Ask about this productRelated genes to: FEN1 Blocking Peptide
- Gene:
- FEN1 NIH gene
- Name:
- flap structure-specific endonuclease 1
- Previous symbol:
- RAD2
- Synonyms:
- FEN-1, MF1
- Chromosome:
- 11q12.2
- Locus Type:
- gene with protein product
- Date approved:
- 1995-02-03
- Date modifiied:
- 2016-10-05
Related products to: FEN1 Blocking Peptide
Related articles to: FEN1 Blocking Peptide
- Lung cancer management remains constrained by a fragmented understanding of the clinical implications of DNA Damage Response (DDR) pathways. This review synthesizes current evidence to position DDR alterations as potential prognostic, predictive, and therapeutic biomarkers. Prognostically, overexpression of FEN1, BRCA1, and XRCC4/5/6 correlates with poor survival in non-small cell lung cancer, whereas low ERCC1 expression and specific EXO1 or RPA polymorphisms are associated with enhanced responsiveness to platinum-based chemotherapy. As well, deleterious mutations in ATM, ERCC family genes, and mismatch repair genes (MSH2, PMS2) may support the identification of patients more likely to benefit from immune checkpoint inhibitors, driven by increased tumor mutational burden and neoantigen load. Therapeutically, PARP and ATR inhibitors may offer an opportunity within precision strategies through synthetic lethality, with particular promise in difficult-to-treat subsets, including KRAS-mutated adenocarcinoma and patients progressing on standard targeted therapies. However, clinical implementation faces significant technical limitations regarding testing variability (particularly isoform specificity), geographic biases toward Asian populations, and severe overlapping toxicities in combination trials. To facilitate the integration of DDR biomarkers into routine practice, future research must prioritize assay standardization, broader ethnic representation, and mechanistic exploration of DDR-mediated remodeling of the tumor microenvironment. Integrating these complex molecular interactions is essential to bridge the gap between biological activity and personalized clinical application in lung cancer. - Source: PubMed
Publication date: 2026/08/15
Durán-Toribio Ana-KarlaJiménez-Díaz Ignacio FCaballé-Pérez EnriqueLucio-Lozada JoséCastillo-Ruiz CesarBarrios-Bernal PedroRomero-Núñez EuniceHernández-Pedro NormaArrieta Oscar - In this study, we modeled gene expression profile data from Acute Myeloid Leukemia (AML) and healthy cases. At first, the GEO-GSE9476 dataset was processed, and a total of 341 genes were identified as differentially expressed genes (DEGs) in patients, and 599 DEGs in healthy individuals. Gene Ontology and pathway analysis on DEGs led to the identification of 5 Transcription Factors for patients and 3 for healthy cases. Analysis of the respective metabolic pathways revealed a common region in the metabolic pathway between AML and Tuberculosis (TB) that confirmed the validity of our procedure due to the consistency with similar reports. Upon PPI network analysis, Hub genes and three modules containing 41 up-regulated and down-regulated genes in AML patients were identified. Survival analysis on these genes results in reducing the number of identified effective genes into 3 upregulated (ITGAM, ITGAL and CD163) and 5 downregulated genes (MCM2, MCM3, RFC4, RFC5 and FEN1). Finally, drug sensitivity analysis was performed on these genes demonstrating complexity in drug-resistance due to the pattern of gene expression. This knowledge could potentially enable personalized treatment approaches based on individual patient responses due to the epigenetics and life style which affect gene expression pattern. - Source: PubMed
Publication date: 2026/07/27
Aghajan BehnamGhaemi Mohammad RezaMosammam Ali MHeshmati EmranKhalifeh Khosrow - Although the acute phase of the SARS-CoV-2 pandemic has subsided, viral persistence and variant evolution continue to challenge existing antiviral strategies. Here, we investigated an intranasal nanomedicine formulation comprising flap-endonuclease 1 (FEN1) and a panel of hairpin-structured DNA probes (hpDNAs), which we designed to concurrently target the highly conserved nucleocapsid RNA and host-derived Cathepsin L mRNA. This dual-targeting approach aims to interfere with both viral genetic integrity and the host-dependent entry pathway. Replacing conventional siRNA/sgRNA with stable, economical hpDNAs may improve the practicality of nucleic acid-based antivirals. Additionally, the co-administration of the anti-inflammatory agent baicalein was examined to assess its potential to improve the nanomedicine's cellular biodistribution. Our portable intranasal drop, a multi-target treatment co-administered with baicalein, elicited a partial reduction in the viral load in mice infected with SARS-CoV-2, suggesting that this multi-target strategy may offer an alternative antiviral modality for further development. - Source: PubMed
Publication date: 2026/08/03
Cao JiyanuoWan MengGu JiayuWang PeiliangGao YuanWei LibinGuo YongjianZhao LingzhiXu Shu - Dry eye disease (DED), a prevalent ocular condition, has seen rising incidence rates. Aberrant inflammation and immune dysregulation are key pathogenic factors in DED. However, the underlying mechanisms linking autoimmunity to DED therapy remain incompletely understood. Herbal medicine's potential in treating DED warrants further exploration due to rendering monotherapy insufficient for clinical needs. - Source: PubMed
Publication date: 2026/07/18
Long XiLiu GuichengLiu PeiJiang PengfeiPeng JunPeng Qinghua - The yeast RAD27 gene encodes the Rad27/Fen1 nuclease, which contributes to genome stability during Okazaki fragment maturation (OFM), DNA mismatch repair (MMR), base excision repair, and other processes. Here, we analyze whole genome mutation accumulation in Saccharomyces cerevisiae lacking RAD27 and show that its loss elevates diverse mutation classes arising through multiple mechanistic pathways. Overall mutation rates in rad27Δ cells are over 60-fold higher than in wild type and only modestly lower than in MMR-deficient strains. However, most mutations in rad27Δ cells cannot be explained by defective MMR, elevated translesion synthesis, or defects in other Rad27-associated repair processes. Instead, mutation spectra implicate aberrant processing of Okazaki fragment intermediates via DNA terminus slippage before ligation (SBL) and template switching (TS). The latter may arise through replication-associated processes such as transient primer relocation (TPR) or through recombination-mediated mechanisms including homoeologous recombination. SBL accounts for the majority of insertion mutations in rad27Δ cells, while TS explains substantial fractions of substitutions, insertions, deletions, and copy number variants, often involving non-local templates. Our results indicate that Rad27 suppresses genome instability through multiple mechanistically distinct roles. Together, these findings reveal Rad27/Fen1 to be a determinant of replication-associated genome stability on par with MMR. - Source: PubMed
Publication date: 2026/07/17
Lujan Scott AArana Mercedes EWilkins HunterWilliams Jessica SGarbacz Marta ABebenek KatarzynaKunkel Thomas A