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β-Arrestin acts as a clathrin adaptor in endocytosis of the β_2-adrenergic receptor

机译：β-Arrestin充当网格蛋白衔接子，参与β_2-肾上腺素受体的内吞

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摘要

The ability of a system to regulate its responsiveness in the presence of a continuous stimulus, often termed desensitization, has been extensively characterized for the β_2-adrenergic receptor (β_2AR). β_2AR signalling is rapidly attenuated through receptor phosphorylation and subsequent binding of the protein β-arrestin. Ultimately the receptor undergoes internalization, and although the molecular mechanism is unclear, receptor phosphorylation and β-arrestin binding have been implicated in this process. Here we report that β-arrestin and arrestin-3, but not visual arrestin, promote β_2AR internalization and bind with high affinity directly and stoichiometrically to clathrin, the major structural protein of coated pits. Moreover, β-arrestin/ arrestin chimaeras that are defective in either β_2AR or clathrin binding show a reduced ability to promote β_2AR endocytosis. Immunofluorescence microscopy of intact cells indicates an agonist-dependent colocalization of the β_2AR and β-arrestin with clathrin. These results show that β-arrestin functions as an adaptor in the receptor-mediated endocytosis pathway, and suggest a general mechanism for regulating the trafficking of G-protein-coupled receptors.
机译：对于β_2-肾上腺素能受体（β_2AR），已广泛表征了系统在连续刺激（通常称为脱敏）存在下调节其响应能力的能力。 β_2AR信号通过受体的磷酸化和随后蛋白β-arrestin的结合而迅速减弱。最终，受体经历了内在化，尽管分子机制尚不清楚，但受体磷酸化和β-arrestin结合已牵涉到该过程中。在这里我们报道β-arrestin和arrestin-3，而不是视觉arrestin，促进β_2AR内化并以化学计量比直接和高亲和力与网格蛋白（包被的小孔的主要结构蛋白）结合。此外，在β_2AR或网格蛋白结合方面有缺陷的β-arrestin/ restin嵌合体显示出降低的促进β_2AR内吞作用的能力。完整细胞的免疫荧光显微镜检查表明，β_2AR和β-arrestin与网格蛋白的激动剂依赖性共定位。这些结果表明，β-arrestin在受体介导的胞吞途径中起衔接子的作用，并提出了调节G蛋白偶联受体运输的一般机制。

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