Novel beta2-adrenergic receptor signaling pathways.
Novel beta2-adrenergic receptor signaling pathways.
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DOI：
10.1067/mai.2002.129370
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发表时间：
2002-12-01
影响因子：
14.2
通讯作者：
Benovic, Jeffrey L.
中科院分区：
文献类型：
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作者：
Benovic, Jeffrey L.
β2 肾上腺素受体 (beta2AR) 可能是所有 G 蛋白偶联受体中研究最彻底的。虽然 beta2AR 信号传导的经典途径涉及激动剂促进受体与异三聚鸟苷三磷酸结合蛋白 Gs 的结合、腺苷酸环化酶的激活以及环磷酸腺苷 (cAMP) 的产生，但目前的证据表明 beta2AR 信号传导是通过与多种蛋白质的相互作用来调节的。这些相互作用分为 3 个主要组：三磷酸鸟苷结合蛋白，例如 Gs 和 Gi；蛋白激酶，例如cAMP依赖性蛋白激酶、蛋白激酶C、G蛋白偶联受体激酶和酪氨酸激酶；以及接头蛋白，例如视紫红质抑制蛋白、A-激酶锚定蛋白和 Na+/H+-交换调节因子。这篇综述讨论了这些不同的相互作用，特别强调它们在调节 beta2AR 信号传导和运输中的作用。
The beta2-adrenergic receptor (beta2AR) is perhaps the most thoroughly investigated of all G-protein-coupled receptors. Although the classical pathway of beta2AR signaling involves agonist-promoted binding of the receptor to the heterotrimeric guanosine triphosphate-binding protein Gs, activation of adenylyl cyclase, and production of cyclic adenosine monophosphate (cAMP), current evidence suggests that beta2AR signaling is regulated by interaction with multiple proteins. These interactions fall into 3 major groups: guanosine triphosphate-binding proteins such as Gs and Gi; protein kinases such as the cAMP-dependent protein kinase, protein kinase C, G-protein-coupled receptor kinases, and tyrosine kinases; and adaptor proteins such as arrestins, A-kinase anchoring proteins, and the Na+/H+-exchanger regulatory factor. This review discusses these various interactions with particular emphasis on their role in regulating beta2AR signaling and trafficking.