Seeking Ligand Bias: Assessing GPCR Coupling to Beta-Arrestins for Drug Discovery.
Seeking Ligand Bias: Assessing GPCR Coupling to Beta-Arrestins for Drug Discovery.
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DOI：
10.1016/j.ddtec.2010.06.005
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发表时间：
2010
期刊：
影响因子：
--
通讯作者：
McDonald, Patricia H
中科院分区：
文献类型：
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作者：
Bohn, Laura M;McDonald, Patricia H
G蛋白偶联受体（GPCR）是内源性激素和神经递质的主要作用部位。早期的药物发现工作集中在确定配体是否可以参与G蛋白偶联，并随后激活或抑制同源的“第二信使”。那些简单的日子已经一去不复返了，因为我们现在意识到受体也可以偶联β抑制蛋白。当我们深入研究配体介导的信号传导和受体体支架的复杂性时，我们面临着受体-配体介导的事件引发的似乎无穷无尽的可能性。
G protein-coupled receptors (GPCR) are the major site of action for endogenous hormones and neurotransmitters. Early drug discovery efforts focused on determining whether ligands could engage G protein coupling and subsequently activate or inhibit cognate “second messengers.” Gone are those simple days as we now realize that receptors can also couple βarrestins. As we delve into the complexity of ligand-directed signaling and receptosome scaffolds, we are faced with what may seem like endless possibilities triggered by receptor-ligand mediated events.