Ask about this productRelated genes to: FLJ20628 antibody
- Gene:
- TRMT61B NIH gene
- Name:
- tRNA methyltransferase 61B
- Previous symbol:
- -
- Synonyms:
- FLJ20628
- Chromosome:
- 2p23.2
- Locus Type:
- gene with protein product
- Date approved:
- 2009-01-09
- Date modifiied:
- 2014-11-19
Related products to: FLJ20628 antibody
Related articles to: FLJ20628 antibody
- Pancreatic cancer, characterized by an unfavourable prognosis, necessitates early diagnosis and prompt therapeutic intervention. This study aimed to delineate the functional implications of m6A/m1A/m5C-related genes in pancreatic carcinogenesis and establish a prognostic model. Utilizing data from the TCGA-PAAD cohort (n=178) combined with GTEx normal pancreatic tissues (n=332), we identified 43 genes associated with mA/mA/mC methylation pathways. Significant expression differences in these genes were observed between neoplastic and non-neoplastic tissues, correlating with multiple biological pathways. Consensus clustering divided pancreatic cancer patients into two distinct molecular subtypes exhibiting pronounced survival differences. A prognostic risk-scoring model was developed based on nine mA/mA/mC-related genes, demonstrating efficacy in predicting patient outcomes. We constructed a nomogram integrating clinical variables with the risk score to enhance prognostic precision. Among these genes, a comprehensive investigation was conducted using immunohistochemistry and multicolor immunofluorescence to elucidate that higher TRMT61B expression in tumour tissues is significantly associated with higher pancreatic cancer stage, and might relate to an immunosuppressive and dysfunctional tumour immune microenvironment. This study reveals the role of mA/mA/mC associated genes, especially TRMT61B, in the epigenetic regulation of pancreatic cancer, providing evidence supporting their potential as novel prognostic biomarkers. - Source: PubMed
Wang YunyangHong XueqingCao DinggeWang MingzhenTuergong AbulaihaitiLiu HongruiGuo YuxuanTing XiaLiu XujunHuo XiaoSi Wenzhe - Despite recent advances in technology to map RNA chemical modifications transcriptome-wide, the distribution of N1-methyladenosine (m1A) in messenger RNA (mRNA) remains contested, hindering a clear understanding of its function. Additionally, the enzyme(s) that installs the majority of reported mRNA m1A sites has yet to be identified. In this study, we characterized TRMT61B, an m1A methyltransferase known to methylate mitochondrial RNAs, but whose sequence preferences have been underexplored. By integrating cellular overexpression of TRMT61B and in vitro methylation of a synthetic pool of diverse human mRNA sequences, we identified a preference for a YMRA consensus motif in single-stranded RNA regions. In these experiments, TRMT61B methylated thousands of novel human mRNA sites, revealing activity on cytosolic mRNAs. We used these novel m1A-modifiable sequences to test the effects of m1A on translation of luciferase reporters and on ribosome recruitment to modified transcripts in the pool. We found that m1A addition can significantly affect translation and ribosome recruitment, but that these effects vary by transcript. Taken together, our results inform future studies of TRMT61B and mRNA modifications, and emphasize that studies of m1A regulation of mRNA must be carried out and interpreted in a highly context-aware manner. - Source: PubMed
Fang DorthyBabich John MStanton RyanVock Isaac WAbdallah KyrillosZhu MingyiLetchuman RajLi RichardSimon Matthew DGilbert Wendy VNachtergaele Sigrid - Despite recent advances in technology to map RNA chemical modifications transcriptome-wide, the distribution of N-methyladenosine (mA) in mRNA remains contested, hindering a clear understanding of its function. Additionally, the enzyme(s) that installs the majority of reported mRNA mA sites has yet to be identified. In this study, we characterized TRMT61B, an mA methyltransferase known to methylate mitochondrial RNAs, but whose sequence preferences have been underexplored. By integrating cellular overexpression of TRMT61B and methylation of a synthetic pool of diverse human RNA sequences, we identified a preference for a YMRA consensus motif in single stranded RNA regions. In these experiments, TRMT61B methylated thousands of novel human mRNA sites, revealing activity on cytosolic mRNAs. We used these novel mA-modifiable sequences to test the effects of mA on translation of luciferase reporters and on ribosome recruitment to modified transcripts in the pool. We found that mA addition can significantly affect translation and ribosome recruitment, but that these effects are vary by transcript. Taken together, our results can inform future studies of TRMT61B and mRNA, and emphasize that studies of mA regulation of mRNA must be carried out and interpreted in a highly context-aware manner. - Source: PubMed
Publication date: 2025/12/08
Fang DorthyBabich John MStanton RyanVock Isaac WAbdallah KyrillosZhu MingyiLi RichardSimon Matthew DGilbert Wendy VNachtergaele Sigrid - Neuroblastoma tightly linked with genetic abnormality. The core genes responsible for RNA N-methyladenosine (mA) modification are critical in tumor development. Nevertheless, few reports revealed the function of mA modification core gene polymorphisms and the neuroblastoma risk. We carried out this study to verify the association of 12 single-nucleotide polymorphisms (SNPs) with neuroblastoma susceptibility. This study recruited 898 cases with newly diagnosed neuroblastoma and 1734 Healthy controls from eight medical centers. We selected 12 SNPs from mA modification genes ALKBH1, TRMT6, TRMT61B, and TRMT10C, and genotypes were determined by the TaqMan method. We used univariable and multivariable logistic regression models to analyze the association of SNPs with neuroblastoma risk, followed by stratified analysis. Statistical analysis showed that TRMT6 rs236170 GG (AOR = 1.23, 95% CI = 1.02-1.50, P = 0.034), rs451571 CC (AOR = 1.46, 95% CI = 1.01-2.11, P = 0.043), rs236188 AA (AOR = 2.65, 95% CI = 1.16-6.07, P = 0.021), rs236110 AA (AOR = 1.91, 95% CI = 1.29-2.82, P = 0.001), and ALKBH1 rs6494 AA (AOR = 4.27, 95% CI = 1.31-13.93, P = 0.016), rs176942 GG (AOR = 1.98, 95% CI = 1.35-2.89, P = 0.0005) were neuroblastoma risk variants; the ALKBH1 rs1048147 CC (AOR = 0.80, 95% CI = 0.68-0.94, P = 0.007) was inverse associated with neuroblastoma risk. The eQTL analysis showed that functional annotation of rs6494 T > A may be potential function variants through decreasing ALKBH1 gene expression mRNA, rs451571 T > C, rs236188 G > A, rs236110 C > A are associated with neuroblastoma risk through increasing the expression of its nearby genes RP5-967N21.11 and lowering the expression of MCM8. Our research showed some SNPs in the mA modification core genes are related to neuroblastoma.Clinical perspectives(i) Few reports have revealed the function of mA modification core gene polymorphisms in neuroblastoma risk.(ii) After genotyping 12 SNPs with potential functions in four mA modification core genes in children with neuroblastoma and healthy controls, we found several neuroblastoma predisposition loci, including TRMT6 rs236170, rs451571, rs236188, rs236110, and ALKBH1 rs6494, rs176942, and rs1048147. The eQTL assessment demonstrated that rs6494 T > A may be a potential functional variant by decreasing ALKBH1 mRNA expression.(iii) Our research is the first to reveal mA modification core gene SNPs and neuroblastoma risk. - Source: PubMed
Publication date: 2025/10/17
Jiang SusuDong SiqiLi YongLin LeiChen LipingZhang WenliZhu JinhongZhang XinxinYang ZhonghuaZhang JiaoCheng JiwenLi LiZhou HaixiaLi SuhongYang WenhanHe JingZhuo Zhenjian - RNA modifications, including m6A, m1A, m5C, m7G, and ac4C, may play a role in the occurrence and development of cancer, such as proliferation. However, the effects of RNA modification-related genes (RRGs) in the development of oral squamous cell carcinoma (OSCC) have not been fully elucidated. The present study aimed to evaluate the effects and mechanisms of RRGs on OSCC development progression. - Source: PubMed
Publication date: 2025/07/01
Lu Cheng-HuiYin Xue-LaiHuang Zhuo-DengLv Si-AngWu JunWei Jie