关键词: G protein-coupled receptors diabetes metabolism mutant mice obesity β-arrestins

Mesh : Animals Diabetes Mellitus / metabolism Disease Models, Animal Energy Metabolism Glucose / metabolism Mice Obesity / metabolism Receptors, G-Protein-Coupled / metabolism Signal Transduction beta-Arrestin 1 / metabolism beta-Arrestin 2 / metabolism

来  源:   DOI:10.3390/ijms23010495

Abstract:
The two β-arrestins (β-arrestin-1 and -2; alternative names: arrestin-2 and -3, respectively) are well known for their ability to inhibit signaling via G protein-coupled receptors. However, β-arrestins can also act as signaling molecules in their own right. Although the two proteins share a high degree of sequence and structural homology, early studies with cultured cells indicated that β-arrestin-1 and -2 are not functionally redundant. Recently, the in vivo metabolic roles of the two β-arrestins have been studied using mutant mice selectively lacking either β-arrestin-1 or -2 in cell types that are of particular relevance for regulating glucose and energy homeostasis. These studies demonstrated that the β-arrestin-1 and -2 mutant mice displayed distinct metabolic phenotypes in vivo, providing further evidence for the functional heterogeneity of these two highly versatile signaling proteins.
摘要:
两种β-抑制蛋白(β-抑制蛋白-1和-2;替代名称:分别为抑制蛋白-2和-3)的能力是众所周知的通过G蛋白偶联受体抑制信号传导的能力。然而,β-抑制素本身也可以充当信号分子。尽管这两种蛋白质具有高度的序列和结构同源性,对培养细胞的早期研究表明β-抑制蛋白-1和-2在功能上不是多余的.最近,已经使用在与调节葡萄糖和能量稳态特别相关的细胞类型中选择性缺乏β-抑制素-1或-2的突变小鼠研究了两种β-抑制素的体内代谢作用。这些研究表明,β-arrestin-1和-2突变小鼠在体内表现出不同的代谢表型,为这两种高度通用的信号蛋白的功能异质性提供了进一步的证据。
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