry of the conformation of CFTR channel pore.

机构信息

Department of Cell Physiology, National Institute for Physiological Sciences, Okazaki, Japan.

出版信息

J Physiol Sci. 2011 Jul;61(4):267-78. doi: 10.1007/s12576-011-0144-0. Epub 2011 Apr 3.

DOI:10.1007/s12576-011-0144-0
PMID:21461971
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10717511/
Abstract

Despite substantial efforts, the entire cystic fibrosis transmembrane conductance regulator (CFTR) protein proved to be difficult for structural analysis at high resolution, and little is still known about the actual dimensions of the anion-transporting pathway of CFTR channel. In the present study, we therefore gauged geometrical features of the CFTR Cl(-) channel pore by a nonelectrolyte exclusion technique. Polyethylene glycols with a hydrodynamic radius (R (h)) smaller than 0.95 nm (PEG 300-1,000) added from the intracellular side greatly suppressed the inward unitary anionic conductance, whereas only molecules with R (h) ≤ 0.62 nm (PEG 200-400) applied extracellularly were able to affect the outward unitary anionic currents. Larger molecules with R (h) = 1.16-1.84 nm (PEG 1,540-3,400) added from either side were completely excluded from the pore and had no significant effect on the single-channel conductance. The cut-off radius of the inner entrance of CFTR channel pore was assessed to be 1.19 ± 0.02 nm. The outer entrance was narrower with its cut-off radius of 0.70 ± 0.16 nm and was dilated to 0.93 ± 0.23 nm when a non-hydrolyzable ATP analog, 5'-adenylylimidodiphosphate (AMP-PNP), was added to the intracellular solution. Thus, it is concluded that the structure of CFTR channel pore is highly asymmetric with a narrower extracellular entrance and that a dilating conformational change of the extracellular entrance is associated with the channel transition to a non-hydrolytic, locked-open state.

摘要

尽管已经付出了大量努力,但整个囊性纤维化跨膜电导调节因子 (CFTR) 蛋白仍难以进行高分辨率的结构分析,人们对 CFTR 通道阴离子转运途径的实际尺寸仍知之甚少。因此,在本研究中,我们采用非电解质排斥技术来测量 CFTR Cl(-) 通道孔的几何特征。从细胞内侧添加的水力学半径 (R (h)) 小于 0.95nm 的聚乙二醇 (PEG 300-1,000) 极大地抑制了内向单阴离子电导,而仅当 R (h) ≤ 0.62nm(PEG 200-400)的分子从细胞外侧施加时,才能影响外向单阴离子电流。从两侧添加的 R (h) = 1.16-1.84nm(PEG 1,540-3,400)的较大分子完全被排斥在孔外,对单通道电导没有显著影响。CFTR 通道孔内入口的截止半径被评估为 1.19 ± 0.02nm。外入口更窄,其截止半径为 0.70 ± 0.16nm,当向细胞内溶液中添加非水解型 ATP 类似物 5'-腺嘌呤核苷酰亚咪唑二磷酸 (AMP-PNP) 时,外入口会扩张至 0.93 ± 0.23nm。因此,可以得出结论,CFTR 通道孔的结构具有高度的不对称性,外入口较窄,并且外入口的扩张构象变化与通道向非水解、锁定开放状态的转变有关。