Ask about this productRelated genes to: URP1 antibody
- Gene:
- FERMT1 NIH gene
- Name:
- fermitin family member 1
- Previous symbol:
- C20orf42
- Synonyms:
- FLJ20116, URP1, KIND1, UNC112A
- Chromosome:
- 20p12.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-21
- Date modifiied:
- 2015-09-11
Related products to: URP1 antibody
Related articles to: URP1 antibody
- Pancreatic ductal adenocarcinoma (PDAC) remains a highly lethal cancer due to its strong resistance to chemotherapeutic agents that induce apoptosis. As conventional treatments gradually lose their effectiveness over time, necroptosis has become a key therapeutic target worth exploiting. Necroptosis is a regulated cell death independent of caspases. It is driven by the receptor-interacting protein kinase 1/3 (RIPK1/3) and mixed lineage kinase domain-like pseudokinase (MLKL) signaling axis. This systematic review summarizes the complex role of necroptosis in PDAC. We clarify how necroptosis can be triggered or manipulated pharmacologically, and how it can be induced by accumulating reactive oxygen species (ROS). We also critically analyze its tumor-promoting side. Persistent necroptotic signaling reshapes the tumor microenvironment (TME) by releasing damage-associated molecular patterns (DAMPs) and activating inflammatory cascades. We also highlight the growing clinical significance of necroptosis-related genes (NRGs), long non-coding RNAs (lncRNAs), and specific biomarkers such as fermitin family member 1 (FERMT1). Finally, we propose a new, context-dependent therapeutic framework. This framework proposes a combination of strategies for controlling necroptosis induction and immunomodulatory agents, offering a reasonable strategy for PDAC management. - Source: PubMed
Publication date: 2026/04/20
Fan Yu-JieLiu Wei-JiaLiu ChangZhu Yi-WenChu TiHan Hang-ShenWu Dong-Dong - - Source: PubMed
Publication date: 2026/02/11
Oh JaslynChin Hui-LinPulido JoseChan Hwei Wuen - University Town, Nanjing 210023, China; Faculty of Chinese Medicine and State Key Laboratory of Mechanism and Quality of Chinese Medicine, Macau University of Science and Technology, Macau, China. Email: njwych@126.com; Min Chen, PhD. Faculty of Chinese Medicine and State Key Laboratory of Mechanism and Quality of Chinese Medicine, Macau University of Science and Technology, Avenida Wai Long, Taipa, Macau 999078, China. Email: mchen@must.edu.mo. - Source: PubMed
Publication date: 2026/01/27
Chen PeiXiao LuLv ChaoxiangZhang QiqiWu YunchuanChen Min - Very early onset inflammatory bowel disease presents a rare condition with an enrichment of monogenic disorders. This cohort study aims to investigate the prevalence of IBD-like monogenic disorders as well as genotypic and phenotypic characteristics in an Iranian cohort of VEO-IBD patients. - Source: PubMed
Publication date: 2026/01/17
Haghipanah MahyaRohani PejmanRohlfs MeinoShahrokh ShabnamFarahmand FatemehAnvari Maryam SotoudehWitzel MaximilianAhmadipour ShokoufehSohouli MohammadhassanDehghani Seyed MohsenKlein ChristophKotlarz DanielSoltani Bahram MTotonchi Mehdi - BackgroundAlzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline, memory loss and neuronal dysfunction. While amyloid-β plaques and tau tangles remain central to AD pathology, emerging evidence implicates ferroptosis, an iron-dependent, regulated form of cell death marked by lipid peroxidation and oxidative stress, as a critical contributor to disease progression.ObjectiveThis study investigates the interplay between major AD risk factors including chronic alcoholism, alcohol-nicotine co-abuse, aging, genetic predisposition, comorbidities and lifestyle habits and ferroptosis-related molecular pathways.MethodsGEO datasets and 115 ferroptosis-related genes were analyzed using z-score/FDR and Limma, followed by GO/KEGG/GSEA enrichment, machine-learning-based gene selection with ROC-AUC validation, immune-cell profiling using CIBERSORT, and hub gene-miRNA network construction via NetworkAnalyst.ResultsOur findings demonstrate that these risk factors converge on shared mechanisms involving iron dysregulation, oxidative stress and lipid imbalance which are hallmarks of ferroptosis. We identified seven ferroptosis-associated biomarker genes CYBB, FERMT1, BAX, SOD1, ACSL4, TP53, and FTH1 as being significantly dysregulated in AD. Integrative gene-miRNA interaction analysis revealed several hub miRNAs including hsa-miR-34a (TP53, SOD1, BAX), hsa-miR-34b and hsa-miR-34c (TP53, FERMT1), hsa-miR-125a-5p (FERMT1, TP53) and hsa-miR-20a-5p (ACSL4, BAX) suggesting a network of coordinated post-transcriptional regulation. Additionally, we observed strong neuroinflammatory signatures in AD with increased infiltration of pro-inflammatory macrophages (M1), CD8 T cells, monocytes and neutrophils. This heightened immune activity may be exacerbated by ferroptotic cell death and associated oxidative stress forming a vicious cycle of neurodegeneration. Finally, we propose glutathione and alpha-tocopheral (vitamin E) as potential therapeutic compounds due to their antioxidative role in preventing ferroptosis.ConclusionsOverall, our study provides novel insights into the mechanistic connections between ferroptosis, miRNA regulation, immune responses and AD pathology highlighting potential biomarkers and therapeutic targets. - Source: PubMed
Publication date: 2026/01/07
Singh PratibhaRath Soumya Lipsa