RG9MTD1 Blocking Peptide
- Known as:
- RG9MTD1 Blocking Peptide
- Catalog number:
- 33r-4449
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- RG9MTD1 Blocking Peptide
Related genes to: RG9MTD1 Blocking Peptide
- Gene:
- TRMT10C NIH gene
- Name:
- tRNA methyltransferase 10C, mitochondrial RNase P subunit
- Previous symbol:
- RG9MTD1
- Synonyms:
- FLJ20432, MRPP1
- Chromosome:
- 3q12.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-03-04
- Date modifiied:
- 2015-09-25
Related products to: RG9MTD1 Blocking Peptide
Related articles to: RG9MTD1 Blocking Peptide
- The role of m1A as a novel biomarker is gaining increasing attention in the context of cancer. Our study aims to systematically evaluate the prognostic and diagnostic value of m1A in various cancers. - Source: PubMed
Publication date: 2026/03/20
Luo YingDai ZiyaoLi YulinXie XiantingXu Tao - Lipid metabolism disorders and increased angiogenesis play key roles in the tumorigenesis of hepatocellular carcinoma (HCC). Intracellular metal ion disorders such as cuproptosis and ferroptosis have been progressively identified. However, whether copper ions have other effects outside the already recognized mechanisms of cell death is just as worthy of investigation. In particular, the effects on lipid metabolism and angiogenesis have important roles in the development of HCC. Our study revealed that disulfiram (DSF), a copper ion carrier, not only had a significant antitumor effect in vitro and in vivo, but also significantly inhibited angiogenesis and reversed abnormal lipid metabolism. Through transcriptome analysis, mA methylation analysis, and functional validation, we identified c-FOS as a key target in DSF-induced methylation changes. In summary, DSF can reduce the modifications of c-FOS caused by the mA methyltransferase TRMT10C, then regulate downstream genes MCAM and PCSK9, ultimately affecting angiogenesis and lipid metabolism. Moreover, high levels of expression of TRMT10C and PCSK9 in human HCC tumor tissues were associated with poor prognosis, while c-FOS showed the opposite pattern, confirming that the TRMT10C-c-FOS-PCSK9 axis is an important mechanism in HCC. In conclusion, copper ion carrier-DSF promotes the expression of c-FOS by inhibiting the mA methyltransferase TRMT10C, thereby reversing the dysregulation of lipid metabolism and inhibiting angiogenesis in HCC. - Source: PubMed
Publication date: 2026/01/09
Qi ZhuoranKong XiuyanWu JinlanDu XiaojingJiang MatteoYu ZhijieShen XizhongFang YuanXia Jinglin - RNase P enzymes of widely varying architectures recognize the 5'-leader/acceptor-stem junction and the D/T loop-interaction region of precursor tRNAs to direct cleavage to the 5' end of tRNAs. In contrast, human mitochondrial RNase P (mtRNase P) encases the entire tRNA with the aid of the methyltransferase subcomplex TRMT10C-SDR5C1. Here, we performed a kinetic analysis of substrate recognition by mtRNase P using substrate and protein variants. Surprisingly, processing by mtRNase P was found to be more efficient for tRNA precursors with longer 5' extensions and decreased sharply at a leader length of 1 nt. MtRNase P also employs a more rigid "measuring mechanism" for cleavage-site selection than the related single-subunit enzymes, so that even substrates with a G:C base-pair extension of the acceptor stem are cleaved predominantly at the canonical site. The specific contacts of TRMT10C-SDR5C1 with the anticodon loop are not crucial for efficient processing, but without interactions with the pre-tRNA, TRMT10C-SDR5C1 is unable to stimulate cleavage by the nuclease subunit PRORP, also explaining why mtRNase P reaches its limits with the D-armless mitochondrial tRNASer(AGY). Our findings set human mtRNase P apart in terms of substrate recognition from all other known forms of RNase P, including the related single-polypeptide PRORPs. - Source: PubMed
Hazisllari EnxhiRadovanović DanijelaToth UrsulaVilardo ElisaHartmann Roland KRossmanith Walter - This study investigates the impact of the m1A regulator TRMT6 on prognosis and the tumor microenvironment in ovarian cancer. - Source: PubMed
Publication date: 2025/10/30
Zhao JingWang XiaonaWang YazhuoLi Na - 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