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更新于：2024-11-01

TrpRS

更新于：2024-11-01

基本信息

别名

hWRS、IFI53、IFP53

+ [10]

简介

Isoform 1, isoform 2 and T1-TrpRS have aminoacylation activity while T2-TrpRS lacks it. Isoform 2, T1-TrpRS and T2-TrpRS possess angiostatic activity whereas isoform 1 lacks it. T2-TrpRS inhibits fluid shear stress-activated responses of endothelial cells. Regulates ERK, Akt, and eNOS activation pathways that are associated with angiogenesis, cytoskeletal reorganization and shear stress-responsive gene expression.

关联

项与 TrpRS 相关的药物

M-101AI

靶点

TrpRS

作用机制

TrpRS inhibitors

在研机构

MirimGENE Co. Ltd.初创企业

原研机构

MirimGENE Co. Ltd.初创企业

在研适应症

脓毒症

非在研适应症-

最高研发阶段临床前

首次获批国家/地区-

首次获批日期1800-01-20

M-207AN

靶点

TrpRS

作用机制

TrpRS inhibitors

在研机构

MirimGENE Co. Ltd.初创企业

原研机构

MirimGENE Co. Ltd.初创企业

在研适应症

结核

非在研适应症-

最高研发阶段临床前

首次获批国家/地区-

首次获批日期1800-01-20

100 项与 TrpRS 相关的临床结果

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100 项与 TrpRS 相关的转化医学

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0 项与 TrpRS 相关的专利（医药）

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402

项与 TrpRS 相关的文献（医药）

2024-12-01·Cellular and Molecular Life Sciences

Tryptophanylation of insulin receptor by WARS attenuates insulin signaling

Article

作者: Zhao, Shi-Min ; Yuan, Yi-Yuan ; Zhang, Kai-Hui ; Hu, Song-Hua ; Zhou, Qian ; Xu, Wei ; Sun, Wen-Xing ; Lin, Yan

Increased circulating amino acid levels have been linked to insulin resistance and development of type 2 diabetes (T2D), but the underlying mechanism remains largely unknown. Herein, we show that tryptophan modifies insulin receptor (IR) to attenuate insulin signaling and impair glucose uptake. Mice fed with tryptophan-rich chow developed insulin resistance. Excessive tryptophan promoted tryptophanyl-tRNA synthetase (WARS) to tryptophanylate lysine 1209 of IR (W-K1209), which induced insulin resistance by inhibiting the insulin-stimulated phosphorylation of IR, AKT, and AS160. SIRT1, but not other sirtuins, detryptophanylated IR^W-K1209 to increase the insulin sensitivity. Collectively, we unveiled the mechanisms of how tryptophan impaired insulin signaling, and our data suggested that WARS might be a target to attenuate insulin resistance in T2D patients.

2024-08-01·The Journal of Immunology

Single-Cell RNA Sequencing Identifies WARS1+ Mesenchymal Stem Cells with Enhanced Immunomodulatory Capacity and Improved Therapeutic Efficacy

Article

作者: Sun, Xuxu ; Sun, Yang ; Li, Qun ; Jin, Xinping ; Li, Xiangxiao ; Cai, Xiaojie ; Zhang, Fengjiao ; Wang, Zhikai ; Fan, Li ; Wang, Honglin ; Xu, Zhenyao ; Lou, Fangzhou ; Gao, Min ; Tang, Sibei ; Wu, Yue ; Deng, Siyu ; Sun, Libo

AbstractPsoriasis is a common inflammatory skin disorder with no cure. Mesenchymal stem cells (MSCs) have immunomodulatory properties for psoriasis, but the therapeutic efficacies varied, and the molecular mechanisms were unknown. In this study, we improved the efficacy by enhancing the immunomodulatory effects of umbilical cord–derived MSCs (UC-MSCs). UC-MSCs stimulated by TNF-α and IFN-γ exhibited a better therapeutic effect in a mouse model of psoriasis. Single-cell RNA sequencing revealed that the stimulated UC-MSCs overrepresented a subpopulation expressing high tryptophanyl-tRNA synthetase 1 (WARS1). WARS1-overexpressed UC-MSCs treat psoriasis-like skin inflammation more efficiently than control UC-MSCs by restraining the proinflammatory macrophages. Mechanistically, WARS1 maintained a RhoA-Akt axis and governed the immunomodulatory properties of UC-MSCs. Together, we identify WARS1 as a master regulator of UC-MSCs with enhanced immunomodulatory capacities, which paves the way for the directed modification of UC-MSCs for escalated therapeutic efficacy.

2024-06-26·Biochemical Society Transactions

The high-affinity tryptophan uptake transport system in human cells

Review

作者: Wakasugi, Keisuke ; Yokosawa, Takumi

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.