- 14-9865-80 - Invitrogen Antibodies H2AX antibody

Submitted references The mitotic checkpoint is a targetable vulnerability of carboplatin-resistant triple negative breast cancers.

Moens S, Zhao P, Baietti MF, Marinelli O, Van Haver D, Impens F, Floris G, Marangoni E, Neven P, Annibali D, Sablina AA, Amant F
Scientific reports 2021 Feb 4;11(1):3176

MAU2 and NIPBL Variants Impair the Heterodimerization of the Cohesin Loader Subunits and Cause Cornelia de Lange Syndrome.

Parenti I, Diab F, Gil SR, Mulugeta E, Casa V, Berutti R, Brouwer RWW, Dupé V, Eckhold J, Graf E, Puisac B, Ramos F, Schwarzmayr T, Gines MM, van Staveren T, van IJcken WFJ, Strom TM, Pié J, Watrin E, Kaiser FJ, Wendt KS
Cell reports 2020 May 19;31(7):107647

Synergistic lethality between PARP-trapping and alantolactone-induced oxidative DNA damage in homologous recombination-proficient cancer cells.

Wang H, Zhang S, Song L, Qu M, Zou Z
Oncogene 2020 Apr;39(14):2905-2920

Evaluation of cisplatin-induced injury in human kidney organoids.

Digby JLM, Vanichapol T, Przepiorski A, Davidson AJ, Sander V
American journal of physiology. Renal physiology 2020 Apr 1;318(4):F971-F978

ATR maintains chromosomal integrity during postnatal cerebellar neurogenesis and is required for medulloblastoma formation.

Lang PY, Nanjangud GJ, Sokolsky-Papkov M, Shaw C, Hwang D, Parker JS, Kabanov AV, Gershon TR
Development (Cambridge, England) 2016 Nov 1;143(21):4038-4052

More than just a focus: The chromatin response to DNA damage and its role in genome integrity maintenance.

Lukas J, Lukas C, Bartek J
Nature cell biology 2011 Oct 3;13(10):1161-9

ATM phosphorylates histone H2AX in response to DNA double-strand breaks.

Burma S, Chen BP, Murphy M, Kurimasa A, Chen DJ
The Journal of biological chemistry 2001 Nov 9;276(45):42462-7

Histone H2AX is phosphorylated in an ATR-dependent manner in response to replicational stress.

Ward IM, Chen J
The Journal of biological chemistry 2001 Dec 21;276(51):47759-62

DNA double-stranded breaks induce histone H2AX phosphorylation on serine 139.

Rogakou EP, Pilch DR, Orr AH, Ivanova VS, Bonner WM
The Journal of biological chemistry 1998 Mar 6;273(10):5858-68

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Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Immunocytochemistry of fixed and permeabilized MCF7 cells treated for 30 minutes with 10 uM camptothecin and stained with 5 µg/mL of Anti-Human/Mouse phospho-H2AX (S139) Purified followed by 5 µg/mL of F (ab')2 Anti-Mouse IgG eFluor® 570.Nuclei are stained with DAPI.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Immunohistochemistry of formalin-fixed paraffin embedded human tonsil stained with 5 µg/mL of Anti-Human/Mouse phospho-H2AX (S139) Purified followed by Anti-Mouse IgG Biotin, Streptavidin HRP, and DAB visualization.Nuclei are counterstained with hematoxylin.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Jurkat cells were stimulated for 4 hours with staurosporine and then stained intracellularly, using the Foxp3/Transcription Factor Staining Buffer Set (Product # 00-5523-00) and protocol, with PARP1 (Cleaved) Monoclonal Antibody, PE (Product # 12-6668-42) and 0.015 µg Mouse IgG1 kappa Isotype Control (Product # 14-4714-85) (left) or 0.015 µg phospho-H2AX (S139) Monoclonal Antibody (right) followed by IgG1 Monoclonal Antibody, APC (Product # 17-4015-82). Total cells were used for analysis.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Fig. 4 ATL synergizes with olaparib to induce intense replication stress in cancer cells. a Immunofluorescent staining of gammaH2AX and EdU. PC-3 cells were treated by 10 muM ATL, 10 muM olaparib (Ola) or the combination of the two, with or without 10 mM NAC or 5 muM aphidicolin (APC), for 12 h. At the end of drug treatment, cells were pulse-labeled with 10 uM EdU for 20 min (scale bar: 20 mum). b , c gammaH2AX and EdU positive cells were measured using the ImageJ software and the data were processed by the Prism software. d Western blot detection of gammaH2AX. PC-3 cells were treated by the combination of 10 muM ATL and 10 muM Ola or 10 muM ATL and 10 muM veliparib (Vel), with or without 5 muM aphidicolin (APC), for 24 h. e Western blot analysis of the indicated proteins. PC-3 cells were treated by 10 muM ATL, 10 muM olaparib (Ola) or the combination of the two for the indicated times. f Immunofluorescent staining of RPA32 foci. PC-3 cells were treated by 10 muM ATL, 10 muM olaparib (Ola) or the combination of the two for 12 h (scale bar: 10 mum). g Nuclear RPA32 intensity was measured using the ImageJ software and the data were processed by the Prism software. h Western blot detection of chromatin bound RPA32 and gammaH2AX. PC-3 cells were treated by 10 muM ATL, 10 muM olaparib (Ola) or the combination of the two for the indicated times. n.s. not significant, ** p < 0.01, **** p < 0.0001 vs. vehicle control.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Fig. 7 Coadministration of ATL and olaparib induces regression of tumor xenografts. PC-3 cells (2 x 10 6 ) in 1:1 matrigel were inoculated subcutaneously into the left flanks of male athymic BALB/c nude mice. When the tumor volume reached approximately 150 mm 3 (15 days after inoculation), mice were treated once daily with 50 mg/kg ATL oral gavage or 50 mg/kg olaparib intraperitoneal injection or both for 15 days. a Photograph of tumors dissected out from each mouse at the time of study termination. b Tumor volumes measured on the indicated days of treatment. Results were shown as mean +- SD. c Tumor weight measured at the end of the study. d Representative images of immunohistochemical staining of gammaH2AX and TUNEL in tumor tissues (scale bar: 20 mum). e Hematoxylin-eosin staining of liver, heart, and kidney tissue sections (magnification: x400). n.s. not significant, *** p < 0.001 vs. vehicle control.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Proteome re-wiring of carboplatin-resistant 468-R cells protects from carboplatin-induced oxidative and genotoxic stress. ( A,B ) Hierarchical clustering of differentially expressed proteins (DE) ( A ) and Ingenuity Pathway Analysis ( B ) of the proteome alterations in MDA-MB-468 and 468-R cells treated with vehicle or 2 uM carboplatin for 5 days. Protein expression was analyzed by LC/MS-MS, and DE proteins were identified by ANOVA followed by Tukey's HSD test with an adjusted P value < 0.05. The top 10 significantly enriched pathways are shown. P value < 0.05 was used to determine significantly enriched pathways; the -log10 ( P value) was not shown if the pathway was not significantly enriched. N = 3. ( C,D ) ROS levels in MDA-MB-468 and 468-R cells treated with vehicle or 2 uM carboplatin for 5 days. Total ROS levels ( C ) were measured by the cellROX assay, and mitochondrial specific superoxide levels ( D ) were measured by the mitoSOX assay. Median flow of cytometric intensities were normalized to MDA-MB-468 vehicle condition. Data are shown as Mean +- SEM. P values were calculated by two-way ANOVA with Geisser-Greenhouse and Tukey's correction. N = 3. ( E ) NAD/NADH ratio as measured by NAD/NADH-Glo kit. Data are shown as Mean +- SEM. P values were calculated by two-way ANOVA with Geisser-Greenhouse and Tukey's correction. N = 3. ( F ) gamma-H2AX staining of MDA-MB-468 and 468-R cells treated with vehicle or 2 uM carboplatin for 5 days as analyzed by flow cytometry. P va

14-9865-80

Antibody data