NSUN4 Antibody (C-term)
- Known as:
- NSUN4 Antibody (C-terminus)
- Catalog number:
- AP11159b-ev20
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- NSUN4 Antibody (C-term)
Related genes to: NSUN4 Antibody (C-term)
- Gene:
- NSUN4 NIH gene
- Name:
- NOP2/Sun RNA methyltransferase 4
- Previous symbol:
- -
- Synonyms:
- MGC22960, SHTAP
- Chromosome:
- 1p33
- Locus Type:
- gene with protein product
- Date approved:
- 2004-08-25
- Date modifiied:
- 2019-02-26
Related products to: NSUN4 Antibody (C-term)
Related articles to: NSUN4 Antibody (C-term)
- Thyroid eye disease (TED) is the most common extra-thyroidal complication of Graves' disease, but its molecular pathogenesis is not fully understood. This study explored the mechanism associated with methyltransferase like 3 (METTL3), NOP2/Sun RNA methyltransferase 4 (NSUN4), and solute carrier family 2 member 3 (SLC2A3) in an in vitro TED model. Human normal orbital fibroblasts were stimulated with platelet-derived growth factor BB (PDGF-BB) to establish in vitro TED model. Differentially expressed genes were screened using online databases. Western blotting was performed for protein detection, and qPCR was used for mRNA quantification. CCK-8 assay and EdU assay were conducted to examine metabolic viability and proliferation, respectively. Hyaluronan (HA) production and glycolysis metabolism were assessed via commercial kits. Methylated RNA immunoprecipitation (MeRIP), RIP, dual-luciferase reporter assay, and RNA-protein pull-down assay were utilized for interaction analysis. Bioinformatics screening obtained 1139 differential genes and 45 glycolytic genes, yielding 2 overlapping genes that were considered as glycolysis-related genes in TED. SLC2A3 was highly expressed in TED and PDGF-BB-stimulated orbital fibroblasts, and silencing SLC2A3 suppressed PDGF-BB-induced cell proliferation, HA production and glycolysis. NSUN4 mediated the m5C methylation modification to increase SLC2A3 expression in an YBX1-dependent manner. NSUN4 inhibition restrained PDGF-BB-induced effects via downregulating SLC2A3. METTL3 mediated m6A methylation modification to reduce NSUN4 expression, with YTHDF2 as a reader protein. The influences of PDGF-BB on human orbital fibroblasts were significantly alleviated by METTL3 overexpression to down-regulate NSUN4. NSUN4 downregulation caused by METTL3-induced m6A modification of NSUN4 mRNA regulated m5C modification of SLC2A3 mRNA, thereby ameliorating PDGF-BB-induced proliferation, HA generation and glycolysis of human orbital fibroblasts in TED. The evidence uncovered the specific molecular mechanism underlying TED pathogenesis. - Source: PubMed
Publication date: 2026/05/16
Liu Shu-YanWang HongLiu Bao-ZhongJia LeiWang TingZhou Lin-FeiXu Xiao-LiHou Bao-HuaYang BoSun Li-ShaPang Hui - This study aimed to investigate the biological role and molecular mechanism of the RNA mC methyltransferase NSUN4 in cervical cancer progression, with a focus on its involvement in ferroptosis regulation. - Source: PubMed
Publication date: 2026/04/28
Tian DuanchengDu MingZheng ZhenWang WeidiWang HaoyuMaisaidi ReyilanmuXiang Yang - Glaucoma, a leading global cause of blindness, is characterized by progressive retinal neuronal loss. NOP2/Sun RNA methyltransferase 4 (NSUN4), a writer of 5-methylcytosine (m5C) RNA modifications, has established roles in methylation and mitoribosome assembly, yet its function in retinal cell survival remains unexplored. In this study, integrated methylated RNA immunoprecipitation sequencing (MeRIP-seq) and RNA-seq analysis in an NMDA-induced retinal injury model revealed widespread mRNA hypomethylation enriched in the Sonic Hedgehog (SHH) signaling pathway, accompanied by significant downregulation of Nsun4. To investigate the underlying mechanisms, we utilized the R28 retinal cell line, a widely accepted model for studying retinal neuroprotection. In glutamate-stimulated R28 cells, NSUN4 overexpression mitigated excitotoxic injury, attenuating Ca² ⁺ overload, mitochondrial dysfunction, and apoptosis. Mechanistically, NSUN4 enhanced m5C methylation on key SHH pathway transcripts (Shh, Gli1, and Gli2). Crucially, the neuroprotective effect of NSUN4 was abolished upon pharmacological inhibition of the SHH pathway using Vismodegib, confirming that pathway activation is essential for NSUN4-mediated protection. Clinically, NSUN4 levels were significantly reduced in the aqueous humor of patients with primary open-angle glaucoma compared to controls. Together, these findings establish NSUN4 as an m5C-dependent activator of the SHH pathway that protects retinal cells against excitotoxic injury, nominating it as a novel candidate for glaucoma neuroprotection. - Source: PubMed
Publication date: 2026/04/15
Li YahongLi DianGeng ChaoWei RuihuaDuan Yajian - A significant proportion of patients with recurrent and refractory diffuse large B-cell lymphoma (DLBCL) exhibit high levels of BCL-2 expression. However, some of these patients are resistant to BCL-2 inhibitors, and the underlying mechanisms remain unclear. In venetoclax-resistant DLBCL cell line, a Cell Counting Kit-8 (CCK8) assay was used to determine the half-maximal inhibitory concentration (IC50) value. Flow cytometric was performed to determine mitochondrial membrane potential (MMP), reactive oxygen species (ROS), and cell apoptosis rates, respectively. The construction of NSUN4 knockdown/overexpression cell line using CRISPR-Cas9 technology. KEGG pathway enrichment analysis indicated that NSUN4 modulates venetoclax resistance. Furthermore, we used Western blotting to explore the mechanism underlying venetoclax-resistant. Finally, the antileukemic activity was further evaluated in an in vivo xenograft model. We identified that NSUN4, an m5C methyltransferase, is highly expressed not only in the venetoclax-resistant cell line but also in the lymph nodes of recurrent and refractory DLBCL patients primarily by inhibiting the p53 signaling pathway, although the precise mechanism warrants further investigation, and is correlated with poor prognosis. Moreover, we discovered that Apatinib could reduce NSUN4 expression and effectively reverse venetoclax resistance. These findings suggest that NSUN4 is a critical target for overcoming venetoclax resistance in DLBCL patients. Our study reveals the role of NSUN4 and the p53 signaling pathway in venetoclax resistance at the molecular, cellular, and animal levels. Understanding how m5C methylation mediates venetoclax resistance and regulates the p53 pathway will provide a theoretical foundation for overcoming venetoclax resistance in patients with recurrent and refractory DLBCL. - Source: PubMed
Publication date: 2026/03/22
Shi YuanfeiWen HeliCao TianleZhao YanchunXu YiSun JianaiZheng XiaolongJin JieTong HongyanXie Wanzhuo - RNA methylation has emerged as a critical frontier in epitranscriptomics, with 5-methylcytosine (mC) drawing particular attention for its multilayered roles in post-transcriptional gene regulation. Recent studies demonstrate that mC modulates diverse biological processes by stabilizing RNA transcripts, promoting nuclear export, shaping translational efficiency, and orchestrating noncoding RNA function. Analogous to DNA methylation, mC is dynamically reversible and governed by a finely tuned regulatory system composed of "writers" (such as the NSUN family and DNMT2/TRDMT1), "readers" (including YBX1 and ALYREF), and "erasers" (TET enzymes and ALKBH1), which collectively dictate its spatial and temporal distribution. In lung cancer, disruption of this regulatory axis is increasingly recognized as a driver of tumor phenotypic remodeling, metabolic adaptation, and immune evasion. Notably, writer enzymes such as NSUN2, NSUN4, and NSUN6 promote malignant progression by stabilizing oncogenic transcripts, enhancing translation, and rewiring metabolic networks. Meanwhile, reader proteins YBX1 and ALYREF maintain the stability of mC-modified RNAs and activate proliferative and pro-invasive signaling pathways, including PI3K/AKT, mTOR, and Hippo/Wnt. In addition, mC plays a pivotal role in shaping the tumor immune microenvironment and modulating immune checkpoint activity, thereby influencing the responsiveness and resistance of lung cancer to radiotherapy, chemotherapy, targeted therapy, and immunotherapy. - Source: PubMed
Publication date: 2026/01/07
Zhong XiaoyouWang WenjingLv JiajiaFan WeifeiWang Lin