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丝氨酰-tRNA 合成酶的非规范活性与血管发育。

Noncanonical activity of seryl-transfer RNA synthetase and vascular development.

机构信息

Department of Structural Analysis, National Cardiovascular Center Research Institute, Suita, Osaka, 565-8565, Japan.

出版信息

Trends Cardiovasc Med. 2009 Aug;19(6):179-82. doi: 10.1016/j.tcm.2009.11.001.

Abstract

Seryl-transfer RNA synthetase (Sars) is one of the 20 aminoacyl-transfer RNA synthetases that are enzymes essential for protein synthesis; however, the developmental function of Sars has not been elucidated. In zebrafish, impairment of zygotic Sars function leads to a significant dilatation of the aortic arch vessels and aberrant branching of cranial and intersegmental vessels. This abnormal vascular branching in sars mutants can be suppressed by a form of Sars that lacks canonical function, indicating that a noncanonical activity of Sars regulates vascular development. Inhibition or knockdown of vascular endothelial growth factor (Vegf) signaling, which plays pivotal roles in the establishment of the vascular network, suppresses the abnormal vascular branching observed in sars mutants. Here, we discuss the possible functional relationship between Sars function and Vegf signaling.

摘要

丝氨酰-tRNA 合成酶(Sars)是 20 种氨酰-tRNA 合成酶之一,是蛋白质合成所必需的酶; 然而,Sars 的发育功能尚未阐明。在斑马鱼中,合子 Sars 功能的损伤导致主动脉弓血管显著扩张和颅神经和节间血管分支异常。Sars 突变体中这种异常的血管分支可以被一种缺乏经典功能的 Sars 形式所抑制,表明 Sars 的非经典活性调节血管发育。抑制血管内皮生长因子(Vegf)信号通路,该信号通路在建立血管网络中起着关键作用,可抑制 Sars 突变体中观察到的异常血管分支。在这里,我们讨论了 Sars 功能与 Vegf 信号之间可能存在的功能关系。

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