Ask about this productRelated genes to: RNF217 Blocking Peptide
- Gene:
- RNF217 NIH gene
- Name:
- ring finger protein 217
- Previous symbol:
- C6orf172, IBRDC1
- Synonyms:
- MGC26996, dJ84N20.1
- Chromosome:
- 6q22.31
- Locus Type:
- gene with protein product
- Date approved:
- 2003-06-17
- Date modifiied:
- 2017-12-15
Related products to: RNF217 Blocking Peptide
Related articles to: RNF217 Blocking Peptide
- Excess iron induces tissue toxicity in various conditions, including hereditary hemochromatosis (HH). Hepcidin, a liver-derived hormone encoded by the HAMP gene, plays a pivotal role in regulating systemic iron by mediating the degradation of ferroportin (FPN), the sole cellular iron exporter. Previous research found that the E3 ubiquitin ligase RNF217 is a key regulator of iron homeostasis by directly affecting FPN degradation; however, the role of RNF217 overexpression in iron-overload disorders such as HH is poorly understood. To address this question, we generated both global and intestine-specific Rnf217-overexpressing mice and then crossed these mice with hemojuvelin knockout (Hjv-/-) mice, a model for studying hemochromatosis. We found that both global and intestine-specific Rnf217 overexpression caused an identical rescue of the HH phenotype, implicating duodenal enterocytes as the main site where RNF217 overexpression exerts its beneficial effects. Moreover, we found that intestinal Rnf217 overexpression significantly reduced iron accumulation in the serum and in vital organs; importantly, these effects were not correlated with hepcidin levels. In summary, our findings demonstrate that intestinal RNF217 overexpression can directly suppress iron absorption by modulating FPN protein levels, bypassing hepcidin. This suggests a possible therapeutic strategy for iron-overload disorders, warranting further study to establish its clinical potential. - Source: PubMed
Publication date: 2026/04/20
Yu YingyingJiang LiLin ZhitingLiu YutongLiang WeiliangSu YunxingWu QianMin JunxiaWang Fudi - Resistance to chemoradiotherapy is a crucial factor limiting the efficacy of therapy and prognosis of esophageal cancer. It is necessary to elucidate the key genes and regulatory mechanisms responsible for therapeutic resistance in esophageal squamous cell carcinoma (ESCC). In this study, we found a relationship between ferroptosis and therapeutic sensitivity in ESCC and identified the ring finger protein 217 (RNF217) as a new regulator of ferroptosis associated with resistance to chemoradiotherapy in ESCC. Mechanistically, RNF217 interacts with kelch like ECH associated protein 1 (KEAP1) and promotes its ubiquitination and degradation, resulting in nuclear factor erythroid 2-related factor 2 (NRF2) evading KEAP1-mediated degradation and, consequently, enhanced NRF2 signaling and led to ferroptosis resistance. Furthermore, NRF2 facilitated the transcription of RNF217 by binding to antioxidant response elements in the RNF217 promoter upon irradiation. Overall, our findings indicate that the RNF217-KEAP1-NRF2 feedback loop is a previously unrecognized mechanism regulating resistance to chemoradiotherapy in ESCC and could be a target to overcome therapeutic resistance in ESCC. - Source: PubMed
Publication date: 2025/08/29
Wang SifenZhang ChaoZhou ShaLiu ShiliangLi QiaoqiaoCheng XingyuanWang RuixiChen BaoqingLi YueXi Mian - This study aims to explore the effect of the long non-coding RNA (lncRNA) RNF217-AS1 on the proliferation and migration of esophageal cancer cells, and to uncover the molecular mechanisms through which RNF217-AS1 regulates these processes. - Source: PubMed
Publication date: 2025/07/07
Liang JieNiu XiaoliWang GaoyanWang Minghui - Hydrogen sulfide (H2S) is a signaling molecule that regulates plant senescence. In this study, we found that H2S delays dark-induced senescence in tomato (Solanum lycopersicum) leaves. Transcriptome and reverse transcription quantitative PCR (RT-qPCR) analyses revealed an ethylene response factor ERF.D3 is quickly induced by H2S. H2S also persulfidated ERF.D3 at amino acid residues C115 and C118. CRISPR/Cas9-mediated gene editing, and gene overexpression analyses showed that ERF.D3 negatively regulates leaf senescence and fruit ripening. Abscisic acid (ABA) levels were reduced by ERF.D3 overexpression, suggesting ERF.D3 might regulate ABA metabolism. Additionally, the ABA 8'-hydroxylase-encoding gene CYP707A2, which is required for ABA degradation, was identified as an ERF.D3 target gene through transcriptome data, RT-qPCR, dual-luciferase reporter assays, and electrophoretic mobility shift assays. ERF.D3 persulfidation enhanced its transcriptional activity toward CYP707A2. Moreover, the E3 ligase RNF217 ubiquitinated ERF.D3, which may accelerate fruit ripening during the late stage of fruit development. Overall, our study provides valuable insights into the roles of a H2S-responsive ERF.D3 and its persulfidation state in delaying leaf senescence and fruit ripening and provides a link between H2S and ABA degradation. - Source: PubMed
Hu KangdiGeng MeihuiMa LinYao GaifangZhang MinZhang Hua - This study aimed to identify feature genes and explore the molecular mechanisms of keratoconus (KC). We downloaded data files from NCBI GEO public database. The Limma package was used for differential expression analysis of gene profiles. Lasso regression was used to identify the feature genes. The CIBERSORT algorithm was used to infer the proportion of immune-infiltrating cells and analyse the correlation between gene expression levels and immune cells. Related transcription factors and miRNAs of key genes were predicted using the Cistrome DB and Mircode databases. Analysis of expression differences in disease genes was based on the GeneCards database. The CMap was used to analyse targeted therapeutic drugs. IHC was performed to verify the expression levels of ATOH7 and MYRF in corneas. Exactly 593 upregulated and 473 downregulated genes were identified. Lasso regression analysis identified ATOH7, DBNDD1, RNF217-AS1, ARL11, MYRF and SNORA74B as feature genes for KC. All key genes were correlated with immune infiltration and the levels of activated memory CD4+ T cells and plasma cells were significantly increased. miRNA, IRF and STAT families were correlated to feature genes. The expression levels of key genes were significantly correlated to KC-related genes. Entinostat, ochratoxin-a, diphencyprone and GSK-3-inhibitor-II were predicted as potential KC medications. The expression of MYRF was significantly higher in the KC samples, contrary to the expression of ATOH7. KC is related to both immune infiltration and genetic factors. MYRF and ATOH7 were newly identified and verified feature genes of KC. - Source: PubMed
Lyu NingDai YiqinWu JiawenFan YidanLyu ZhaoyuanGu JiayuCheng JingyiXu Jianjiang