XRCC4 MaxPab Antibody
- Known as:
- XRCC4 MaxPab Antibody
- Catalog number:
- ENZ-007518-B01
- Product Quantity:
- 0.05ml
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- XRCC4 MaxPab Antibody
Related genes to: XRCC4 MaxPab Antibody
- Gene:
- XRCC4 NIH gene
- Name:
- X-ray repair cross complementing 4
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 5q14.2
- Locus Type:
- gene with protein product
- Date approved:
- 1990-10-16
- Date modifiied:
- 2016-06-02
Related products to: XRCC4 MaxPab Antibody
Related articles to: XRCC4 MaxPab Antibody
- Silver diamine fluoride (SDF) is widely used for its caries-arresting, antimicrobial, and remineralizing effects. However, its cytotoxic, inflammatory, and genotoxic effects in oral cells are unclear. In this study, the effects of increasing concentrations of silver diamine fluoride SDF on cell viability, inflammation, DNA integrity, and functional properties, were evaluated. - Source: PubMed
Publication date: 2026/10/01
Bernard VictoriaYochim Ji MinRajasingh SheejaEyre Clarice LawAl Dayeh AymanRajasingh Johnson - 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 variants 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 variants 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, synthetic lethality of PARP and ATR inhibitors may offer an opportunity in difficult-to-treat subsets progressing on standard targeted therapies. However, clinical implementation of DDR-related findings faces significant technical limitations regarding testing variability, geographic biases toward Asian populations, and overlapping toxicities in combination trials. To facilitate their integration into routine practice, future research must prioritize assay standardization, broader ethnic representation, and mechanistic exploration of DDR-mediated effects in tumor biology. 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 - Ataxia Telangiectasia Mutated (ATM) kinase deficiency results in cancer susceptibility and drug hypersensitivity. Deficiency in either the BRCA1 interacting A complex or XRCC4/Ligase 4 confers resistance to Topoisomerase I or PARP1 inhibitors in ATM-deficient cells. This suggests that BRCA1-A directs toxicity to fork-damaging agents in ATM mutated cells via illegitimate end-joining. Here, we show that ATM inhibition triggers combined SUMO and ubiquitin mediated BRCA1-A damaged fork recognition to restrict end-resection and cause Topoisomerase I inhibitor hypersensitivity. BRCA1-A deficient cells display elevated chromatin accessibility and nuclease activity at damaged forks, coupled with restored resection and drug resistance. Electron microscopy evidence demonstrates that ATM inhibition prevents replication fork reversal, which is restored by BRCA1-A loss to generate substrates for end resection. These findings reveal that BRCA1-A enforces a restrictive chromatin state to suppress the genesis of resection substrates, implicating fork reversal as a key determinant of chemotherapy response in ATM deficient cells. - Source: PubMed
Publication date: 2026/07/04
Datta ArindamJackson JessicaMorozov Yaroslav IQiu JinghanVindigni AlessandroGreenberg Roger A - Premature ovarian insufficiency (POI) is a heterogeneous reproductive disorder, with genetic factors, particularly defects in DNA damage response pathways, increasingly implicated in its pathogenesis. DNA ligase IV (LIG4) is a key enzyme in the non-homologous end joining (NHEJ) pathway responsible for repairing DNA double-strand breaks (DSBs). However, its role in non-syndromic POI remains unclear. This study aimed to investigate the potential contribution of LIG4 variants to non-syndromic POI. - Source: PubMed
Publication date: 2026/06/24
Yu ShaZhou XingyuLai YunhuiTang ShuyanChen Shiling - The DNA damage response (DDR) is a complex network of cellular pathways that ensures the faithful maintenance of our genomes upon a wide array of genomic insults. To elucidate the functional architecture of this network, we conducted unbiased genetic interaction screens using the Cas12a genome editor to disrupt 233 DDR genes frequently mutated in cancer and other genetic diseases, either individually or in pairwise combinations. This approach enabled us to assess the phenotypic effects induced by the disruption of >27,000 DDR gene pair combinations under unperturbed cell growth conditions. From this analysis, we identified over 750 high-confidence positive (buffering) or negative (synthetic lethal/sick) gene-gene interactions, along with multiple connections between previously unlinked DDR pathways and modules, allowing us to define novel aspects of the cellular response to spontaneous, DNA replication-associated DNA damage. Among the identified genetic interactions, we uncovered profound synthetic lethal interactions between genes encoding 1) the translesion polymerase REV1-Pol ζ complex and the MCM8-MCM9-HROB DNA helicase complex; 2) Fanconi Anemia (FA) proteins and the mitotic DNA repair factors GEN1, CIP2A, and RHINO; and 3) the DNA translocase SMARCAL1 and components of the FANCM complex, suggesting novel opportunities for targeted therapies in tumors carrying mutations in these genes. Additionally, we identified robust suppressor interactions between the gene encoding the nuclease APOLLO and the core non-homologous end joining (NHEJ) genes , , and , suggesting that NHEJ impairs the fitness of APOLLO-deficient cells. This work provides a functional map of the DDR network and demonstrates the power of Cas12a-based screens for identifying synthetic lethal and buffering interactions with therapeutic potential. - Source: PubMed
Publication date: 2026/06/08
Hayward Samuel BVaitsiankova AlinaLama-Diaz TomasChou JuihsuanTaglialatela AngeloHuang Jen-WeiWijesekarahanthi YodharaudshaniHeyza Joshua RLeuzzi GiuseppeChen ChuanyuanWong NancyLhakhang TenzinFu XiBuendia Alejandro LGheorghe VeronicaAnvar Nazanin EsmaeiliSchmidt Jens CNussenzweig AndreRabadan RaulCostanzo VincenzoGuérois RaphaëlHart TraverCiccia Alberto