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在大鼠P2X(2)受体的第一个跨膜结构域中鉴定出的参与门控的氨基酸残基。

Amino acid residues involved in gating identified in the first membrane-spanning domain of the rat P2X(2) receptor.

作者信息

Jiang L H, Rassendren F, Spelta V, Surprenant A, North R A

机构信息

Institute of Molecular Physiology, University of Sheffield, Alfred Denny Building, Western Bank, Sheffield S10 2TN, United Kingdom.

出版信息

J Biol Chem. 2001 May 4;276(18):14902-8. doi: 10.1074/jbc.M011327200. Epub 2001 Feb 6.

Abstract

The first hydrophobic segment of the rat P2X(2) receptor extends from residue Leu(29) to Val(51). In the rat P2X(2) receptor, we mutated amino acids in this segment and adjoining flanking regions (Asp(15) through Thr(60)) individually to cysteine and expressed the constructs in human embryonic kidney cells. Whole-cell recordings were used to measure membrane currents evoked by brief (2-s) applications of ATP (0.3-100 microM). Currents were normal except for Y16C, R34C, Y43C, Y55C, and Q56C (no currents but normal membrane expression by immunohistochemistry), Q37C (small currents), and F44C (normal current but increased sensitivity to ATP, as well as alphabeta-methylene-ATP). We used methanethiosulfonates of positive, negative, or no charge to test the accessibility of the substituted cysteines. D15C, P19C, V23C, V24C, G30C, Q37C, F44C, and V48C were strongly inhibited by neutral, membrane-permeant methanethiosulfonates. Only V48C was also inhibited by positively and negatively charged methanethiosulfonates, consistent with an extracellular position; however, accessibility of V48C was increased by channel opening. V48C could disulfide with I328C, as shown by the large increase in ATP-evoked current caused by reducing agents. The results suggest that Val(48) at the outer end of the first hydrophobic segment takes part in the gating movement of channel opening.

摘要

大鼠P2X(2)受体的第一个疏水片段从亮氨酸(Leu)29位延伸至缬氨酸(Val)51位。在大鼠P2X(2)受体中,我们将该片段及相邻侧翼区域(天冬氨酸(Asp)15位至苏氨酸(Thr)60位)的氨基酸逐个突变为半胱氨酸,并在人胚肾细胞中表达构建体。采用全细胞记录法测量由短暂(2秒)施加ATP(0.3 - 100微摩尔)诱发的膜电流。除了Y16C、R34C、Y43C、Y55C和Q56C(无电流,但免疫组化显示膜表达正常)、Q37C(小电流)和F44C(正常电流,但对ATP以及α,β-亚甲基-ATP的敏感性增加)外,电流均正常。我们使用带正电荷、负电荷或不带电荷的甲硫基磺酸盐来检测取代半胱氨酸的可及性。D15C、P19C、V23C、V24C、G30C、Q37C、F44C和V48C被中性、可透过膜的甲硫基磺酸盐强烈抑制。只有V48C也被带正电荷和负电荷的甲硫基磺酸盐抑制,这与细胞外位置一致;然而,通道开放会增加V48C的可及性。如还原剂导致ATP诱发电流大幅增加所示,V48C可与I328C形成二硫键。结果表明,第一个疏水片段外端的缬氨酸48参与通道开放的门控运动。

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