HT Gamma H2AX Elisa Kit
- Known as:
- HT Gamma H2AX Elisa Kit
- Catalog number:
- 4418-096-k
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Trevigen
- Gene target:
- Gamma H2AX Elisa Kit
Related genes to: HT Gamma H2AX Elisa Kit
- 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
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- Chromatin organization changes during aging, accompanied by alterations in higher-order chromosome architecture, contributing to the acquisition of senescent cell-specific functions. Recent studies have revealed that chromatin states and their regulatory mechanisms vary between individual cells. However, analyses of higher-order chromosome structure have been performed mostly at the population level. Therefore, approaches capable of directly quantifying such alterations at the single-cell level are required. Here, we applied persistent homology (PH), a topological data analysis framework, to quantify spatial features of γH2AX foci and DAPI-stained chromatin in single-cell fluorescence images. Using a model of pathological senescence induced by impaired acetylation-dependent histone H2AX exchange, we extracted topological features followed by machine learning analysis. Unsupervised analysis revealed spatial patterns associated with pathological senescence in both γH2AX and DAPI signals. Notably, classifications derived from γH2AX foci showed correspondence with those from DAPI-based chromatin organization, suggesting that local DNA damage patterns reflect global chromatin structure. Supervised models further distinguished normal and pathological senescent cells, with DAPI-derived features highlighting the contribution of nuclear intensity gradients. These findings demonstrate that PH enables quantitative characterization of nuclear architecture at the single-cell level and provides a framework for dissecting chromatin reorganization during cell state transitions. - Source: PubMed
Furuya KanjiUmeno YoshitakaIkura MasaeIkura YasukaNishikawa SeiyaIkura Tsuyoshi - Ultraviolet B (UVB; 280 to 320 nm) radiation damages DNA in epidermal cells and contributes to the development of skin cancer. In response, keratinocytes activate a DNA damage response (DDR) that regulates DNA repair through signaling pathways involving the protein kinases ATR (ataxia telangiectasia and Rad3-related), ATM (ataxia telangiectasia mutated), and DNA-PKcs (DNA-dependent protein kinase catalytic subunit). Activation of these kinases promotes recruitment of DNA repair proteins, including phosphorylated H2AX and p53, to sites of DNA damage. Treatment of primary human neonatal foreskin epidermal keratinocytes and HaCaT keratinocytes with UVB (2.5 to 50 mJ/cm2) resulted in dose- and time-dependent activation of DDR proteins. In HaCaT cells, DDR signaling was most pronounced in S phase compared with cells in G0/G1 or G2/M, as determined by flow cytometry and cell cycle synchronization. Confocal microscopy revealed the accumulation of phosphorylated DNA-PKcs and phosphorylated H2AX in discrete subnuclear foci in S-phase cells, consistent with recruitment to sites of DNA double-strand breaks. UVB also induced oxidative stress in HaCaT cells, as reflected by increased intracellular reactive oxygen species (ROS). Depletion of intracellular glutathione using buthionine sulfoximine significantly enhanced UVB-induced ROS production but had little or no effect on activation of DDR signaling. These findings demonstrate that UVB induces cell cycle-dependent DNA damage in human keratinocytes that is independent of oxidative stress. Understanding mechanisms of UVB activation of the DDR in keratinocytes will be important for elucidating molecular pathways contributing to skin carcinogenesis. - Source: PubMed
An YunqiJan Yi-HuaLaskin Jeffrey D - 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 - The phosphorylation of H2AX at serine 139 (γH2AX) is a marker of DNA damage response, well characterized after ionizing radiation (IR) exposure. In this work we compared γH2AX activation in different human cell lines exposed to X-rays, up to 5 Gy, or UV-C light (below ionization threshold), up to 40 J/m. We selected HeLa, Caco-2 and HaCaT cells as models with different origins and radiosensitivity, conventionally screened with the clonogenic assay. We integrated data from fluorescence microscopy and flow cytometry. Results highlight that γH2AX spatial pattern is determined by the genotoxic agent: X-rays induce discrete, countable foci (associated with DNA double-strand breaks), while UV-C leads to pan-nuclear signal distributions. Instead, dose-response curves are strongly dependent on the cell-line, showing linear or saturating trends, not attributable to the readout technique. After 5 Gy X-rays, γH2AX signal peaks within 1 hour. The residual intensity at 24 hours is compatible with the control for all cell lines; however, cells show different clonogenic survival fractions at 7 days. The kinetics of γH2AX positive cells following 20 J/m UV-C exposure is completely different, with a slower accumulation and persistent signaling from viable cells (not restricted to the S-phase) up to 24 hours, but with a loss of clonogenic potential in the long-term. These findings emphasize that γH2AX marker may be considered as a functional sensor of DNA damage response rather than a marker of specific DNA lesions, and that both radiation quality and cellular context must be considered for its correct interpretation. - Source: PubMed
Publication date: 2026/05/22
Guardamagna IsabellaLonati LeonardoIaria OmbrettaMentana AliceParodi DanielePeterlin GiuliaSemerano RossellaRiani CeciliaPrevitali AndreaTricarico Annade Fatis Paola TabarelliIvaldi Giovanni BattistaPerucca PaolaCazzalini OrnellaBaiocco Giorgio - Based on Monte Carlo simulations and biological experiments, this study aimed to quantitatively analyze the spatial distribution and complexity of DNA double-strand breaks (DSBs) induced by carbon-ion radiation. - Source: PubMed
Publication date: 2026/05/17
Kong XianghuiLi XiaomanHua LingJin XiaodongZhao TingLiu JinyuZhang QiuningLiu XinguoLi QiangLi TianZhang Yibao