PDF(Pubmed)
Abstract：
Our previous study demonstrated that L-tryptophan (Trp)-depleted cells display a marked enhancement in Trp uptake facilitated by extracellular tryptophanyl-tRNA synthetase (TrpRS). Here, we show that Trp uptake into TrpRS-overexpressing cells is also markedly elevated upon Trp starvation. These findings indicate that a Trp-deficient condition is critical for Trp uptake, not only into cells to which TrpRS protein has been added but also into TrpRS-overexpressing cells. We also show that overexpression of TrpRS mutants, which cannot synthesize tryptophanyl-AMP, does not promote Trp uptake, and that inhibition of tryptophanyl-AMP synthesis suppresses this uptake. Overall, these data suggest that tryptophanyl-AMP production by TrpRS is critical for high-affinity Trp uptake.
摘要：
我们先前的研究表明，L-色氨酸（Trp）耗尽的细胞在细胞外色氨酸-tRNA合成酶（TrpRS）的促进下显示出Trp摄取的显着增强。这里,我们表明，在Trp饥饿后，Trp对TrpRS过表达细胞的摄取也显着升高。这些发现表明Trp缺乏对Trp摄取至关重要，不仅进入已添加TrpRS蛋白的细胞,而且进入过表达TrpRS的细胞。我们还显示TrpRS突变体的过表达，不能合成色氨酰-AMP，不促进Trp摄取，色氨酸-AMP合成的抑制抑制了这种吸收。总的来说,这些数据表明，TrpRS产生色氨酸-AMP对于高亲和力Trp摄取至关重要。
