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
Related products to: Anti_Phosphorylated Histone H2AX Sample[DISCONTINUED]
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))
DISCONTINUED See D448642 CAS: Formula: C27H38D9N(2E)-2-Butenedioic Acid (R)-(+)-Timolol Ester
DISCONTINUED CAS: Formula: C17H26N4O6S(2E)-2-Butenedioic Acid (S)-(-)-Timolol Ester
DISCONTINUED CAS: Formula: C17H26N4O6S(2E)-[4-(Acetylthio)-1-[2-cyclopropyl-1-(2-fluorophenyl)-2-oxoethyl]-3-piperidinylidene]acetic Acid Ethyl Ester (Mixture of Diastereomers)
DISCONTINUED C22H26FNO4S CAS: 204206-08-6(3,4-Diaminophenyl)-(2-thienyl)methanone, Dihydrochloride
Discontinued. See D416601 C11H12Cl2N2OS CAS: 355115-86-5(3,4-Diaminophenyl)-(2-thienyl)methanone, Dihydrochloride
Discontinued. See D416601 CAS: 355115-86-5 Formula: C11H12Cl2N2OS(3R,5RS,6RS)-6-(3-Chlorophenyl)-6-hydroxy-5-methyl-3-thiomorpholine Carboxylic Acid
(Bupropion Impurity)
DISCONTINUED CAS: 1246812-57-6 Formula: C12(3β)-Androsta-5,16-diene-3,17-diol 3-Acetate 17-(Trifluoromethanesulfonate)
Discontinued C22H29F3O5S CAS: 115375-60-5(3β)-Androsta-5,16-diene-3,17-diol 3-Acetate 17-(Trifluoromethanesulfonate)
Discontinued CAS: 115375-60-5 Formula: C22H29F3O5S(3β,20S)-20-Formyl-3-hydroxy-5-pregnene 3-O-Acetate
Discontinued C24H36O3 CAS: 10211-88-8(3β,20S)-20-Formyl-3-hydroxy-5-pregnene 3-O-Acetate
Discontinued CAS: 10211-88-8 Formula: C24H36O3(9E)-Erythromycin 9-[O-[[(2-Methoxyethoxy)methoxy]methyl]oxime]
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]
- Concurrent cisplatin and radiotherapy frequently cause severe acute hematologic toxicity. This study investigated whether lymphocyte apoptosis, quantified via the γ-H2AX pan-nuclear immunostaining assay, can serve as a reliable biomarker for the acute hematologic side effects of combined chemoradiation. - Source: PubMed
Publication date: 2026/09/05
Sak AliMladenov EmilAlberti YaseminStuschke Martin - DNA double-strand breaks (DSBs) which arise in G1- or G0-phase normal human cells are repaired by nonhomologous end-joining (NHEJ), a pathway which is important for cell survival but can cause mutations at the break sites. DSB repair by NHEJ is very efficient at high damage levels of 1 or more DSBs per cell, much less efficient at lower damage levels and almost absent if only ~0.05 DSBs per cell are induced. Here, we have analyzed the repair of high and low levels of radiation-induced DSBs in primary fibroblasts from 136 childhood cancer survivors, half of whom developed a second independent tumor later in life, and compared it to the response of primary fibroblasts from 68 individually matched cancer-free individuals. We measured the DSB repair efficiency by quantifying residual γH2AX foci with an automated scoring system at 24 h after irradiation with doses of 2.5, 5, 10, and 100 mGy, which induce about 0.0625, 0.125, 0.25, and 2.5 DSBs per cell, respectively. Although childhood cancer survivors and cancer-free individuals repaired DSBs after 10 and 100 mGy equally efficiently, their response to lower doses differed drastically. While repair in cancer-free individuals was inefficient after 2.5 mGy, childhood cancer survivors repaired DSBs after this dose as efficiently as after higher doses. These results indicate that most of the childhood cancer survivors analyzed here may harbor a genetic alteration that affects their response to low levels of DSBs. We suggest that such alterations may be either inherited or caused by previous tumor treatments. - Source: PubMed
Publication date: 2026/08/26
Mirsch JohannaCordoni Ratna NSchmitt CorneliaDehnert Melina ISchulze AliciaGaletzka DanutaZahnreich SebastianScholz-Kreisel PeterHankeln ThomasMarron ManuelaBlettner MariaRonckers Cécile MSchmidberger HeinzLöbrich Markus - Radiosensitizers are being investigated to improve the therapeutic efficacy of radiotherapy by enhancing tumor cell sensitivity while minimizing damage to normal tissues. Dihydroquinine (DHQ), a naturally occurring Cinchona alkaloid with diverse biological activities, has not previously been evaluated for radiosensitizing potential. In this study, human cervical cancer (HeLa) cells were pretreated with an IC20 concentration of DHQ and exposed to 6 MV X-ray irradiation. Clonogenic survival was assessed after irradiation at 2, 4, and 6 Gy, while intracellular ROS, γ-H2AX immunofluorescence, and apoptosis were evaluated following DHQ pretreatment and 2 Gy irradiation. DHQ pretreatment reduced clonogenic survival, yielding sensitizer enhancement ratio values of 1.37 and 1.55 at surviving fractions of 0.20 and 0.37, respectively, indicating modest-to-moderate enhancement of radiosensitivity. DHQ was also associated with increased ROS production, elevated γ-H2AX positivity, and enhanced apoptosis compared with irradiation alone. These findings suggest that DHQ enhances the radiation response in HeLa cells and is associated with increased radiation-induced cellular responses. Although the radiosensitizing effect was modest, the consistent findings across multiple biological endpoints support further investigation of DHQ as a potential adjunct to radiotherapy. Further studies are warranted to validate these findings in more clinically relevant preclinical models. - Source: PubMed
Publication date: 2026/08/18
Prapan AusanaiAissara PimvareeSoonthornchookiat PeerawitSuwannasing ChanyatipJongjitwimol JirapasPattaweerakul ChatrawutXiong YuChaiwaree SaranyaBäumler Hans - This study aimed to links between ATP7B, CTR1, GPX4, 53BP1, p-H2AX and p-ATM expression, platinum sensitivity and prognosis in patients with epithelial ovarian cancer (EOC). - Source: PubMed
Publication date: 2026/08/13
Gao MaiWang Xuan FengLong QianYang DanZhu HongZhu Jun - Fanconi anemia (FA) is a rare disease with a deficient homologous recombination DNA repair pathway and high sensitivity to mitomycin C (MMC). In FA cells, hydroxyurea (HU), when applied in the G2 phase of the cell cycle, exacerbates the chromosomal aberrations (CAs) induced by MMC. Here, we study how exposure to HU in the G2 phase results in an increased CAs frequency in FA cells with or without prior treatment with MMC. We performed chromosome aberration analysis, flow cytometry, and mRNA and protein expression in lymphoblastoid cell lines. We found that HU alone induces post-replicative DNA damage in the form of DNA double-strand breaks (DSBs) in both wild-type and FA cells and a similar increase in the activation of DSBs marker ɣH2AX. HU potentiates the amount of CAs only in MMC-treated FA cells by multiple mechanisms, including (1) hindering the ɣH2AX signal, (2) impairing the translocation of ribonucleotide reductase (RNR) into the cell nucleus, and (3) promoting the activity of WIP1 phosphatase. Concomitantly, increased levels of cell death were observed in FA cell cultures. HU induces DNA damage and potentiates pre-existent damage in FA cells by preventing the translocation of the RNR component p53R2 into the nucleus and activating checkpoint recovery, thus allowing the survival of a proportion of FA cells that have adapted to DNA damage. - Source: PubMed
Publication date: 2026/07/29
Bustamante BenjaminSosa DavidMelendez-Zajgla JorgeLópez-Velázquez GabrielOstrosky-Wegman PatriciaRodriguez AlfredoTorres LedaJuárez-Figueroa UlisesSánchez-Olea RobertoCervantes-Ríos ElsaOrtiz-Muñiz RocíoMolina BerthaFrias Sara