人细胞中高亲和力色氨酸摄取转运系统。
The high-affinity tryptophan uptake transport system in human cells.
机构信息
Komaba Organization for Educational Excellence, The University of Tokyo, 3-8-1 Komaba, Meguro-ku, Tokyo 153-8902, Japan.
Department of Life Sciences, Graduate School of Arts and Sciences, The University of Tokyo, 3-8-1 Komaba, Meguro-ku, Tokyo 153-8902, Japan.
出版信息
Biochem Soc Trans. 2024 Jun 26;52(3):1149-1158. doi: 10.1042/BST20230742.
The L-tryptophan (Trp) transport system is highly selective for Trp with affinity in the nanomolar range. This transport system is augmented in human interferon (IFN)-γ-treated and indoleamine 2,3-dioxygenase 1 (IDO1)-expressing cells. Up-regulated cellular uptake of Trp causes a reduction in extracellular Trp and initiates immune suppression. Recent studies demonstrate that both IDO1 and tryptophanyl-tRNA synthetase (TrpRS), whose expression levels are up-regulated by IFN-γ, play a pivotal role in high-affinity Trp uptake into human cells. Furthermore, overexpression of tryptophan 2,3-dioxygenase (TDO2) elicits a similar effect as IDO1 on TrpRS-mediated high-affinity Trp uptake. In this review, we summarize recent findings regarding this Trp uptake system and put forward a possible molecular mechanism based on Trp deficiency induced by IDO1 or TDO2 and tryptophanyl-AMP production by TrpRS.
色氨酸（Trp）转运系统对 Trp 具有高度选择性，亲和力在纳摩尔范围内。该转运系统在人干扰素（IFN）-γ处理和吲哚胺 2,3-双加氧酶 1（IDO1）表达的细胞中得到增强。细胞对 Trp 的摄取增加导致细胞外 Trp 减少，并引发免疫抑制。最近的研究表明，IDO1 和色氨酰-tRNA 合成酶（TrpRS）都在 IFN-γ的作用下上调，在人类细胞中高亲和力摄取 Trp 中发挥关键作用。此外，色氨酸 2,3-双加氧酶（TDO2）的过表达对 TrpRS 介导的高亲和力 Trp 摄取产生与 IDO1 相似的作用。在这篇综述中，我们总结了最近关于该 Trp 摄取系统的发现，并提出了一种可能的分子机制，该机制基于 IDO1 或 TDO2 诱导的 Trp 缺乏和 TrpRS 产生色氨酰-AMP。
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