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SS-Arrestin and dishevelled coordinate biased signaling

机译：SS-Arrestin和散乱的坐标偏向信号

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摘要

The adaptor proteins p-arrestins 1 and 2 are ubiquitously expressed and were originally discovered for desensitizing G protein-mediated signal transduction by the cell-surface seven-transmembrane receptors (7TMRs or GPCRs) (1). 7TMRs constitute the largest family of cell-surface receptors, and their signaling regulates almost every aspect of mammalian physiology, including vision, olfaction, behavior, heart rate, blood pressure, inflammatory, and digestive processes. Although 7TMR signaling was originally thought to involve only G proteins, accumulating evidence indicates that p-arrestins not only block G protein signaling, but also facilitate receptor endocytosis and mediate G protein-independent signaling (2, 3). Studies have also illuminated receptor ligands called biased agonists that specifically activate p-arrestin signaling while blocking G proteins or vice versa (4). Such biased ago-riism can be exploited to develop better drugs acting at the 7TMRs with reduced side effects (5). In PNAS, Soh and Trejo report a cytoprotective p-arrestin-biased signaling pathway emanating from the 7TMR, protease activated receptor-1 (PAR1), which could be important in reducing sepsis-induced inflammation (6).
机译：衔接子蛋白p-arrestin 1和2普遍表达，最初发现它们是通过细胞表面七种跨膜受体（7TMR或GPCR）使G蛋白介导的信号转导脱敏的（1）。 7TMR构成细胞表面受体的最大家族，其信号传导调节哺乳动物生理的几乎所有方面，包括视觉，嗅觉，行为，心率，血压，炎症和消化过程。尽管最初认为7TMR信号传导仅涉及G蛋白，但越来越多的证据表明p-arrestins不仅阻断G蛋白信号传导，而且还促进受体内吞并介导G蛋白非依赖性信号传导（2、3）。研究还阐明了称为偏向激动剂的受体配体，该受体配体可特异性激活p-arrestin信号传导，同时阻断G蛋白，反之亦然（4）。可以利用这种有偏见的前种族主义来开发对7TMR起作用​​且副作用减少的更好的药物（5）。在PNAS中，Soh和Trejo报告了从7TMR蛋白酶激活的受体1（PAR1）发出的具有细胞保护作用的p-arrestin偏向的信号传导途径，这对减少败血症引起的炎症可能很重要（6）。

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    Gunnar Schulte; Sudha K. Shenoy;

  • 作者单位

    Department of Physiology and Pharmacology, Section of Receptor Biology and Signaling, Karolinska Instituted S-171 77 Stockholm, Sweden;

    Departments of Medicine and Cell Biology, Duke University Medical Center, Durham, NC 27710;

  • 收录信息 美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
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