NSUN6 antibody - N-terminal region (ARP41188_P050)
- Known as:
- NSUN6 (anti-) - N-terminal region (ARP41188_P050)
- Catalog number:
- arp41188_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- NSUN6 antibody - N-terminal region (ARP41188_P050)
Related genes to: NSUN6 antibody - N-terminal region (ARP41188_P050)
- Gene:
- NSUN6 NIH gene
- Name:
- NOP2/Sun RNA methyltransferase 6
- Previous symbol:
- NOPD1, ARL5B-AS1
- Synonyms:
- FLJ23743
- Chromosome:
- 10p12.31
- Locus Type:
- gene with protein product
- Date approved:
- 2003-11-21
- Date modifiied:
- 2019-02-26
Related products to: NSUN6 antibody - N-terminal region (ARP41188_P050)
Related articles to: NSUN6 antibody - N-terminal region (ARP41188_P050)
- Endometrial cancer (EC) constitutes a leading gynecologic malignancy for which advanced or metastatic disease presents limited therapeutic options. While RNA modifications are acknowledged as key regulatory elements in cancer, the role of 5-methylcytosine (mC) and its modifying enzymes in EC is still largely unstudied. Here, it demonstrates that the mC methyltransferase NSUN6 is significantly upregulated in EC tissues, and its expression correlates with higher tumor grade and unfavorable prognosis. Functional studies employing gain- and loss-of-function models revealed that NSUN6 specifically enhances EC cell migration and invasion both in vitro and in vivo, without altering proliferation or apoptosis. Mechanistically, NSUN6 drives EMT by catalyzing mC modification on Snail mRNA, which in turn stabilizes the transcript of this key EMT transcription factor. AL398 was identified through structure-based virtual screening as a novel small-molecule inhibitor that binds potently to the NSUN6 active site and suppresses its methyltransferase activity. Treatment with AL398 effectively inhibited the NSUN6/mC/Snail axis, reversed the EMT phenotype, and attenuated EC cell migration, invasion, and metastasis in preclinical models. Collectively, it both validates the NSUN6/mC/Snail axis as a critical EC vulnerability and provides a proof-of-concept inhibitor, AL398, laying the groundwork for the development of first-in-class RNA methylation-targeted therapies against metastatic EC. - Source: PubMed
Publication date: 2026/08/28
Zhao XiangzhuanYang LinlinChen HuanxiangGuo ChenfengLu HongshenZhu YingWang XuanzhiLi YangZhang RuikeHuang ZichongChen YifangJin KeyuXu ZeduoMeng LingxiuZhang LongfengHan YuanyuanYan YicongKang QiaozhenWan JunhuLiu Hongyang - mRNA plays a pivotal role in cellular processes of genetic information transfer, and post-transcriptional modifications of its nucleotides enable regulation of these processes with each particular mRNA. m5C methylation is a specific RNA modification that is rather common in tRNA, rRNA, lncRNA and other types of non-coding RNAs, whereas in mRNA it is found not very often. However, the functioning of m5C-methylated mRNAs differs from the non-methylated ones quite dramatically. Of the eight m5C RNA methyltransferases in humans, only two, NSUN2 and NSUN6, were found to be capable of modifying the main portion of cellular mRNAs. A deficiency of NSUN2 and NSUN6 causes global changes in the transcriptome and translatome, and a corruption of the gene in humans is associated with neurodegenerative diseases and intellectual disability. Despite intensive research of m5C mRNA methylation in recent years, many aspects of this phenomenon and its significance remain problematic and far from understood. In this review, we discuss the available information on mRNA methylome biogenesis, methods for its study and analysis, effects of m5C modification on mRNA life, and place it in the general context of cell biology, attempting to draw the biological relevance of m5C mRNA methylation. We highlight the main inconsistencies and difficulties that arise, analyze their possible causes, and propose potential directions for further research that could clarify the controversial issues and provide a link between the NSUN2 deficiency and neurodegenerative diseases. - Source: PubMed
Publication date: 2026/07/25
Babaylova Elena SZolotenkova Elizaveta AMalygin Alexey A - Brain arteriovenous malformations (bAVMs) are high-risk vascular lesions prone to intracranial hemorrhage, with unclear upstream regulatory mechanisms. We integrated 5-methylcytosine (mC) RNA methylation sequencing and transcriptomics in ruptured and unruptured bAVMs to identify differentially methylated non-coding RNAs. Functional validation was performed in human tissues, HUVECs, and zebrafish models. mC profiling revealed global methylation remodeling in ruptured bAVMs, with enrichment of EndMT and Wnt/β-catenin pathways. USP2-AS1 emerged as a key lncRNA showing increased methylation and expression, predominantly in endothelial cells. In HUVECs, USP2-AS1 promoted EndMT-like changes and migration, while its knockdown had opposite effects. NSUN6 was identified as the primary methyltransferase mediating mC modification of USP2-AS1. NSUN6-driven methylation enhanced endothelial plasticity in vitro and induced vascular abnormalities and hemorrhage in zebrafish. Mechanistically, USP2-AS1 activated Wnt/β-catenin signaling, which was essential for these effects and reversible by pathway inhibition. These findings identify a NSUN6-USP2-AS1-Wnt/β-catenin axis that drives endothelial dysfunction and bAVM rupture, suggesting potential therapeutic targets for vascular stabilization. - Source: PubMed
Publication date: 2026/08/11
Li GangleiLiu MingjianZhang HongfeiLi SichenLiu YingjunPan TonglinShen ShiyuLi ZongzeZhu Wei - Cadmium (Cd) is an environmental toxicant associated with pancreatic dysfunction and disordered glucose metabolism. Although ferroptosis has been implicated in Cd toxicity, whether Cd exposure is accompanied by changes in selected RNA 5-methylcytosine (mC) regulatory proteins in pancreatic β-cell-related systems remains unclear. Here, mouse NIT-1 cells were exposed to CdSO (4 μmol/L), and ferroptosis-related injury was evaluated using ferrostatin-1 (Fer-1) and erastin together with assays of cell viability, LDH release, reactive oxygen species (ROS), malondialdehyde (MDA), intracellular Fe, and ferroptosis-related proteins. Mouse pancreatic tissue was analyzed after chronic CdSO exposure. CdSO reduced NIT-1 cell viability and increased LDH activity, ROS, MDA, and Fe levels. Fer-1 partially improved cell viability and attenuated ROS and MDA, whereas erastin exacerbated Cd-associated injury. Cd exposure increased FTL abundance and decreased SLC7A11 and GPX4 in NIT-1 cells; chronic CdSO exposure in mice was accompanied by altered ferroptosis-related proteins, increased pancreatic Fe, and reduced serum insulin. In addition, Cd exposure was associated with altered abundance of selected m5C regulatory proteins, including decreased NSUN2 and increased TET2 in NIT-1 cells, and altered NSUN2, NSUN6, ALYREF, and TET2 in mouse pancreatic tissue. Overall, this preliminary descriptive study indicates that CdSO exposure is associated with ferroptosis-related redox/iron imbalance in NIT-1 cells and mouse pancreatic tissue, accompanied by altered abundance of selected m5C regulatory proteins. However, because serum and pancreatic Cd burdens, formal replicate-level correlation analyses, global or transcript-specific mC marks, and causal regulatory experiments were not assessed, these findings should be interpreted as associative and descriptive evidence rather than as proof of an internal Cd burden-response relationship or a direct mC-mediated mechanism of ferroptosis regulation. - Source: PubMed
Publication date: 2026/08/10
Mei ZongqinLiu XiaoyuWang NanDai JiaoGu ShiyanHe Zuoshun - Portal vein tumor thrombus is a lethal complication of HCC for which effective biomarkers are urgently needed. - Source: PubMed
Publication date: 2026/07/17
Li XutongXu HonghaiChang YuZhang YaniXu HuiYin XinZhang WanxiangLuo YiLu WantingFan WenhuRuan WanwanShen JiapeiLi ZhenxingDu ShuchengBentum-Ennin LutterodtNi JingGao WeiLi JiabinHu WanglaiYang WanshuiGao YufengGu Hao