Anti_Phosphorylated Histone H2AX Sample[DISCONTINUED]
- Known as:
- Anti_Phosphorylated Histone H2AX Sample[DISCONTINUED]
- Catalog number:
- 4411-PC-020
- Product Quantity:
- 20 ul
- Category:
- -
- Supplier:
- Trevigen
- Gene target:
- Anti_Phosphorylated Histone H2AX Sample[DISCONTINUED]
Related genes to: Anti_Phosphorylated Histone H2AX Sample[DISCONTINUED]
- 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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Alkaline Phosphatase Conjugated Affinity Purified anti-Swine IgG (H&L) [Goat] Secondary_Antibodies(1’R,2’R)-2’-Dihydro Boceprevir
(Boceprevir Metabolite M31+M28 (Mixture of Diastereomers)
DISCONTINUED See D448640 CAS: Formula: C27H47N5O5(1’R,2’R)-2’-Dihydro Boceprevir-d9
(Boceprevir Metabolite M31-d9+M28-d9 (Mixture of Diastereomers))
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DISCONTINUED CAS: Formula: C17H26N4O6S(2E)-2-Butenedioic Acid (S)-(-)-Timolol Ester
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Discontinued. See D416601 C11H12Cl2N2OS CAS: 355115-86-5(3,4-Diaminophenyl)-(2-thienyl)methanone, Dihydrochloride
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(Bupropion Impurity)
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Discontinued C22H29F3O5S CAS: 115375-60-5(3β)-Androsta-5,16-diene-3,17-diol 3-Acetate 17-(Trifluoromethanesulfonate)
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DISCONTINUED C42H78N2O16 CAS: 425365-64-6(9E)-Erythromycin 9-[O-[[(2-Methoxyethoxy)methoxy]methyl]oxime]
DISCONTINUED CAS: 425365-64-6 Formula: C42H78N2O16 Related articles to: Anti_Phosphorylated Histone H2AX Sample[DISCONTINUED]
- This prospective single-center study investigated the impact of iodinated contrast agents (Ultravist/iopromide and Visipaque/iodixanol) on DNA double-strand breaks during pediatric chest computed tomography (CT). Twenty-six children underwent medically indicated chest CT between March 2022 and November 2024: unenhanced ( = 7), Ultravist-enhanced ( = 10), and Visipaque-enhanced ( = 9). Blood samples were collected before and 30 min post-CT. DNA damage was quantified by analyzing γ-H2AX and 53BP1 foci formation in peripheral lymphocytes using immunofluorescence microscopy. All groups showed significant increases in DNA damage following CT. The absolute increases were 0.915 ± 0.250 foci/cell (unenhanced), 0.972 ± 0.279 (Ultravist), and 1.261 ± 0.251 (Visipaque), representing 6.2% and 37.8% higher values in contrast groups. However, these differences between groups were not statistically significant ( = 0.579, Kruskal-Wallis test), with small effect sizes (Cohen's d < 0.5 for all comparisons). Contrast-enhanced protocols employed higher radiation doses than unenhanced scans (CTDIvol: 4.04-4.57 mGy vs. 2.66 mGy). When DNA damage was normalized for CTDIvol, no significant differences were observed between groups ( = 0.659). DNA damage showed no significant correlation with dosimetric parameters. When accounting for radiation dose differences, iodinated contrast agents do not enhance radiation-induced DNA double-strand breaks in pediatric chest CT, confirming the safety of contrast-enhanced CT. - Source: PubMed
Publication date: 2026/07/09
Nuta OtiliaKenessova AinurSarno AntonioJumadilova DinaraDautov Tairkhan - The evaluation of compound genotoxicity is of great significance for drug safety assurance, and the existing evaluation methods have the problems of false-positive/negative, low throughput, or complicated operation. Although enzyme-linked immunosorbent assays (ELISA) kits targeting some genotoxic targets have high throughput, there are limitations in sensitivity and stability due to the use of horseradish peroxidase (HRP). In this study, an integrated evaluation platform based on novel sea urchin-like platinum-coated gold nanoparticles (Pt/Au NPs) was developed to address the above problems. Pt/Au NPs nanozymes were synthesized by deposition of a platinum layer on the surface of gold seeds. The nanozymes exhibited excellent peroxidase activity as well as superior stability compared to natural enzymes. Pt/Au NPs nano-enzymes were replaced for the construction of nano-enzyme-linked immunosorbent assay (NLISA), which has better sensitivity and stability, decreasing the acquired amount of test compounds. Through quantification of genotoxicity damage markers, phosphorylated histone H2AX (γH2AX) and phosphorylated histone H3 (p-H3) in metabolic human hepatocytes, this study has proposed a "see-saw" model to differentiate the genotoxic compounds of DNA breakage or aneuploidy: the breakage agent can significantly increase γH2AX levels, whereas the aneuploidy agent can increase p-H3 levels. Therefore, this microplate-based high-throughput colorimetric detection method can provide an efficient assessment tool for drug safety. - Source: PubMed
Publication date: 2026/06/22
Zhu HongtanXu LuWang XueyingXiao YutongFeng FengZheng FengMeng XiaoliNaisbitt DeanLiu WenyuanHan Lingfei - Inhibitors of ATR, a central kinase controlling DNA replication origin firing and cellular checkpoints, are undergoing clinical trials, yet mechanisms underpinning sensitivity to ATR inhibitors (ATRi) and patient stratification biomarkers are lacking. Here, we perform in parallel, proteomics, transcriptomics and functional analyses and demonstrate that sensitive cancer cell lines have higher expression of DNA replication initiation factors, and exhibit higher origin firing, increased pan-nuclear γH2AX signals and cell death upon ATRi treatment. ATRi sensitivity is causally associated with origin firing rates, since we could modulate ATRi sensitivity by either up- or down-regulating origin firing capacity using CDC7 inhibition, CDK2 inhibition or CDC45 overexpression in both breast and colorectal cancer cells. High expression of replication initiation factors predicts ATRi sensitivity across cell lines from multiple cancer types and acute myeloid leukemia patient samples. This study reveals a contribution of lethal origin firing capacity to ATR sensitivity, providing key steps towards developing a multimodal clinically applicable biomarker. - Source: PubMed
Publication date: 2026/06/19
Lumeau APfuderer P LScarth J AManiati EGuscott M AShaikh NCopley F BGerdes HDe Angelis SAlard E LWang JCutillas P RMardakheh F KBoemo M AForment J VMcClelland S E - 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