Ask about this productRelated genes to: YTHDF3 antibody
- Gene:
- YTHDF3 NIH gene
- Name:
- YTH N6-methyladenosine RNA binding protein 3
- Previous symbol:
- -
- Synonyms:
- FLJ31657
- Chromosome:
- 8q12.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-06-01
- Date modifiied:
- 2016-04-12
Related products to: YTHDF3 antibody
Related articles to: YTHDF3 antibody
- The ORF3 protein of swine hepatitis E virus (HEV-4) is a key virulence factor involved in viral assembly, egress, and host signaling regulation. The mammalian target of rapamycin (mTOR) pathway plays a pivotal role in autophagy, metabolism, and immunity, and is often modulated by viruses to promote replication. However, it remains unknown whether HEV-4 ORF3 modulates the mTOR pathway via circular RNAs (circRNAs). - Source: PubMed
Publication date: 2026/04/03
Li JiyaWu ShengpingWang LingjieCao XinYin YulongWang LeliJiao Hanwei - Idiopathic Parkinson's disease (iPD) represents the most prevalent form of Parkinson's disease; however, the molecular mechanisms underlying its development remain only partially understood. N6-methyladenosine (m6A), the most abundant internal RNA modification in eukaryotic mRNA, has emerged as a key regulator of gene expression and has been implicated in neurodegenerative disorders. In this study, we performed integrated differential expression, weighted gene co-expression network analysis (WGCNA), and differential co-expression (DECO) analyses using peripheral blood RNA-seq data from Latin American controls and early iPD patients to investigate m6A-associated transcriptional alterations. WGCNA and differential expression analyses identified 1207 hub genes and 237 differentially expressed genes, respectively. The integration of these datasets with curated m6A-related genes yielded 12 overlapping candidate genes associated with early iPD. Subsequent DECO analysis revealed three significant m6A regulator-target differential co-expression links involving the m6A factors , , and . Experimental validation in an independent exploratory cohort confirmed altered expression of these regulators and increased m6A enrichment of and transcripts. To our knowledge, this study represents the first integrative transcriptomic evaluation of m6A-associated regulatory patterns in early iPD within a Latin American population. Collectively, our findings suggest that selective m6A-associated transcriptional network alterations may contribute to the systemic molecular signatures observed in early iPD, warranting further validation in larger and mechanistically oriented studies. - Source: PubMed
Publication date: 2026/04/01
Leiva FranciscoConstandil LuisChana-Cuevas PedroVidal Rene LMorales BernardoVidal Rodrigo - Breast cancer, a malignant tumour that frightens women, ruthlessly claims the lives of tens of thousands of women around the world every year. However, the mechanism by which YTHDF3 regulates the occurrence and development of breast cancer is still imperfect. In this study, we used bioinformatics to analyse the expression of YTHDF3 in breast cancer and verified it in clinical specimens. In addition, YTHDF3 knockdown breast cancer cell lines were used to determine the biological role of YTHDF3 in breast cancer through functional experiments such as CCK-8 assay, transwell assay, clonal proliferation and cell cycle assay. Lactate analysis, seahorse assay, RT-qPCR and Western blot were used to explore the downstream mechanism of YTHDF3, and rescue experiments were performed with small molecule activators to repeatedly confirm the downstream targets. Finally, YTHDF3 knockout breast cancer cell lines were used to establish cell line-derived xenograft (CDX) mouse models to further confirm the biological function of YTHDF3 in breast cancer and the possible regulatory mechanism. Our results showed that YTHDF3 was highly expressed in breast cancer cells and clinical tissues, and YTHDF3 enhanced the proliferation and migration ability of breast cancer. Mechanistically, YTHDF3 enhances the expression of HIF1α and LDHA and glycolysis by inducing the phosphorylation of mTOR, and finally promotes the occurrence and development of breast cancer. In addition, YTHDF3 can be used as a helpful biomarker in various cancers, including breast cancer. We aimed to elucidate the role of YTHDF3 in breast cancer development and provide evidence for improving the diagnosis and treatment of breast cancer. In this study, we elucidated that YTHDF3 regulates the glycolysis level, proliferation and migration of breast cancer through the mTOR-HIF1α-LDHA axis. Interference of the YTHDF3 expression is a potential target for breast cancer treatment, which provides strong evidence for improving diagnosis and treatment methods. - Source: PubMed
Liu ZiQianJiang TengFeiLi PengDong KeWang XiMeiGeng ChenChenZhang XiaoDongZuo DanZhao GuangHui - Retinal ganglion cells (RGCs) are particularly vulnerable to damage during the early stages of diabetic retinopathy (DR). Emerging evidence indicates that dysregulated expression of N6-methyladenosine (m6A) methylation regulators contributes to DR pathogenesis. In particular, the m6A reader protein YTHDF3 has been found to be highly expressed in human proliferative DR membranes although its functional role in DR progression remains unclear. In this study, diabetic rat models were established via streptozotocin injection. Subsequently, YTHDF3 expression was knocked down in the retina by intravitreal delivery of AAV-sh-YTHDF3. Additionally, high glucose (HG) conditions were used to induce injury in RGCs in vitro. Our results demonstrated that downregulation of YTHDF3 significantly mitigated HG-induced RGC damage both in vivo and in vitro. YTHDF3 silencing reduced HG-triggered RGC apoptosis by suppressing mitochondrial dysfunction and PINK1-Parkin-mediated excessive mitophagy. Moreover, YTHDF3 functioning as an m6A reader enhanced the translation of PHB2 in an m6A-dependent manner. Notably, PHB2 overexpression effectively counteracted the protective effects of YTHDF3 knockdown, reinstating HG-induced mitochondrial damage and mitophagy. In conclusion, our findings indicate that YTHDF3 exacerbates RGC injury under high glucose conditions by promoting m6A-dependent PHB2 translation, which in turn aggravates mitochondrial damage and PINK1-Parkin-driven mitophagy, thereby contributing to DR progression. - Source: PubMed
Publication date: 2026/04/23
Lv ZeyiLv PeilinPang LongSong YanminKong DerenGui Fulan - Long non-coding RNA PAR5 (lncRNA-PAR5) is downregulated in glioma and has been confirmed to inhibit glioma progression; however, the specific regulatory mechanism underlying its downregulation remains unclear. - Source: PubMed
Xu LiuFeiXu YuanDuan YongBinWang BoLuo YiYuWang XiangPeng