Ask about this productRelated genes to: H2AFX antibody
- Gene:
- H2AFX NIH gene
- Name:
- H2A histone family member X
- Previous symbol:
- H2AX
- Synonyms:
- -
- Chromosome:
- 11q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1994-11-22
- Date modifiied:
- 2018-11-05
Related products to: H2AFX antibody
Related articles to: H2AFX antibody
- External stressors, particularly heat stress, induce DNA damage and genomic instability in cells. However, the mechanisms by which cells rapidly respond to such DNA damage remain largely unknown. In this study, we found that heat shock factor 1 (HSF1), the major transcription factor in the heat shock response, activated several non-homologous end joining (NHEJ) pathway-associated genes, particularly NHEJ1, through puncta formation, thereby maintaining the stability of NHEJ pathway and alleviating the repair burden of DNA double-strand breaks caused by heat stress. Furthermore, N6-methyladenosine (m6A) RNA modification and its reader YTH domain-containing protein 1 (YTHDC1) contributed to this process by promoting the splicing of NHEJ1. Knockdown of HSF1 or YTHDC1 increased nuclear intensity of phosphorylation of histone variant H2AX at Ser-139 (γH2AX) in heat-stressed cells, whereas NHEJ1 overexpression rescued this effect. Moreover, HSF1 or YTHDC1 overexpression increased NHEJ repair efficiency in heat-stressed cells, supporting the existence of an HSF1/YTHDC1-NHEJ1-DNA double-strand repair axis. Our findings reveal a mechanism by which cells repair DNA damage during the heat shock response, providing new insights into how cells maintain genomic stability under external stress conditions. - Source: PubMed
Ding WenqingDeng QidongWang TianyuLiu RuoqianXiang YunfanHuang LuluLiu Jun - KDM8 is a histone demethylase initially characterized for its activity on H3K36me2, although its function is now more widely recognized as a hydroxylase. Through a high-throughput screening on histone demethylases, we identified KDM8 as a regulator of the γH2AX response following ionizing radiation. Experiments using specific reporter substrates revealed that KDM8 depletion increases homologous recombination (HR), while its overexpression reduces HR. This shift is counterbalanced by a concomitant decrease in non-homologous end joining (NHEJ), an effect partly independent of its demethylase activity and unrelated to cell cycle alterations. Despite this imbalance, cellular sensitivity to DNA-damaging agents - such as ionizing radiation, mitomycin C, and camptothecin - remains unchanged. FRET experiments in living cells demonstrated an interaction between KDM8 and Rad51 after DNA damage induced by camptothecin. These findings identify KDM8 as a key player in DSB repair, specifically influencing HR. - Source: PubMed
Publication date: 2026/04/19
Fages JérémieBergoglio ValérieJulia EmmanuelCintori LuanaChailleux CatherineFourez Anne-LisePonsolle NatachaTrouche DidierCanitrot Yvan - Ionizing radiation is a potent genotoxic carcinogen. In this study, acute DNA damage-related biomarker responses were evaluated in peripheral blood lymphocytes of adults undergoing radiographic investigations for orthodontic treatment. Patients (n = 22) for orthodontic treatment were divided into two groups: Group 1 - conventional radiographs (Orthopantomogram (OPG), Lateral Cephalogram (LC) and two Intra-oral periapical radiographs); Group 2 - Cone Beam Computed Tomography (CBCT). Peripheral blood samples (3 mL) were collected before and after radiography imaging. Gamma-H2AX (γ-H2AX) focus formation, micronucleus (MN) formation, and ferredoxin reductase (FDXR) gene expression were evaluated as biomarkers of exposure and response. The frequency of γ-H2AX focus and micronuclei increased significantly (p < 0.05 and p < 0.001) from pre- and post-radiography in both groups. FDXR showed significant upregulation and downregulation in Groups 1 and 2, respectively indicating divergent early transcriptional response between the groups. Conventional radiographs and low-dose CBCT exerted acute DNA damage-related biomarker responses in adult orthodontic patients. FDXR gene showed greater upregulation with conventional radiographs than CBCT. Group 1 and group 2 post-radiography showed no statistical difference when assessed with the three biomarkers for acute damage. Future studies with larger samples and long-term follow-up are needed to validate the findings and provide a basis for safety recommendations. - Source: PubMed
Publication date: 2026/02/28
Murali SandhyaKannan NandhiniKailasam VigneshPerumal VenkatachalamMandodi Mohammed - Background and objectives Radiotherapy for advanced cervical cancer (CaCx) often results in unintended genitourinary toxicities, notably bladder damage. Predicting such radiation-induced toxicity remains challenging. γ-H2AX, a marker of DNA double-strand breaks (DSBs), offers promise as a predictive biomarker for radiosensitivity. This study aimed to evaluate γ-H2AX foci kinetics in peripheral blood lymphocytes (PBLs) as a surrogate for DNA damage response and a predictor of bladder toxicity in CaCx patients undergoing pelvic radiotherapy. Methods In this prospective study, 43 FIGO stage IIIB CaCx patients were enrolled. Stage I (n=31) assessed γ-H2AX induction post-CT simulation (2-6 mGy); Stage II (n=34) evaluated γ-H2AX kinetics across three radiotherapy fractions (FR1, FR13, FR25) during external beam radiotherapy (50 Gy in 25 fractions ± cisplatin). Blood samples were collected at baseline, 1-, 4-, and 24-h post-irradiation. γ-H2AX foci were quantified via flow cytometry. Bladder toxicity was graded usingRadiation Therapy Oncology Group (RTOG) criteria. Results CT and radiotherapy both induced significant γ-H2AX foci, peaking at 1 h. Patients without bladder toxicity showed higher foci induction and faster decay (1→4h: 48.9% vs. 39.4%; 1→24h: 43.6% vs. 12.8%) across all fractions. Persistent foci at 24 h correlated with increased toxicity risk, indicating deficient DNA repair capacity. Interpretation and conclusions γ-H2AX foci kinetics effectively reflect in vivo DNA repair efficiency and predict radiation-induced bladder toxicity. This minimally invasive biomarker may guide personalized radiotherapy, enabling early identification of high-risk patients and potential use of radioprotectors or treatment modifications. - Source: PubMed
John GeofreyGhanekar ShubhamDominic DonilGawde Jitendra RamakantDora TapasChopra Supriya JayantGoda Jayant S - The phosphorylated form of the histone H2AX (γH2AX), a sensor of DNA double-strand breaks (DSB), can serve as a biomarker of DNA damage and therapy response. This study aimed to evaluate the association between γH2AX expression and pathological, molecular, and immune features in colorectal cancer (CRC). - Source: PubMed
Berrino EnricoBellomo Sara ErikaAquilano Maria CostanzaFalcinelli MartaChesta AnitaValtorta EmanueleZampieri DanielaMauri GianlucaSala GiuseppeMarsoni SilviaBardelli AlbertoSartore-Bianchi AndreaSiena SalvatoreSapino AnnaBonoldi Emanuelad'Adda di Fagagna FabrizioMarchiò Caterina