XRCC3 Antibody
- Known as:
- XRCC3 Antibody
- Catalog number:
- XW-7922
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- XRCC3 Antibody
Related genes to: XRCC3 Antibody
- Gene:
- XRCC3 NIH gene
- Name:
- X-ray repair cross complementing 3
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 14q32.33
- Locus Type:
- gene with protein product
- Date approved:
- 1995-08-11
- Date modifiied:
- 2018-08-14
Related products to: XRCC3 Antibody
Related articles to: XRCC3 Antibody
- Background Occupational exposure to pesticides has been associated with a range of adverse health outcomes among agricultural workers. Genetic polymorphisms in detoxification and DNA repair pathway genes may influence individual susceptibility to these effects. Grape farmers in southwestern Maharashtra, India, represent a high-risk occupational group facing routine and intensive pesticide exposure throughout the cultivation season, yet molecular epidemiological data from this population remain limited. Methods A cross-sectional exploratory study was conducted among 204 pesticide-exposed grape farmers from Sangli and nearby districts of southwestern Maharashtra, India. Demographic characteristics, exposure patterns, and self-reported symptoms experienced following pesticide exposure were recorded using a structured questionnaire. Oxidative stress markers, including malondialdehyde (MDA) and ferric reducing antioxidant power (FRAP), were measured as secondary biological indicators. Genotyping of paraoxonase 1 () polymorphisms (Q192R, L55M), apurinic/apyrimidinic endonuclease 1 (), and X-ray repair cross-complementing proteins (, , and ) was performed using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Associations between genotypes, exposure-related parameters, and self-reported symptoms were evaluated using chi-square tests and odds ratios (ORs) with 95% confidence intervals (CIs). A p-value ≤ 0.05 was considered statistically significant. Results The majority of participants were male, 177 (86.8%), with most falling in the 31-50 year age group, 110 (53.9%). A total of 170 (83.3%) reported daily exposure of ≥6 hours, and none reported use of personal protective equipment. The mean MDA was 5.24 ± 2.02 µmol/L, and the mean FRAP was 443.39 ± 250.90 µmol/L. Overall, 80 (39%) participants reported at least one symptom following pesticide exposure. Prolonged daily exposure (≥6 hours) was significantly associated with increased odds of symptom experience (OR = 3.5; 95% CI: 1.38-8.9; p = 0.006). L55M heterozygosity showed a borderline significant association with increased likelihood of self-reported reactions (OR = 1.79; 95% CI: 0.99-3.2; p = 0.049). The rs25487 variant genotype was inversely associated with symptom experience (OR = 0.25; 95% CI: 0.07-0.92; p = 0.034), though this finding requires cautious interpretation given the low variant cell count. Conclusion Prolonged daily pesticide exposure was independently associated with increased likelihood of self-reported health reactions. The borderline association of L55M and the exploratory finding for rs25487 represent preliminary signals requiring confirmation in larger studies with objective exposure assessment and validated clinical outcomes. - Source: PubMed
Publication date: 2026/05/11
Garud AishwaryaPawar SatyajeetDatkhile KailasDurgawale Pratik PKakade Satish VPatil Satish R - Nowadays, against the backdrop of a global increase in cancer incidence, the search for prognostic markers to assess individual risks is particularly relevant. Early identification of altered DNA methylation patterns may serve as a reliable indicator of malignant transformation and be used for diagnostic purposes. The objective of this study was to assess the methylation level of CpG dinucleotides in the promoter regions of DNA repair genes (AKT1, DDB2, GADD45A, XPC and XRCC3) in the blood of chronically exposed individuals who subsequently developed cancers. The study was conducted in individuals who were affected by chronic low dose-rate exposure in 1950-1960s in the Southern Urals. The main group included exposed individuals in the latent period of cancer development-104 people, the comparison group consisted of exposed individuals without cancers-188 people. The methylation level was assessed in bisulfite-converted DNA samples using methylation-specific high-resolution melting. It was established that in exposed individuals from the main group, there was a statistically significant decrease in the methylation level in the AKT1 and GADD45A gene promoter, relative to the comparison group (4.37 versus 7.23%, p < 0.001 and 10.73 versus 19.58%, p < 0.001, respectively). As for the XRCC3 gene, there was an increase in the methylation level of CpG dinucleotides in the promoter in individuals from the main group relative to the comparison group (5.38 versus 6.18%, p < 0.001). When the prognostic potential of methylation parameters of the AKT1, GADD45A, XRCC3 gene promoters was assessed for the purposes of early diagnosis of cancer development risk, it was found that when these loci were analyzed together, the AUC was 0.89 (95% CI: 0.85-0.93) at p < 0.001. - Source: PubMed
Korechenkova A VBlinova E AAkleyev A V - Hexavalent chromium [Cr(VI)] is a lung carcinogen. Central to its carcinogenic mechanism are Cr(VI)-induced DNA double strand breaks and chromosome instability. While breaks are usually repaired in healthy cells, Cr(VI) inhibits homologous recombination repair by targeting RAD51. RAD51 paralogs (RAD51B, RAD51C, RAD51D, XRCC2, and XRCC3) are responsible for RAD51 loading and the stabilization of nucleoprotein filaments necessary for DNA strand exchange and repair. This study aimed to investigate the effects of Cr(VI) exposure on RAD51 paralogs. WTHBF-6 cells, a human lung cell line, were exposed to various environmentally and occupationally relevant concentrations of zinc chromate for acute (24 h) and prolonged (120 h) exposure times. After exposure to Cr(VI), we collected RNA for sequencing and assessed the ability of DNA repair proteins to form foci using immunofluorescence. Protein levels were measured with western blotting, RNA-Seq was validated with RT-qPCR, and protein-protein interactions were assessed with the Proximity Ligation Assay (PLA) assay. Cr(VI) transcriptionally repressed all RAD51 paralogs. Further functional analyses showed that Cr(VI) inhibited the foci formation of RAD51D after acute and prolonged exposures and of XRCC2 and XRCC3 after prolonged exposure. Cr(VI) also inhibited overall RAD51D protein expression, as well as its interaction with RAD51. These findings suggest that Cr(VI) inhibits all RAD51 paralogs, but RAD51D might be an early target of Cr(VI), leading to the loss of RAD51 filament formation and function and the overall inhibition of homologous recombination repair. - Source: PubMed
Publication date: 2026/03/23
Williams Aggie RMeaza IdoiaLu HaiyanWise James T FDiven Sandra SToyoda Jennifer HKouokam J CalvinWise John Pierce - Genetic susceptibility is believed to contribute to leukemia development. This study aimed to systematically evaluate the association between DNA repair gene polymorphisms, particularly xeroderma pigmentosum (XP) and excision repair cross-complementing (XRCC) genes, and leukemia risk. - Source: PubMed
Publication date: 2026/04/23
Ye HonghuiFang JinyongJin Pei - Homologous recombination (HR) repairs DNA double-strand breaks and stabilizes stressed replication forks, and HR deficiency promotes genome instability and cancer. HR requires assembly of RAD51 nucleoprotein filaments on single-stranded DNA (ssDNA), a process regulated by the human RAD51 paralogs RAD51C, XRCC3, RAD51D and XRCC2. Here, using cryo-electron microscopy, we find that the RAD51-XRCC3-RAD51C complex (RAD51-X3C) assembles into an octamer in which XRCC3 engages the RAD51 DNA-binding surface and RAD51 subunits adopt a misaligned configuration incompatible with filament formation. These features define an autoinhibited RAD51-X3C state that limits nonproductive RAD51 binding to double-stranded DNA or RNA-DNA hybrids while preserving RAD51 availability for ssDNA-dependent strand exchange. We further show that the RAD51D-XRCC2 paralog complex remodels RAD51-X3C into a pentameric RAD51-X3CDX2 assembly by engaging the exposed RAD51C surface and disrupting contacts that stabilize the octamer. This remodeling exposes the RAD51 DNA-binding interface, enhances RAD51-ssDNA filament assembly, and promotes strand exchange on RPA-coated ssDNA, and yields a filament-compatible paralog assembly that integrates into ssDNA-bound RAD51 filaments. Together, these findings establish paralog exchange as a mechanism that converts an autoinhibited RAD51-X3C octamer into an activated RAD51-X3CDX2 pentamer to regulate RAD51 filament formation during HR and replication fork preservation. - Source: PubMed
Publication date: 2026/04/22
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