Ask about this productRelated genes to: RDM1 Blocking Peptide
- Gene:
- RDM1 NIH gene
- Name:
- RAD52 motif containing 1
- Previous symbol:
- RAD52B
- Synonyms:
- MGC33977
- Chromosome:
- 17q12
- Locus Type:
- gene with protein product
- Date approved:
- 2004-02-19
- Date modifiied:
- 2016-10-05
Related products to: RDM1 Blocking Peptide
Related articles to: RDM1 Blocking Peptide
- RDM1 is linked to poor prognosis in hepatocellular carcinoma (HCC) chemotherapy. We investigated its post-transcriptional regulation and developed a targeted co-delivery strategy to enhance chemosensitivity. - Source: PubMed
Publication date: 2026/03/23
Cai XiaoniWang XiangZhang QiongdanGao FanXu SongLyu WenqiaoYe JiayuanLiu FeiZhang Luting - Emerging evidence has demonstrated that pseudouridylation regulates mRNA translation and gene expression, yet its molecular characteristics in hepatocellular carcinoma (HCC) remain unknown. Using public databases, we developed pseudouridylation-related molecular subtype and risk score model to assess HCC patient prognosis and disclose their clinical feature, molecular mechanism and immune landscape. Furthermore, quantitative polymerase chain reaction (qPCR) was performed to verify the expression of RDM1, CDCA3 and FLVCR1. Specifically, functional enrichment analysis revealed pseudouridylation-related genes (PRGs) predominantly regulate transcriptional and translational regulation. Prognostic PRGs stratified HCC into two distinct subtypes, the cluster 1 had a poor prognosis and was characterized by high alpha fetoprotein level, poor differentiation, advanced tumor stage, large tumor size, frequent TP53 mutation, up-regulation of cell cycle- and mitosis-associated genes, which was similar to the aggressive proliferation subtype of HCC. In contrast, the cluster 2 exhibited good prognosis and increased infiltration of immune cells, resembling the non-proliferation subtype of HCC, and suggesting its potential responsiveness to immunotherapy. Survival analysis discovered that the risk score model served as an independent prognostic factor, with high-risk group exhibiting significantly shorter overall survival and recurrence-free survival than low-risk group. Notably, receiver operating characteristic analysis revealed that the risk model had a powerful predictive performance for 1- and 3- year survival (AUC=0.806). In addition, functional enrichment analysis suggested that upregulated genes of high-risk group displayed an enrichment of cell cycle progression, mitotic division, and some oncogenic signaling pathways (PLK1, FOXM1, and p53 signaling pathways). qPCR experiment confirmed the significant overexpression of RDM1, CDCA3, and FLVCR1 in HCC tissues, being consistent with public database analysis. In conclusion, pseudouridylation related-molecular subtype and risk model may effectively predict the prognosis and therapeutic response of HCC. - Source: PubMed
Publication date: 2025/08/16
Lan ChenluGao DonghuaWei YongguangHuang HuashengLv XianweiZhou XinQin WeiLiao XiwenZhu GuangzhiPeng Tao - Kidney cancer may result from different gene mutations, each contributing to different histological subtypes and prognoses. RAD52 motif-containing 1 (RDM1) regulates multiple cancer pathways, but its role in ccRCC is unknown to date. According to our results, RDM1 expression increased in ccRCC cells, which was correlated to poor survival in ccRCC patients. Knockdown of RDM1 arrested the cell cycle, promoted cell apoptosis, and apparently suppressed ccRCC cell growth in vitro and in vivo. From the mechanism perspective, RDM1 drove MCM2 to modulate ccRCC cell cycle. Thus, RDM1 inhibition blocks cell cycle progression, suppresses ccRCC cell growth, and is a promising approach for treating ccRCC. - Source: PubMed
Publication date: 2025/07/02
Li XiumingLiu HuiWei YujieWang AnxinLv ChengchengZeng Yu - Forward genetic screens have uncovered numerous genes involved in DNA methylation regulation, but these methods are often time-intensive, costly, and labor-intensive. To address these limitations, this study utilized CRISPR technology to knockout selected co-expressed genes, enabling the rapid identification of low luciferase (LUC) luminescence mutants in the Col-LUC line, which harbors a LUC transgene driven by a 2 × 35S promoter in Arabidopsis. As proof of concept, the repressor of silencing 1 (ROS1) and RNA-directed DNA methylation 1 (RDM1) genes were used as controls, while the increased DNA methylation 3 (IDM3) gene, co-expressed with ROS1, was selected as the target for gene knockout experiments. The results demonstrated that combining co-expression analysis with CRISPR technology is an effective strategy for generating low LUC luminescence mutants in the Col-LUC line. Notably, a new mutant, named reduced luminescence 1 (rl1), was identified through this approach. The rl1 mutant exhibited genome-wide DNA hypermethylation, and its reduced luminescence phenotype was largely reversed by treatment with the DNA methylation inhibitor 5-Aza-2'-deoxycytidine, confirming its anti-silencing role in DNA methylation regulation. This study presents a novel and efficient approach for obtaining low luminescence mutants in the Col-LUC line and identifies RL1 as a previously uncharacterized protein involved in DNA methylation regulation. - Source: PubMed
Publication date: 2024/12/27
Miao WeiDai JieZhang LiLiang ZhileSun XiaoxuanHuang MeiziZhang AqinZheng LongLi YongjunLi Ying - RNA polymerase V (Pol V) and Pol IV are known to be specialized for RNA-directed DNA methylation (RdDM). Here we report that Pol V, but not Pol IV, regulates hundreds of genes including jasmonic acid-responsive genes and confers plant defence to Botrytis cinerea and Spodoptera exigua. About half of the Pol V-regulated genes are associated with Pol V transcripts (PVTs). We thus hypothesized that some PVTs could regulate gene expression in an RdDM-independent manner. To test this hypothesis, we studied three PVTs, PVT-ERF5a/b and PVT-ERF6, as models. PVT-ERF5a/b and PVT-ERF6 are transcribed from the upstream regions of ERF5 and ERF6 and positively regulate their transcription, thereby regulating plant defence. Such regulation involves PVT-dependent H3K4me3 deposition and requires the DRD1-DMS3-RDM1 complex that mediates Pol V recruitment to the target loci. These findings highlight an unprecedented role for PVTs in regulating gene transcription, apart from serving as scaffold RNAs to direct DNA methylation. - Source: PubMed
Publication date: 2024/08/26
Yuan YuxiangLiu YujieHan LuLi YanQi Yijun