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Last update 08 May 2025

TRMT5

Last update 08 May 2025

Basic Info

Synonyms

KIAA1393, M1G-methyltransferase, TRM5

+ [5]

Introduction

Involved in mitochondrial tRNA methylation (PubMed:26189817). Specifically methylates the N1 position of guanosine-37 in various tRNAs. Methylation is not dependent on the nature of the nucleoside 5' of the target nucleoside. This is the first step in the biosynthesis of wybutosine (yW), a modified base adjacent to the anticodon of tRNAs and required for accurate decoding.

Drugs associated with TRMT5

Thienopyrimidinone derivative

Target

TRMT5

Mechanism

TRMT5 inhibitors

Active Org.

Nanyang Technological University [+1]

Originator Org.

Singapore-MIT Alliance for Research & Technology [+1]

Active Indication

Mycobacterium Infections

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with TRMT5

100 Translational Medicine associated with TRMT5

0 Patents (Medical) associated with TRMT5

Literatures (Medical) associated with TRMT5

01 Oct 2024·Small

Circulating B Cell‐Derived Small RNA Delivered by Extracellular Vesicles: A Dialogue Mechanism for Long‐Range Targeted Renal Mitochondrial Injury in Obesity

Article

Author: Han, Yi ; Wang, Cunchuan ; Yin, Lianghong ; Li, Hongyue ; Meng, Yu ; Hu, Bo ; Liu, Xiayun ; Zheng, Zirun ; Liu, Huanhuan ; Huang, Sibo ; Chen, Ruichang ; Xiao, Zhangzhang ; Yang, Wah ; Ma, Ke ; Liu, Jinfeng ; Li, Xiaqing ; Zhao, Qian

AbstractThe intricate processes that govern the interactions between peripatetic immune cells and distal renal injury in obesity are not fully understood. Employing transcriptomic analysis of circulating extracellular vesicles (EVs), a marked amplification of small RNA (miR‐3960) is discerned within CD3−CD19+ B cells. This RNA is found to be preferentially augmented in kidney tissues, contrasting with its subdued expression in other organs. By synthesizing dual‐luciferase reporter assay with co‐immunoprecipitation analysis, it is pinpointed that miR‐3960 specifically targets the nuclear gene TRMT5, a pivotal actor in the methylation of mitochondrial tRNA. This liaison instigates aberrations in the post‐transcriptional modifications of mitochondrial tRNA, engendering deficiencies within the electron respiratory chain, primarily attributable to the diminution of the mitochondrial bioenergetic compound (NDUFA7) complex I. Such perturbations lead to a compromised mitochondrial respiratory capacity in renal tubular cells, thereby exacerbating tubular injury. In contrast, EV blockade or miR‐3960 depletion markedly alleviates renal tubular injury in obesity. This investigation unveils a hitherto unexplored pathway by which obesity‐induced circulating immune cells remotely manipulate mitochondrial metabolism in target organs. The strategic targeting of obese EVs or infiltrative immune cells and their specifically secreted RNAs emerges as a promising therapeutic avenue to forestall obesity‐related renal afflictions.

01 Jul 2024·Translational Cancer Research

Novel mitochondrial-related gene signature predicts prognosis and immunological status in glioma

Article

Author: Chen, Guangliang ; Cai, Lize ; Liu, Yongsheng ; Yao, Lin ; Zhang, Kai ; Zhou, Youxin ; Wang, Hao

BackgroundMitochondria are the center of cellular metabolism. The relationship between mitochondria and diseases has also been studied for a long time. However, the prognostic role of mitochondrial-related genes (MRGs) in patients with glioma and their biological effects are still unclear. The aim of the study was to construct a mitochondria-related model to assess prognosis and potential biological effects like immune infiltration, gene pathway and mutation, and give some predictive chemotherapeutic agents.MethodsThe data of 675 patients from The Cancer Genome Atlas (TCGA) database were used to identify MRG signature and construct a prognostic model. After validating its robustness in Chinese Glioma Genome Atlas (CGGA), two risk groups derived from the prognostic model were then conducted with Gene Set Enrichment Analysis (GSEA), immune status, mutation status and chemotherapeutic agents prediction.ResultsThe prognostic model built from six gene signatures can successfully predict the prognosis and reflect clinicopathological characteristics. Patients in high-risk group displayed significantly worse overall survival (OS), immunosuppression effects, and mutation markers with worse prognosis. Twelve chemotherapeutic agents with strongly correlated sensitivity and risk scores were selected as potential agents.ConclusionsThe novel MRG signatures (TYMP, TSFM, MGME1, BOLA3, TRMT5, NDUFA9) can predict prognosis and immunological status in glioma.

01 Nov 2023·International Journal of Biological Macromolecules

Restricted tRNA methylation by intermolecular disulfide bonds in DNMT2/TRDMT1

Article

Author: Chen, Yong ; Li, Huari ; Cheng, Hongjing ; Cai, Chao ; Zhu, Daiyun ; Yang, Yapeng ; Ma, Yunfei ; Xu, Dandan ; Chen, Juan ; Qin, Mian ; Xue, Pingfang

Reportedly, DNMT2/TRDMT1 mainly methylates tRNAs at C38 and prevents them from the cleavage under stress. It also plays an essential role in the survival and physiological homeostasis of organisms. Nevertheless, DNMT2/TRDMT1 exhibits much weaker tRNA methylation activity in vitro than other tRNA methyltransferases, TrmD and Trm5. Here, we explored the restricted tRNA methylation mechanism by DNMT2/TRDMT1. In the current study, the optimized buffer C at 37 °C was the best condition for DNMT2/TRDMT1 activation. Of note, Dithiothreitol (DTT) was an indispensable component for this enzyme catalysis. Moreover, reductants took similar effects on the conformation change and oligomeric formation of DNMT2/TRDMT1. Ultimately, LC-MS/MS result revealed that C292-C292 and C292-C287 were predominant intermolecular disulfide bonds in recombinant DNMT2/TRDMT1. Notably, DNMT2/TRDMT1 existed primarily as dimers via intermolecular disulfide bonds C79-C24, C292-C292, and C222-C24 in HEK293T cells. GSSG stress enhanced tRNA methylation level in the early stage of stress, whereas the DNMT2/TRDMT1 activity might be unfavorable along with this enzyme accumulation in the nucleus. Excitingly, GSH stress downregulated the DNMT2/TRDMT1 expression and promoted tRNA methylation in cells, probably through breaking intermolecular disulfide bonds in this enzyme. Thus, our findings demonstrated restricted tRNA methylation by disulfide bonds in DNMT2/TRDMT1, and will provide important implications for redox stress related-diseases.

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TRMT5

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