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3类信号素信号传导:一个教条的终结。

Class 3 semaphorin signaling: the end of a dogma.

作者信息

Potiron Vincent, Roche Joëlle

机构信息

UMR-CNRS 6187, Institut de Physiologie et Biologie Cellulaires, Université de Poitiers, 40 avenue du recteur Pineau, 86022 Poitiers, France.

出版信息

Sci STKE. 2005 May 24;2005(285):pe24. doi: 10.1126/stke.2852005pe24.

DOI:10.1126/stke.2852005pe24
PMID:15914725
Abstract

Semaphorins--a family of secreted, membrane-bound, and transmembrane proteins--play an important role in the development of various organs, as well as in axonal pathfinding, angiogenesis, tumorigenesis, and the immunological response. Neuropilins 1 and 2 (NRP1 and 2) are receptors for the class 3 secreted semaphorins (SEMA3s) but not for the other classes of semaphorins. NRPs are also coreceptors for vascular endothelial growth factor 165 (VEGF165), suggesting that SEMA3s could inhibit the VEGF165-VEGF receptor (VEGFR) pathway during angiogenesis. Until recently, it was believed that binding of SEMA3s to neuropilins was necessary to initiate signaling from plexins, the active players in semaphorin signal transduction. However, Gu and colleagues have recently described an exception: Their research suggests that SEMA3E signal transduction may be neuropilin independent. This Perspective focuses on this recent finding in the context of semaphorin signaling outside the nervous system.

摘要

信号素——一类分泌型、膜结合型和跨膜蛋白——在各种器官的发育以及轴突导向、血管生成、肿瘤发生和免疫反应中发挥重要作用。神经纤毛蛋白1和2(NRP1和NRP2)是3类分泌型信号素(SEMA3s)的受体,但不是其他类信号素的受体。神经纤毛蛋白也是血管内皮生长因子165(VEGF165)的共受体,这表明SEMA3s在血管生成过程中可能抑制VEGF165-血管内皮生长因子受体(VEGFR)途径。直到最近,人们还认为SEMA3s与神经纤毛蛋白的结合是启动信号素信号转导中的活跃参与者——丛状蛋白信号传导所必需的。然而,顾及其同事最近描述了一个例外情况:他们的研究表明,SEMA3E信号转导可能不依赖神经纤毛蛋白。本观点文章在神经系统之外的信号素信号传导背景下重点关注这一最新发现。

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