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
- 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. Glioblastoma stem cells (GSCs) 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 (NSCs) 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 overcome chemoresistance in GBM. - Source: PubMed
Publication date: 2026/09/21
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 - Symmetric histone recycling is vital for maintaining epigenetic inheritance upon eukaryotic DNA replication. Recent genome-wide studies have uncovered key determinants of this process, but how these factors collectively support parental histone transfer remains incompletely understood. Here, we successfully reconstitute histone recycling with 24 purified proteins and analyze the products digested by Micrococcal nuclease with Repli-pore-seq, the newly developed pipeline combining nanopore sequencing and deep-learning-based classification. As a result, we identify histones symmetrically recycled as tetrasomes or hexasomes on nucleosome-favorable sequences. We also observe the discordance of the recycled position between lagging and leading strands on the GC-rich DNA sequences. Moreover, removal of Pol δ, Pol32, Dpb3/4, Ctf4, Csm3/Tof1, or Mrc1 disrupts the balance of histone recycling between the two daughter strands, whereas removal of Ctf4, Csm3/Tof1, or Mrc1 additionally alters the positions at which histones were recycled. Furthermore, addition of the lagging-strand maturation factors Fen1 and Cdc9 enhances histone recycling to the lagging strand. These findings provide critical insights into the molecular players and mechanisms underlying symmetric histone recycling. - Source: PubMed
Publication date: 2026/08/11
Nagae FritzEndo ShizukoMurayama YasutoTerakawa Tsuyoshi - Carbon dots (CDs) have emerged as promising electrochemiluminescence (ECL) emitters for biosensing due to their low toxicity, facile synthesis and modification, and good biocompatibility. However, most of the reported CDs require a more negative ECL trigger potential than -1.5 V vs Ag/AgCl, which not only induces undesirable electrode side reactions but also compromises the structural integrity of biomolecules, thus limiting their practical utility in complex biological systems. This study explored a bimetallic atom modulation strategy to significantly shift the ECL excitation potential of CDs positively. Concretely, Co-Mn bimetallic atoms were anchored on ultrasmall nitrogen-doped carbon dots (NCDs) to prepare Co-Mn/NCDs. On one hand, the bimetallic atoms effectively narrowed the bandgap of the material, shifting the ECL excitation potential positively to -0.9 V. On the other hand, the synergistic action of the bimetallic atoms significantly enhanced the decomposition efficiency of S2O82-, promoting the generation of reactive intermediates such as SO4•- and OH•, thereby greatly boosting ECL intensity. The excellent low-potential ECL characteristics of Co-Mn/NCDs were integrated with a CRISPR-Cas12a cascade signal amplification strategy to construct an ECL sensing platform for the highly sensitive detection of the cancer biomarker flap endonuclease 1 (FEN1). This work innovatively introduces bimetallic atoms into the CDs-based ECL system, effectively overcoming the issue of the overly negative excitation potential of CDs and providing an attractive low-potential ECL platform. - Source: PubMed
Li RongfangYang GuominHu Fang XinYuan RuoChen Shihong