ARRESTIN FUNCTION IN INACTIVATION OF G-PROTEIN COUPLED RECEPTOR RHODOPSIN INVIVO
ARRESTIN FUNCTION IN INACTIVATION OF G-PROTEIN COUPLED RECEPTOR RHODOPSIN INVIVO
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DOI：
10.1126/science.8316831
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发表时间：
1993-06-25
期刊：
影响因子：
56.9
通讯作者：
ZUKER, CS
中科院分区：
文献类型：
--
作者：
DOLPH, PJ;RANGANATHAN, R;ZUKER, CS
阻滞蛋白参与了许多G蛋白偶联受体信号级联的调控。两个果蝇光感受器特异性捕获基因，捕获蛋白1和捕获蛋白2发生突变。对这些突变体的光响应分析表明，Arr1和Arr2蛋白是视紫红质失活的介质，对体内光传导级联的终止至关重要。过量激活的视紫红质使阻滞蛋白功能饱和，导致光感受器的持续激活状态，即延长的去极化后电位。在没有阻滞的情况下，由于光传导级联的持续活动，光感受器经历光依赖性视网膜变性。这些结果表明，在体内G蛋白偶联受体和信号级联反应的调控中，抑制蛋白家族成员的基本要求。
Arrestins have been implicated in the regulation of many G protein-coupled receptor signaling cascades. Mutations in two Drosophila photoreceptor-specific arrestin genes, arrestin 1 and arrestin 2, were generated. Analysis of the light response in these mutants shows that the Arr1 and Arr2 proteins are mediators of rhodopsin inactivation and are essential for the termination of the phototransduction cascade in vivo. The saturation of arrestin function by an excess of activated rhodopsin is responsible for a continuously activated state of the photoreceptors known as the prolonged depolarized afterpotential. In the absence of arrestins, photoreceptors undergo light-dependent retinal degeneration as a result of the continued activity of the phototransduction cascade. These results demonstrate the fundamental requirement for members of the arrestin protein family in the regulation of G protein-coupled receptors and signaling cascades in vivo.