Ku80 _ XRCC5
- Known as:
- Ku80 _ XRCC5
- Catalog number:
- Y213524
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- Ku80 _ XRCC5
Related genes to: Ku80 _ XRCC5
- Gene:
- XRCC5 NIH gene
- Name:
- X-ray repair cross complementing 5
- Previous symbol:
- -
- Synonyms:
- KU80, KARP-1, Ku86, KUB2
- Chromosome:
- 2q35
- Locus Type:
- gene with protein product
- Date approved:
- 1992-01-22
- Date modifiied:
- 2016-06-02
Related products to: Ku80 _ XRCC5
Related articles to: Ku80 _ XRCC5
- To investigate RNF146 expression in triple-negative breast cancer (TNBC) and its role in modulating sensitivity to the PARP inhibitor olaparib, we analyzed RNF146 expression and its association with patient survival using The Cancer Genome Atlas (TCGA) database. Functional studies were performed in 4T1 cells with stable RNF146 overexpression generated via lentiviral transduction. Cell viability and clonogenic capacity were assessed by CCK-8 and colony formation assays, respectively. An orthotopic nude mouse model was used to evaluate tumor growth and therapeutic response in vivo. Potential substrates of RNF146 were screened using the BioGRID database and validated by Western blot analysis. RNF146 expression was significantly reduced in breast cancer tissues, including TNBC, compared with normal tissues, and low RNF146 expression was associated with poor overall survival. RNF146 overexpression markedly enhanced olaparib sensitivity in vitro and significantly inhibited tumor growth while promoting apoptosis in vivo. XRCC5 was identified as a potential substrate of RNF146 and was confirmed to be downregulated by RNF146 both in vitro and in tumor tissues. These findings indicate that RNF146 enhances olaparib sensitivity in TNBC, at least in part, through downregulation of XRCC5, and suggest that RNF146 may serve as a prognostic biomarker and a potential therapeutic target for improving PARP inhibitor efficacy in TNBC. - Source: PubMed
Publication date: 2026/03/31
Chen MengTang YezhenXiao TingtingMa HongningSun HuihuiWang ZhijunZhao Wei - Epithelioid malignant peripheral nerve sheath tumor (EMPNST) is recognized as a distinct entity in the 2026 World Health Organization classification, defined by characteristic morphology and frequent SMARCB1 (INI1) loss, which differentiates it from conventional MPNST. Limited data suggest EMPNST may have a more favorable prognosis, but prognostic markers remain undefined. We studied 78 primary EMPNSTs and compared them with 60 conventional MPNSTs. Patients with EMPNST included 41 females and 37 males, with a median age of 45 (range, 6-84) years. Necrosis was observed in 20% of cases, cytologic atypia was mild (25%), moderate (57%), or severe (18%), and mitoses ranged from 0 to 42/10 (median 7/10) high-power fields. SMARCB1 loss was observed in 81% of EMPNSTs and correlated with prominent nucleoli (64%, P < .001). EMPNSTs predominantly arose in the lower extremities, with 32% superficial, whereas conventional MPNSTs were mostly truncal. Targeted sequencing in 34 EMPNSTs identified SMARCB1 inactivation in 77% of cases, which was associated with SMARCB1 loss (P < .001), and recurrent alterations targeting 2q35/XRCC5 in 59% of cases. Among 34 patients with follow-up (median, 43 months; range, 0-225), 9 developed local recurrence, 15 metastases, and 10 died of disease. Compared with conventional MPNST, EMPNST demonstrated longer median progression-free survival (34 vs 19 months, P value for global difference of survival curves = .35); overall survival was not reached in EMPNST (vs 85 months in conventional MPNST, P value for global difference of survival curves = .16). In multivariable analysis, tumor size and mitotic rate were independently associated with poor prognosis (hazard ratio [HR], 5.2; 95% CI, 1.5-17.7; HR, 1.1; 95% CI, 1.01-1.2, respectively). A risk score integrating tumor size > 5 cm, mitoses > 7 of 10 high-power fields, and necrosis predicted poor outcomes (HR, 4.1; 95% CI, 1.4-12). In conclusion, EMPNST tumor size and mitotic activity are key prognostic factors, supporting a simple risk stratification model. SMARCB1 inactivation is the most frequent genomic event, followed by gains at 2q35 potentially targeting XRCC5, highlighting molecular underpinnings for this distinct sarcoma subtype. - Source: PubMed
Publication date: 2026/03/23
Richman Lee PMichaels Phillip DNief CorrineJo Vickie YHariri Dana JNielsen G PeturDong FeiMazzola EmanueleHornick Jason LSchaefer Inga-Marie - Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by dopaminergic neuronal loss and α-synuclein aggregation, with evidence implicating impaired DNA double-strand break (DSB) repair in disease pathogenesis. This study aimed to systematically evaluate the association between genetic polymorphisms in DSB repair pathway genes, including , , , , , , , and , and PD risk, along with corresponding mRNA expression and DNA repair capacity. A total of 123 clinically diagnosed PD patients and 492 age- and sex-matched healthy controls of Taiwanese ancestry were genotyped, and transcriptional and functional assays were performed in 52 healthy controls. Nominally significant associations with PD risk were identified for four SNPs: rs5751129 ( = 3.55 × 10⁻⁵), rs28360071 ( = 0.0181), rs2735383 ( = 0.0213) and rs17772583 ( = 0.0411). Among these, rs5751129 remained statistically significant after correction for multiple comparisons. Compared to individuals with the wild-type TT genotype, carriers of the heterozygous variant (TC) and homozygous variant (CC) genotypes exhibited increased PD risks, with odds ratios of 1.86 (95% CI, 1.09–3.17) and 13.82 (95% CI, 2.74–69.54), respectively. Cumulative analysis revealed a dose-dependent increase in PD risk with multiple high-risk genotypes ( for trend = 0.0025). Functionally, the rs5751129 CC variant was associated with reduced mRNA expression ( = 0.0001) and impaired NHEJ and DSB repair capacity ( = 0.0183). These findings suggest that genetic variants in DSB genes , , and are associated with PD susceptibility in a Taiwanese population and provide preliminary functional evidence that variants contribute to compromised DNA repair. Together, the results highlight a critical role of inherited DSB repair deficiencies in PD etiology and suggest potential avenues for personalized risk prediction and prevention. - Source: PubMed
Publication date: 2026/03/11
Chen Chao-HsuanTsai Chia-WenChang Wen-ShinLu Ming-KueiCho Der-YangBau Da-Tian - GenX (HFPO-DA), a short-chain per- and polyfluoroalkyl substance (PFAS) substitute, is implicated in testicular toxicity. GenX-related genes were intersected with aging-associated genes to construct a GenX-Aging gene set. Single-cell RNA sequencing (scRNA-seq) data from human testicular aging (GSE254315) were analyzed to evaluate cell-type-specific aging sensitivity and intercellular communication dynamics. Male infertility transcriptomic datasets (GSE45885/GSE45887) were integrated, and least absolute shrinkage and selection operator (LASSO) regression combined with support vector machine recursive feature elimination (SVM-RFE) were applied to identify hub genes, which were validated by reverse transcription quantitative polymerase chain reaction (RT-qPCR) in GenX-exposed rat testicular tissues. Spermatids exhibited the highest aging sensitivity, with progressive decline in intercellular communication. Four hub genes-SOD1, XRCC5, FOXO3, and POLB-demonstrated diagnostic value for male infertility. RT-qPCR confirmed computational predictions: SOD1, XRCC5, and FOXO3 were upregulated, while POLB was downregulated. Functional enrichment implicated FoxO signaling, cellular senescence, and DNA repair pathways. Molecular docking confirmed favorable GenX-protein binding interactions. SOD1, XRCC5, FOXO3, and POLB are candidate biomarkers for GenX-induced reproductive toxicity, with oxidative stress and genome maintenance as key pathological mechanisms. - Source: PubMed
Publication date: 2026/03/08
Gong ZhuozhiFeng QiujianTang SiyuanChen WenyuLiu Shengjing - The effect of sinusoidal Extremely Low-Frequency Electromagnetic Fields (ELF-EMFs) on gynecological (HeLa, ES-2) and urological (DU-145) cancer cells was investigated. ELF-EMFs with a frequency of 50 Hz and a magnetic flux density of 1.3 mT were applied for 15 and 30 min. The experiment was conceptualized to investigate the short-term effects of ELF-EMFs on cell reactive oxygen species (ROS) formation, the levels of genes and proteins involved in DNA damage response, and epigenetic modifications. Here, we found that ELF-EMFs treatment leads to an elevation in the ROS levels that contribute to distinct scenarios in the studied cancer cells. The most prominent changes in the studied factors were found in ES-2 and DU-145 cells exposed to 30 min of ELF-EMFs. ES-2 cells exhibited upregulation of gene expression and elevated levels of several proteins: TNF-α, RAD51, APE1, XRCC1, and NSUN2. Diminished levels of BCL-2, HSP90, RAD51, and TNF-α, as well as overexpression of VIM and METTL3, were observed in DU-145 cells. In summary, we postulate that short-term exposure to 50 Hz ELF-EMFs may be a promising treatment strategy for gynecological and urological cancer cells. - Source: PubMed
Publication date: 2026/02/07
Betlej GabrielaBator EwelinaKwiatkowska AleksandraRomerowicz-Misielak MariaKoziorowska AnnaKoziorowski MarekRzeszutek Iwona