THUMPD3

Last update 08 May 2025

Basic Info

Synonyms

DKFZP434F091, THUMP domain containing 3, THUMP domain-containing protein 3

+ [2]

Introduction

Methyltransferase which catalyzes the formation of N(2)-methylguanosine at position 6 in a broad range of tRNA substrates containing the characteristic 3'-CCA terminus of mature tRNAs (PubMed:34669960). Also catalyzes the formation of N(2)-methylguanosine at position 7 of tRNA(Trp) (PubMed:34669960). Requires the methyltransferase adapter protein TRM112 for tRNA methyltransferase activity (PubMed:34669960).

100 Clinical Results associated with THUMPD3

100 Translational Medicine associated with THUMPD3

0 Patents (Medical) associated with THUMPD3

Literatures (Medical) associated with THUMPD3

01 Mar 2025·Progress in Neuro-Psychopharmacology and Biological Psychiatry

Unraveling the genetic links between depression and type 2 diabetes

Article

Author: Zhang, Fuquan ; Cao, Hongbao ; Chandhoke, Vikas ; Liu, Dongming ; Baranova, Ancha

BACKGROUNDType 2 diabetes (T2D) is a chronic metabolic disorder that has high comorbidity with mental disorders. The genetic relationships between T2D and depression are far from being well understood.METHODSWe performed genetic correlation, polygenic overlap, Mendelian randomization (MR) analyses, cross-trait meta-analysis, and Bayesian colocalization analysis to assess genetic relationships between T2D and depression, in the forms of major depressive disorder (MDD) and depressed affect (DAF). Then, the summary data-based MR (SMR) analysis was performed to prioritize genes contributing to MDD and to T2D from functional perspective. MDD-driven signaling pathways were constructed to understand the influence of MDD on T2D at the molecular level.RESULTST2D has positive genetic correlations both with MDD (r_g = 0.14) and with DAF (r_g = 0.19). The polygenic overlap analysis showed that about 60 % of causal variants for T2D are shared with MDD and DAF. The MR analysis indicated that genetic liabilities to both MDD (OR: 1.24, 95 % CI: 1.11-1.38) and DAF (OR: 1.48, 95 % CI: 1.23-1.78) are associated with an increased risk for T2D, while genetic liability to T2D is not associated with the risk for MDD (OR: 1.00, 95 % CI: 0.99-1.01) or DAF (OR: 1.01, 95 % CI: 1.00-1.02). The cross-trait meta-analysis identified 271 genomic loci, of which 29 were novel. Genetic predisposition to MDD and T2D shares six overlapping loci, involving some well-characterized genes, such as TCF4 and NEGR1. Colocalization analysis revealed three shared chromosome regions between MDD and T2D, which covers mediator genes including SCYL1, DENND1A, and MAD1L1. Molecular pathway analysis suggests mechanisms that promote the development of T2D through inflammatory pathways overactive in patients with MDD. The SMR analysis and the meta-analysis highlighted seven genes with functional implications for both MDD and T2D, including TNKS2, CCDC92, FADS1, ERI1, THUMPD3, NUCKS1, and PM20D1.CONCLUSIONSOur study points out that depression, in the forms of MDD and DAF, may increase the risk of T2D. Analysis of underlying genetic variation and the molecular pathways, connecting depression and T2D, indicate that the pathophysiological foundations of these two conditions have a notable overlap.

20 Dec 2024·ACS Chemical Biology

PhOxi-seq Detects Enzyme-Dependent m²G in Multiple RNA Types

Article

Author: Chung, Kimberley Chung Kim ; Hili, Ryan ; Zhang, Han ; Klimontova, Marie ; Bannister, Andrew J. ; Kouzarides, Tony

In recent years, RNA-modifying enzymes have gained significant attention due to their impact on critical RNA-based processes and, consequently, human pathology. However, identifying sites of modifications throughout the transcriptome remains challenging largely due to the lack of accurate and sensitive detection technologies. Recently, we described PhOxi-seq as a method capable of confirming known sites of m²G within abundant classes of RNA, namely, purified rRNA and purified tRNA. Here, we further explore the selectivity of PhOxi-seq and describe an optimized PhOxi-seq workflow, coupled to a novel bioinformatic pipeline, that is capable of detecting enzyme-dependent m²G sites throughout the transcriptome. In this way, we generated a database of potential THUMPD3-dependent m²G sites in multiple RNA classes within a human cancer cell line and further identify potential non-THUMPD3 controlled m²G sites. These potential sites should serve as the basis for further confirmation studies for m²G within the human transcriptome.

01 May 2024·Gene

RNA-seq based transcriptomic map reveals multiple pathways of necroptosis in treating myocardial ischemia reperfusion injury

Article

Author: Sun, Xiaotong ; E, Sihan ; Liang, Yingxia ; Zhang, Yijia ; Guan, Xuehao ; Song, Qingbiao ; Juan, Zhaodong ; Zhang, Zhiyu

Necroptosis has been shown to contribute to myocardial ischemia reperfusion injury (MIRI). This study aims to gain new insights into the signaling pathway of necroptosis in rat MIRI using RNA sequencing. MIRI was induced in male rats by ligating the left anterior descending coronary artery for 30 min, followed by reperfusion for 120 min. RNA sequencing was performed to obtain mRNA profiles of MIRI group and MIRI group treated with necrostatin-1 (Nec-1,an inhibitor of necroptosis). Differentially expressed genes (DEGs) were then identified. The DEGs were prominently enriched in the TNF-α signaling pathway, the MAPK signaling pathway and cytokine-cytokine receptor pathways. The majority of the results were associated with genes like Thumpd3,Egr2,Dot1l,Cyp1a1,Dbnl,which primarily regulate inflammatory response and apoptosis, particularly in myocardium. The above results suggested that Nec-1 might be involved in the regulation of necroptosis and the inflammatory response through the above-mentioned genes.

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THUMPD3

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