FEN1 Antibody
- Known as:
- FEN1 Antibody
- Catalog number:
- 32204
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- FEN1 Antibody
Related genes to: FEN1 Antibody
- 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 Antibody
Related articles to: FEN1 Antibody
- High-grade gliomas (HGGs) exhibit marked intratumoral heterogeneity, which is associated with variable survival outcomes among patients receiving standard adjuvant chemotherapy. Conventional methods relying on molecular biomarkers are constrained by technical limitations and tumor heterogeneity. This study aimed to develop a multi-channel 2.5D deep learning framework that integrates Convolutional Neural Network (CNN) and Vision Transformer (ViT) features to noninvasively stratify HGG patients based on expected survival outcomes following postoperative adjuvant temozolomide (TMZ) chemotherapy and to explore the underlying molecular mechanisms. - Source: PubMed
Publication date: 2026/09/29
Li ZehuiDuan XinLian JunjieLi XuanZheng BihuaLiang QianNiu WenjuLiu XuTan YanYang GuoqiangDu JiangfengYang XiangliWang XiaochunZhang Hui - DNA mismatch repair (MMR) corrects DNA replication errors, some forms of chemical damage to DNA bases, and acts in processes such as heteroduplex rejection, triplet repeat expansion, antibody maturation and cytotoxicity of alkylating agents. During MMR, the newly synthesized DNA strand containing the error must be removed and resynthesized to prevent mutations. In bacteria, this strand is displaced by the UvrD DNA helicase. In eukaryotes, this strand is excised by redundant pathways. In the first excision pathway identified, Msh2-Msh6 (or Msh2-Msh3) and/or Mlh1-Pms1 (human MLH1-PMS2) recruit Exo1 to 5' nicks, and 5'-to-3' excision by Exo1 excises the daughter strand containing the mispair to generate a single-stranded gap. The Mlh1-Pms1 endonuclease also mediates excision through extensive nicking of the daughter strand to generate single-stranded gaps. In coupled strand-displacement synthesis coordinated by Msh2-Msh6 (or Msh2-Msh3), DNA polymerase delta and Rad27 (human FEN1)-mediated 5' flap cleavage excise the mispair and resynthesize the daughter strand. Resynthesis in the Exo1- and Mlh1-Pms1-mediated pathways can be performed by both DNA polymerase delta and epsilon, and in all excision pathways the nicked product can be sealed by DNA ligase. Genetic analysis in suggests that these three pathways correspond to all or at least the major excision pathways; however, other factors such as Fan1, Artemis, Mre11, Dna2, Fun30, and the RSC complex have been implicated in eukaryotic MMR but are less well understood. The roles of excision and its redundant pathways have also been less well characterized for other processes involving MMR proteins. - Source: PubMed
Publication date: 2026/10/04
Putnam Christopher DKolodner Richard D - DNA is inherently susceptible to damage from endogenous and exogenous sources. Base excision repair (BER) maintains genomic integrity, with its core enzymes Flap endonuclease 1 (FEN1) and Apurinic/apyrimidinic endonuclease 1 (APE1) implicated in various malignancies. Herein, an integrated microchip electrophoresis (MCE) and exponential strand displacement amplification (ESDA) method is presented for the simultaneous and sensitive detection of FEN1 and APE1. To achieve the simultaneous specific recognition of two enzymes and their ESDA cyclic amplification, two target-specific probes with distinct structures were specially designed: a dumbbell probe M1 for FEN1 and a double-stranded probe M2 for APE1. Other two template strands P1 and P2 were also carefully designed for the ESDA cyclic amplification. Because there were only four probes participating in this ESDA reaction, the background interference was significantly reduced and the detection sensitivity was increased corresponding. This approach achieves the limits of detection as low as 4 × 10⁻ U/μL and 5 × 10⁻ U/μL for FEN1 and APE1 respectively (S/N = 3) under the optimal conditions. Both enzymes were successfully quantified in cancer cell lysates and spiked serum samples with high specificity and sensitivity, indicating that this ESDA-MCE method is promising for the early diagnosis and effective treatment of cancer and related diseases. - Source: PubMed
Publication date: 2026/09/23
Han MengmengGeng XingTang ShuangLv JiananTu FengLi SijinChen ShiqiGu YuxinZhang FanWang Qingjiang - Arthritis is a chronic inflammatory disease characterized by a metabolic imbalance and oxidative stress, which can lead to significant DNA damage. While photobiomodulation (PBM) is a widely recognized non-invasive therapy for managing arthritic pain and inflammation, its effects on the mechanisms of DNA repair, specifically the Base Excision Repair (BER) pathway, remain unexplored in zymosan-induced arthritis. The objective of this study was to evaluate the effects of PBM on the mRNA levels of key BER genes in an experimental model of arthritis. Male C57BL/6 mice were subjected to zymosan-induced arthritis and treated with a low-power infrared laser (830 nm; 10 mW, 0.15 and 1.5 J, 15 and 150 s, 0.05 cm, 200 mW/cm, 3 or 30 J/cm, continuous emission mode). Animals were euthanized at 24, 48, and 72 h post-induction, total mRNA was extracted from joint tissues, and transcription of APE1, POLβ, XRCC1, FEN1, and LIG1 genes was quantified using RT-qPCR. Zymosan-induced inflammation significantly altered relative mRNA levels of BER genes over time, generally increasing the expression of XRCC1, FEN1, and LIG1. PBM at 24 h, both 3 and 30 J/cm fluences, significantly reduced APE1, FEN1, and LIG1 mRNA levels. At 48 h, PBM reduced XRCC1, FEN1, and LIG1 expression but, at 72 h, PBM increased transcription of LIG1 gene. Transcription of POLβ gene was not significantly affected. These findings suggest that PBM modulates the relative mRNA levels of genes involved in both the short-patch and long-patch BER pathways in zymosan-induced arthritis. - Source: PubMed
Publication date: 2026/09/30
Ferreira Victória Batistade Souza Álvaro CarneiroDos Anjos Lúcia Mara Januárioda Silva Ferreira Ana Carolineda Silva Marcelle Abreude Paoli Fláviade Souza da Fonseca Adenilson - Glioblastoma (GBM) is an aggressive brain tumor characterized by therapy resistance and recurrence. GBM stem cells (GSC) are key drivers of tumor maintenance, therapeutic resistance, and relapse, but targeting them remains clinically elusive due to their overlap with normal neural stem cells (NSC) and a lack of actionable vulnerabilities. To identify selective vulnerabilities in GSCs, we performed genome-wide CRISPR-Cas9 loss-of-function screening across patient-derived GSC models under standard-of-care treatment conditions. We identified flap endonuclease 1 (FEN1), a key enzyme in DNA replication and base excision repair, as an essential gene for GSC survival, with enhanced dependency in the context of temozolomide (TMZ) treatment. Genetic knockdown of FEN1 impaired GSC proliferation and self-renewal and extended survival in a patient-derived xenograft model. Pharmacologic inhibition of FEN1 using a small-molecule inhibitor revealed selective cytotoxicity in highly aggressive and recurrent GBM models while sparing NSCs. Notably, FEN1 inhibition synergized with TMZ to induce DNA double-strand breaks and potentiate cell death only in a subset of GSCs sensitive to FEN1 inhibition. Mechanistically, single-cell transcriptomics revealed that FEN1 expression correlates with programs linked to proliferation, stemness, and DNA damage repair, underscoring its role in maintaining the treatment-refractory phenotype. Our findings identify FEN1 as a selective vulnerability in aggressive, proliferative GSCs. FEN1 inhibition not only impairs GSC viability but also restores sensitivity to TMZ in treatment-resistant models, offering a strategy for salvage therapy in recurrent GBM. These results support the development of FEN1-targeted therapies and lay the foundation for a biomarker-guided approach to overcoming chemoresistance in GBM. - Source: PubMed
Brakel Benjamin AMcKenna DillonPuri AnishShaikh Muhammad VaseemSingh ManojSaleh AliTomajian Abdo-JoseMikolajewicz NicholasBeltrami MarcelloTopley MaxwellAnand AlishaMiletic PetarBrown Kevin RTieu DavidMaich WilliamSalim SabraSuk YujinSubapanditha MinomiGendoo Deena M AVenugopal ChitraMoffat JasonKatyal SachinChokshi Chirayu RSingh Sheila K