Histone H2AX (phospho_Ser139) pAb
- Known as:
- Histone H2AX (phospho_Ser139) pAb
- Catalog number:
- ASA905771100
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- Histone H2AX (phospho_Ser139) pAb
Related genes to: Histone H2AX (phospho_Ser139) pAb
- 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: Histone H2AX (phospho_Ser139) pAb
Related articles to: Histone H2AX (phospho_Ser139) pAb
- To investigate the role of circ_000681 in DNA damage caused by cadmium chloride exposure in human bronchial epithelial cells (16HBE cells), and to provide scientific evidence for clarifying the molecular mechanism of respiratory system diseases caused by metal cadmium exposure and exploring early molecular markers. In April 2022, 16HBE cells were used as the research object, and a cell DNA damage model induced by cadmium chloride was constructed. The experiment consisted of a control group (0 μmol/L) and four different dose cadmium chloride exposure groups (2.5, 5, 10, 20 μmol/L), and treated 16HBE cells with each group for 24 h and 48 h respectively. Comet assay was used to analyze the changes in Olive tail moment; Western blot was used to detect the expression of phosphorylated histone H2AX (γ-H2AX), and to identify the degree of cell DNA damage. Real-time fluorescence quantitative PCR was used to detect the expression of significantly differentially expressed circular RNA (circRNA) in cadmium chloride-induced DNA damage. The circ_000681 knockdown and overexpression sequences were constructed, transfected into 16HBE cells, and combined with cadmium chloride exposure. The DNA damage indicators of the cells were analyzed using the above methods to clarify the role of circ_000681 in cadmium chloride-induced DNA damage in 16HBE cells. Data statistics were performed using one-way analysis of variance and Student's -test. After 24 h and 48 h of exposure to different doses of cadmium chloride (2.5, 5, 10, 20 μmol/L) in 16HBE cells, compared with the control group, the Olive tail moment and γ-H2AX protein expression levels in each dose group were significantly increased (<0.05). Compared with the control group, after 24 h of exposure to cadmium chloride at 2.5, 5, 10, and 20 μmol/L, the expression level of circ_000681 was significantly decreased (<0.05). Compared with the 5 μmol/L cadmium chloride exposure group alone, the Olive tail moment and γ-H2AX protein expression in the knockdown circ_000681 combined with 5 μmol/L cadmium chloride exposure group were increased (<0.05), while the Olive tail moment and γ-H2AX protein expression in the overexpression circ_000681 combined with 5 μmol/L cadmium chloride exposure group were decreased (<0.05) . Overexpression of circ_000681 may inhibit DNA damage in bronchial epithelial cells caused by cadmium chloride exposure. - Source: PubMed
Cui J JHao H YHuang L H - Ribosomal DNA (rDNA) arrays are among the most highly transcribed repetitive regions of the genome and therefore require specialized mechanisms to maintain their stability. The nucleolar DNA damage response (n-DDR) safeguards rDNA integrity and is coordinated by the repair scaffold TOPBP1 and the fibrillar center (FC) protein Treacle. Here, we show that Treacle promotes phase separation of TOPBP1 within the FC to establish a spatially confined signaling platform that amplifies nucleolar DDR signaling and coordinates rDNA repair pathway engagement. Using an inducible TOPBP1 oligomerization system together with physiological models of rDNA damage, we demonstrate that phosphorylation of Treacle by CK2 and ATR/ATM enables its interaction with TOPBP1 and nucleates TOPBP1 condensation in the nucleolus. Functionally, Treacle-dependent condensation promotes robust ATR/ATM activation, γH2AX signaling, and recruitment of DNA repair factors. Disruption of this process does not impair the initial removal of rDNA double-strand breaks but shifts repair toward rapid DNA-PK-dependent nonhomologous end joining while attenuating ATR/ATM signaling and reducing engagement of homologous recombination-associated pathways. Treacle-knockout cells exhibit accelerated early rDNA repair but incomplete damage resolution at later stages. Together, our findings identify Treacle-dependent TOPBP1 condensation as a nucleolar signaling platform that promotes accurate maintenance of highly repetitive rDNA arrays. - Source: PubMed
Petrova Nadezhda VDeriglazov Dmitry AKovina Anastasia PLuzhin Artem VShender Victoria OArapidi Georgij PGavrikov Alexey SMishin Alexander SRazin Sergey VVelichko Artem K - 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