XPORT-dependent transport of TRP and rhodopsin.
XPORT-dependent transport of TRP and rhodopsin.
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DOI：
10.1016/j.neuron.2011.09.016
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发表时间：
2011-11-17
期刊：
影响因子：
16.2
通讯作者：
Colley NJ
中科院分区：
文献类型：
--
作者：
Rosenbaum EE;Brehm KS;Vasiljevic E;Liu CH;Hardie RC;Colley NJ
TRP通道已经成为视觉、味觉、嗅觉、听觉和触觉中的关键生物传感器。尽管它们很重要，但实际上对TRP通道在生物合成过程中的折叠和转运一无所知。在这里，我们确定XPORT（视紫红质和TRP的出口蛋白）作为TRP及其G蛋白偶联受体（GPCR），视紫红质（Rh1）的关键伴侣。XPORT是一种常驻ER和分泌途径蛋白，与TRP和Rh1以及Hsp27和Hsp90相互作用。XPORT促进TRP靶向果蝇S2细胞的膜，这一发现为解决TRP成功异源表达的长期问题迈出了关键的第一步。输出突变导致TRP和Rh1的转运缺陷，导致视网膜变性。我们的研究结果确定XPORT作为一种新的分子伴侣，并提供了一个机械连接TRP通道和它们的GPCR在生物合成和运输。
TRP channels have emerged as key biological sensors in vision, taste, olfaction, hearing and touch. Despite their importance, virtually nothing is known about the folding and transport of TRP channels during biosynthesis. Here, we identify XPORT (exit protein of rhodopsin and TRP) as a critical chaperone for TRP and its G-protein coupled receptor (GPCR), rhodopsin (Rh1). XPORT is a resident ER and secretory pathway protein that interacts with TRP and Rh1, as well as with Hsp27 and Hsp90. XPORT promotes the targeting of TRP to the membrane in Drosophila S2 cells, a finding that provides a critical first step towards solving a longstanding problem in the successful heterologous expression of TRP. Mutations in xport result in defective transport of TRP and Rh1, leading to retinal degeneration. Our results identify XPORT as a novel molecular chaperone and provide a mechanistic link between TRP channels and their GPCRs during biosynthesis and transport.
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DOI：
10.1016/j.cub.2009.12.006
发表时间：
2010-02-09
期刊：
Current biology : CB
影响因子：
--
作者：
Fain GL;Hardie R;Laughlin SB
通讯作者：
Laughlin SB
DOI：
10.1073/pnas.152330499
发表时间：
2002-12-10
影响因子：
11.1
作者：
Bonini, NM
通讯作者：
Bonini, NM
影响因子：
56.9
作者：
Hundley, HA;Walter, W;Craig, EA
通讯作者：
Craig, EA
影响因子：
64.5
作者：
COLLEY, NJ;BAKER, EK;ZUKER, CS
通讯作者：
ZUKER, CS
影响因子：
16.2
作者：
HARDIE, RC;MINKE, B
通讯作者：
MINKE, B