A human aminoacyl-tRNA synthetase as a regulator of angiogenesis
A human aminoacyl-tRNA synthetase as a regulator of angiogenesis
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DOI：
10.1073/pnas.012602099
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发表时间：
2002-01-08
影响因子：
11.1
通讯作者：
Schimmel, P
中科院分区：
文献类型：
--
作者：
Wakasugi, K;Slike, BM;Schimmel, P
氨基酰基- trna合成酶催化蛋白质合成的第一步。最近的研究表明，人酪氨酸- trna合成酶（TyrRS）可以分裂成两个具有不同细胞因子活性的片段，从而将蛋白质合成与细胞因子信号通路联系起来。色氨酸- trna合成酶（TrpRS）是TyrRS的密切同源物。一个自然片段，这里被称为迷你trpr，被其他人证明是通过选择性剪接产生的。据报道，ifn - γ刺激了该片段的产生，ifn - γ是一种细胞因子，也刺激了血管抑制因子的产生。迷你trpr在哺乳动物细胞培养系统、鸡胚胎和两个独立的小鼠血管生成实验中显示出血管抑制作用。全长酶在相同的实验中是无活性的。因此，蛋白质合成可能通过trpr的天然片段与血管生成的调节有关。
Aminoacyl-tRNA synthetases catalyze the first step of protein synthesis. It was shown recently that human tyrosyl-tRNA synthetase (TyrRS) can be split into two fragments having distinct cytokine activities, thereby linking protein synthesis to cytokine signaling pathways. Tryptophanyl-tRNA synthetase (TrpRS) is a close homologue of TyrRS. A natural fragment, herein designated as mini TrpRS, was shown by others to be produced by alternative splicing. Production of this fragment is reported to be stimulated by IFN-gamma, a cytokine that also stimulates production of angiostatic factors. Mini TrpRS is shown here to be angiostatic in a mammalian cell culture system, the chicken embryo, and two independent angiogenesis assays in the mouse. The full-length enzyme is inactive in the same assays. Thus, protein synthesis may be linked to the regulation of angiogenesis by a natural fragment of TrpRS.