Regulation of G-protein coupled receptor traffic by an evolutionary conserved hydrophobic signal.
Regulation of G-protein coupled receptor traffic by an evolutionary conserved hydrophobic signal.
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DOI：
10.1111/j.1600-0854.2010.01033.x
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发表时间：
2010-04
期刊：
影响因子：
--
通讯作者：
Hurt CM
中科院分区：
文献类型：
--
作者：
Angelotti T;Daunt D;Shcherbakova OG;Kobilka B;Hurt CM
Plasma membrane (PM) expression of G-protein coupled receptors (GPCRs) is required for activation by extracellular ligands; however mechanisms that regulate PM expression of GPCRs are poorly understood. For some GPCRs, such as alpha2c-adrenergic receptors (α2c-ARs), heterologous expression in non-native cells results in limited PM expression and extensive endoplasmic reticulum (ER) retention. Recently, ER export/retentions signals have been proposed to regulate cellular trafficking of several GPCRs. By utilizing a chimeric α2a/α2c-AR strategy, we identified an evolutionary conserved hydrophobic sequence (ALAAALAAAAA) in the extracellular amino terminal region that is responsible in part for α2c-AR subtype specific trafficking. To our knowledge, this is the first luminal ER retention signal reported for a GPCR. Removal or disruption of the ER retention signal dramatically increased PM expression and decreased ER retention. Conversely, transplantation of this hydrophobic sequence into α2a-ARs reduced their PM expression and increased ER retention. This evolutionary conserved hydrophobic trafficking signal within α2c-ARs serves as a regulator of GPCR trafficking.
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影响因子：
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