Structured Review

Merck KGaA anti γ h2ax
DNA damage after IR increased following treatment with RGD/P-AuNPs. Notes: ( A ) Representative confocal immunofluorescence images of <t>γ-H2AX</t> (red) in MDA-MB-231 cells after treatment with AuNPs and radiation (0 Gy or 4 Gy). Bar, 20 μm. ( B ) Number of γ-H2AX foci per nucleus in MDA-MB-231 cells was counted. Cells pre-cultured with AuNPs were fixed and stained with γ-H2AX antibody 12 h after IR (0 Gy or 4 Gy). At least 50 nuclei were counted in each independent experiment. Columns, mean (n=3), bars, SE, * P
Anti γ H2ax, supplied by Merck KGaA, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/anti γ h2ax/product/Merck KGaA
Average 92 stars, based on 1 article reviews
Price from $9.99 to $1999.99
anti γ h2ax - by Bioz Stars, 2020-09
92/100 stars

Images

1) Product Images from "Targeting integrins with RGD-conjugated gold nanoparticles in radiotherapy decreases the invasive activity of breast cancer cells"

Article Title: Targeting integrins with RGD-conjugated gold nanoparticles in radiotherapy decreases the invasive activity of breast cancer cells

Journal: International Journal of Nanomedicine

doi: 10.2147/IJN.S137833

DNA damage after IR increased following treatment with RGD/P-AuNPs. Notes: ( A ) Representative confocal immunofluorescence images of γ-H2AX (red) in MDA-MB-231 cells after treatment with AuNPs and radiation (0 Gy or 4 Gy). Bar, 20 μm. ( B ) Number of γ-H2AX foci per nucleus in MDA-MB-231 cells was counted. Cells pre-cultured with AuNPs were fixed and stained with γ-H2AX antibody 12 h after IR (0 Gy or 4 Gy). At least 50 nuclei were counted in each independent experiment. Columns, mean (n=3), bars, SE, * P
Figure Legend Snippet: DNA damage after IR increased following treatment with RGD/P-AuNPs. Notes: ( A ) Representative confocal immunofluorescence images of γ-H2AX (red) in MDA-MB-231 cells after treatment with AuNPs and radiation (0 Gy or 4 Gy). Bar, 20 μm. ( B ) Number of γ-H2AX foci per nucleus in MDA-MB-231 cells was counted. Cells pre-cultured with AuNPs were fixed and stained with γ-H2AX antibody 12 h after IR (0 Gy or 4 Gy). At least 50 nuclei were counted in each independent experiment. Columns, mean (n=3), bars, SE, * P

Techniques Used: Immunofluorescence, Multiple Displacement Amplification, Cell Culture, Staining

2) Product Images from "Loss of the Fanconi anemia–associated protein NIPA causes bone marrow failure"

Article Title: Loss of the Fanconi anemia–associated protein NIPA causes bone marrow failure

Journal: The Journal of Clinical Investigation

doi: 10.1172/JCI126215

Nipa -deficient cells display MMC hypersensitivity as a hallmark of FA. ( A ) Western blot analysis of Nipa +/+ and Nipa –/– primary MEFs (untreated and treated +6 hours with 0.5 μM MMC) for FANCD2 and lamin. Quantification of relative non- and monoubiquitinated FANCD2 protein levels of Nipa +/+ and Nipa –/– primary MEFs is shown. n = 7 Nipa +/+ ; n = 7 Nipa –/– . ( B ) Quantification of γ-H2AX foci in untreated and 0.5 μM MMC–treated Nipa +/+ and Nipa –/– primary MEFs. No MMC: data from 2 independent experiments; n = 74 Nipa +/+ , n = 112 Nipa –/– . +6 hours MMC: data from 4 independent experiments; n = 121 Nipa +/+ , n = 93 Nipa –/– . ( C ) Immunofluorescence for γ-H2AX foci in untreated and 6-hour MMC-treated (0.5 μM) Nipa +/+ and Nipa –/– primary MEFs. Representative confocal microscopy images are shown. Original magnification, ×63. ( D ) Representative images of DAPI-stained metaphase spreads of untreated and MMC-treated (5 nM) Nipa +/+ and Nipa –/– spleen cells after 48 hours of in vitro growth. Arrow indicates chromosome radials. Original magnification, ×100. ( E ) Quantification of chromosome radials per cell of untreated and MMC-treated (5 and 10 nM) Nipa +/+ and Nipa –/– spleen cells after 48 hours of in vitro growth. No MMC: n =40 Nipa +/+ ; n = 40 Nipa –/– . +MMC: n = 20 Nipa +/+ ; n = 20 Nipa –/– . ( F ) Cell survival assay of Nipa +/+ , Nipa –/– , and Fancd2 –/– MEFs measured after 5 days of culture with the indicated concentrations of MMC. Data from 2 independent experiments are shown. n = 12 Nipa +/+ ; n = 12 Nipa –/– ; n =12 Fancd2 –/– . One-way ANOVA, P = 6.4 × 10 –7 (5 nM); P = 4.9 × 10 –6 (10 nM); P = 1.7 × 10 –5 (20 nM); P = 1.0 × 10 –4 (50 nM). Reported P values in the figure from unpaired 2-tailed Student’s t test. * P
Figure Legend Snippet: Nipa -deficient cells display MMC hypersensitivity as a hallmark of FA. ( A ) Western blot analysis of Nipa +/+ and Nipa –/– primary MEFs (untreated and treated +6 hours with 0.5 μM MMC) for FANCD2 and lamin. Quantification of relative non- and monoubiquitinated FANCD2 protein levels of Nipa +/+ and Nipa –/– primary MEFs is shown. n = 7 Nipa +/+ ; n = 7 Nipa –/– . ( B ) Quantification of γ-H2AX foci in untreated and 0.5 μM MMC–treated Nipa +/+ and Nipa –/– primary MEFs. No MMC: data from 2 independent experiments; n = 74 Nipa +/+ , n = 112 Nipa –/– . +6 hours MMC: data from 4 independent experiments; n = 121 Nipa +/+ , n = 93 Nipa –/– . ( C ) Immunofluorescence for γ-H2AX foci in untreated and 6-hour MMC-treated (0.5 μM) Nipa +/+ and Nipa –/– primary MEFs. Representative confocal microscopy images are shown. Original magnification, ×63. ( D ) Representative images of DAPI-stained metaphase spreads of untreated and MMC-treated (5 nM) Nipa +/+ and Nipa –/– spleen cells after 48 hours of in vitro growth. Arrow indicates chromosome radials. Original magnification, ×100. ( E ) Quantification of chromosome radials per cell of untreated and MMC-treated (5 and 10 nM) Nipa +/+ and Nipa –/– spleen cells after 48 hours of in vitro growth. No MMC: n =40 Nipa +/+ ; n = 40 Nipa –/– . +MMC: n = 20 Nipa +/+ ; n = 20 Nipa –/– . ( F ) Cell survival assay of Nipa +/+ , Nipa –/– , and Fancd2 –/– MEFs measured after 5 days of culture with the indicated concentrations of MMC. Data from 2 independent experiments are shown. n = 12 Nipa +/+ ; n = 12 Nipa –/– ; n =12 Fancd2 –/– . One-way ANOVA, P = 6.4 × 10 –7 (5 nM); P = 4.9 × 10 –6 (10 nM); P = 1.7 × 10 –5 (20 nM); P = 1.0 × 10 –4 (50 nM). Reported P values in the figure from unpaired 2-tailed Student’s t test. * P

Techniques Used: Western Blot, Immunofluorescence, Confocal Microscopy, Staining, In Vitro, Clonogenic Cell Survival Assay

Nipa –/– HSCs are unable to repair DNA damage and prone to cell death. ( A ) Immunofluorescence for γ-H2AX foci in young (5 months) Nipa +/+ and Nipa –/– HSCs. Representative confocal microscopy images and quantitative graph are shown. Data from 4 independent experiments. n = 53 Nipa +/+ ; n =62 Nipa –/– . Original magnification, ×63. ( B ) Immunofluorescence for γ-H2AX foci in aged (11–18 months) Nipa +/+ and Nipa –/– HSCs. Representative confocal microscopy images and quantitative graph are shown. Data are from 6 independent experiments. n = 136 Nipa +/+ ; n = 78 Nipa –/– . Original magnification, ×63. ( C ) Representative confocal microscopy images and quantitative results for 8-month-old HSCs stained for γ-H2AX 11 hours after 4-Gy irradiation. Data are from 7 independent experiments. n = 183 Nipa +/+ ; n = 230 Nipa –/– . Original magnification, ×63. ( D ) Percentages of early apoptotic cells (annexin V + 7-AAD – ) within hematopoietic subpopulations from Nipa +/+ and Nipa –/– mice older than 20 months. n = 8 Nipa +/+ ; n = 8 Nipa –/– . Lin neg, lineage-negative. ( E ) Heatmap of expression levels of apoptosis-related genes between aged ( > 20 months) untreated Nipa +/+ and Nipa –/– HSCs analyzed by microarray. Color scale represents row Z -score mRNA intensity values. * P
Figure Legend Snippet: Nipa –/– HSCs are unable to repair DNA damage and prone to cell death. ( A ) Immunofluorescence for γ-H2AX foci in young (5 months) Nipa +/+ and Nipa –/– HSCs. Representative confocal microscopy images and quantitative graph are shown. Data from 4 independent experiments. n = 53 Nipa +/+ ; n =62 Nipa –/– . Original magnification, ×63. ( B ) Immunofluorescence for γ-H2AX foci in aged (11–18 months) Nipa +/+ and Nipa –/– HSCs. Representative confocal microscopy images and quantitative graph are shown. Data are from 6 independent experiments. n = 136 Nipa +/+ ; n = 78 Nipa –/– . Original magnification, ×63. ( C ) Representative confocal microscopy images and quantitative results for 8-month-old HSCs stained for γ-H2AX 11 hours after 4-Gy irradiation. Data are from 7 independent experiments. n = 183 Nipa +/+ ; n = 230 Nipa –/– . Original magnification, ×63. ( D ) Percentages of early apoptotic cells (annexin V + 7-AAD – ) within hematopoietic subpopulations from Nipa +/+ and Nipa –/– mice older than 20 months. n = 8 Nipa +/+ ; n = 8 Nipa –/– . Lin neg, lineage-negative. ( E ) Heatmap of expression levels of apoptosis-related genes between aged ( > 20 months) untreated Nipa +/+ and Nipa –/– HSCs analyzed by microarray. Color scale represents row Z -score mRNA intensity values. * P

Techniques Used: Immunofluorescence, Confocal Microscopy, Staining, Irradiation, Mouse Assay, Expressing, Microarray

3) Product Images from "Oridonin Enhances Radiation-Induced Cell Death by Promoting DNA Damage in Non-Small Cell Lung Cancer Cells"

Article Title: Oridonin Enhances Radiation-Induced Cell Death by Promoting DNA Damage in Non-Small Cell Lung Cancer Cells

Journal: International Journal of Molecular Sciences

doi: 10.3390/ijms19082378

Histopathological analysis of H460 tumors following combination treatment with oridonin and radiation. Hematoxylin and eosin (H-E) staining and immunohistochemistry for cleaved caspase-3 and γ-H2AX were performed on tumors harvested at 14 days after IR. Representative images of H-E-stained tumors ( upper images ) and cleaved caspase-3- and γ-H2AX-positive cells ( middle images , brown staining) and quantification of cleaved caspase-3 and γ-H2AX-positive staining with six mice in each group ( lower plots , means ± SEM) are shown; * p
Figure Legend Snippet: Histopathological analysis of H460 tumors following combination treatment with oridonin and radiation. Hematoxylin and eosin (H-E) staining and immunohistochemistry for cleaved caspase-3 and γ-H2AX were performed on tumors harvested at 14 days after IR. Representative images of H-E-stained tumors ( upper images ) and cleaved caspase-3- and γ-H2AX-positive cells ( middle images , brown staining) and quantification of cleaved caspase-3 and γ-H2AX-positive staining with six mice in each group ( lower plots , means ± SEM) are shown; * p

Techniques Used: Staining, Immunohistochemistry, Mouse Assay

4) Product Images from "BRG1 Promotes chromatin remodeling around DNA damage sites"

Article Title: BRG1 Promotes chromatin remodeling around DNA damage sites

Journal: Animal Cells and Systems

doi: 10.1080/19768354.2018.1525429

BRG1 knockdown impairs DNA damage repair. (A) SW13 cells were transfected with the pBJ5 vector or pBJ5-BRG1 plasmids for 48 h. Then, the cells were treated with 10 μM ETO for 20 min and allowed to repair for the indicated time. The cells were fixed, permeabilized and immunostained with BRG1 and γ H2AX antibodies. Images were captured with a fluorescence microscope. The relative γ H2AX levels were quantified by ImageJ software. Scale bar: 10 μm. (B) U2OS cells were transfected with control siRNA or BRG1 siRNA for 48 h. Then, the cells were treated with 10 μM ETO for 20 min and allowed to repair for the indicated time. The cells were fixed, permeabilized and immunostained with BRG1 and γ H2AX antibodies. Images were captured with a fluorescence microscope. The relative γ H2AX levels were quantified by ImageJ software. Scale bar: 10 μm. siCont: control siRNA. siBRG1: BRG1 siRNA.
Figure Legend Snippet: BRG1 knockdown impairs DNA damage repair. (A) SW13 cells were transfected with the pBJ5 vector or pBJ5-BRG1 plasmids for 48 h. Then, the cells were treated with 10 μM ETO for 20 min and allowed to repair for the indicated time. The cells were fixed, permeabilized and immunostained with BRG1 and γ H2AX antibodies. Images were captured with a fluorescence microscope. The relative γ H2AX levels were quantified by ImageJ software. Scale bar: 10 μm. (B) U2OS cells were transfected with control siRNA or BRG1 siRNA for 48 h. Then, the cells were treated with 10 μM ETO for 20 min and allowed to repair for the indicated time. The cells were fixed, permeabilized and immunostained with BRG1 and γ H2AX antibodies. Images were captured with a fluorescence microscope. The relative γ H2AX levels were quantified by ImageJ software. Scale bar: 10 μm. siCont: control siRNA. siBRG1: BRG1 siRNA.

Techniques Used: Transfection, Plasmid Preparation, Fluorescence, Microscopy, Software

5) Product Images from "Depletion of pre-mRNA splicing factor Cdc5L inhibits mitotic progression and triggers mitotic catastrophe"

Article Title: Depletion of pre-mRNA splicing factor Cdc5L inhibits mitotic progression and triggers mitotic catastrophe

Journal: Cell Death & Disease

doi: 10.1038/cddis.2014.117

Depletion of Cdc5L results in kinetochore-microtubule attachment defects and DNA damage. Synchronized HeLa cells transfected with control or  Cdc5L  siRNA were treated with MG132 to prevent anaphase onset ( a – d ). Coverslips were chilled on ice for 10 min ( b ) or fixed immediately ( a ) and stained with anti-centromere antibody (ACA; for kinetochores; red), anti- α -tubulin antibody (microtubules; green) and SYTOX Blue nucleic acid stain (for DNA; blue), scale bar, 10  μ m. For spindle checkpoint analysis( c  and  d ), the cells were stained with anti-Bub1 or BubR1 antibody (green) and ACA (for kinetochores; red), scale bar, 10  μ m. ( e  and  f ) Quantification of Bub1 and BubR1 levels described as in  c  and  d  were analyzed. Bub1 and BubR1 signals were normalized to ACA. For Bub1 quantification, control-knockdown cells ( n =4) and Cdc5L-knockdown cells ( n =10); for BubR1 quantification, control-knockdown cells ( n =7) and Cdc5L-knockdown cells ( n =14). Data are shown as mean±S.D. ( g ) HeLa cells were transfected with control or Cdc5L siRNA, then stained with anti- γ -H2AX antibody (green) and PI (for DNA; red), scale bar, 10  μ m. ( h ) A box-and-whisker plot showing the number of  γ -H2AX foci per cell described as in  g  cells with control siRNA ( n =328) or  Cdc5L  siRNA ( n =276). Outliers are indicated by open circles, extremes by asterisks
Figure Legend Snippet: Depletion of Cdc5L results in kinetochore-microtubule attachment defects and DNA damage. Synchronized HeLa cells transfected with control or Cdc5L siRNA were treated with MG132 to prevent anaphase onset ( a – d ). Coverslips were chilled on ice for 10 min ( b ) or fixed immediately ( a ) and stained with anti-centromere antibody (ACA; for kinetochores; red), anti- α -tubulin antibody (microtubules; green) and SYTOX Blue nucleic acid stain (for DNA; blue), scale bar, 10  μ m. For spindle checkpoint analysis( c and d ), the cells were stained with anti-Bub1 or BubR1 antibody (green) and ACA (for kinetochores; red), scale bar, 10  μ m. ( e and f ) Quantification of Bub1 and BubR1 levels described as in c and d were analyzed. Bub1 and BubR1 signals were normalized to ACA. For Bub1 quantification, control-knockdown cells ( n =4) and Cdc5L-knockdown cells ( n =10); for BubR1 quantification, control-knockdown cells ( n =7) and Cdc5L-knockdown cells ( n =14). Data are shown as mean±S.D. ( g ) HeLa cells were transfected with control or Cdc5L siRNA, then stained with anti- γ -H2AX antibody (green) and PI (for DNA; red), scale bar, 10  μ m. ( h ) A box-and-whisker plot showing the number of γ -H2AX foci per cell described as in g cells with control siRNA ( n =328) or Cdc5L siRNA ( n =276). Outliers are indicated by open circles, extremes by asterisks

Techniques Used: Transfection, Staining, Whisker Assay

6) Product Images from "Oridonin Enhances Radiation-Induced Cell Death by Promoting DNA Damage in Non-Small Cell Lung Cancer Cells"

Article Title: Oridonin Enhances Radiation-Induced Cell Death by Promoting DNA Damage in Non-Small Cell Lung Cancer Cells

Journal: International Journal of Molecular Sciences

doi: 10.3390/ijms19082378

Histopathological analysis of H460 tumors following combination treatment with oridonin and radiation. Hematoxylin and eosin (H-E) staining and immunohistochemistry for cleaved caspase-3 and γ-H2AX were performed on tumors harvested at 14 days after IR. Representative images of H-E-stained tumors ( upper images ) and cleaved caspase-3- and γ-H2AX-positive cells ( middle images , brown staining) and quantification of cleaved caspase-3 and γ-H2AX-positive staining with six mice in each group ( lower plots , means ± SEM) are shown; * p
Figure Legend Snippet: Histopathological analysis of H460 tumors following combination treatment with oridonin and radiation. Hematoxylin and eosin (H-E) staining and immunohistochemistry for cleaved caspase-3 and γ-H2AX were performed on tumors harvested at 14 days after IR. Representative images of H-E-stained tumors ( upper images ) and cleaved caspase-3- and γ-H2AX-positive cells ( middle images , brown staining) and quantification of cleaved caspase-3 and γ-H2AX-positive staining with six mice in each group ( lower plots , means ± SEM) are shown; * p

Techniques Used: Staining, Immunohistochemistry, Mouse Assay

Related Articles

Staining:

Article Title: Targeting integrins with RGD-conjugated gold nanoparticles in radiotherapy decreases the invasive activity of breast cancer cells
Article Snippet: .. The following primary antibodies were used for immunofluorescence staining: anti-α5-integrin (Cell Signaling Technology), anti-αv-integrin (Cell Signaling Technology), anti-LAMP1 (Cell Signaling Technology), anti-EEA1 (Cell Signaling Technology), anti-Rab5 (Cell Signaling Technology), anti-Rab7 (Cell Signaling Technology), anti-Rab9 (Cell Signaling Technology) and anti-γ-H2AX (Merck Millipore). .. Cell viability assay Cell viability and cytotoxicity were examined by the Cell Counting Kit-8 (CCK-8; Dojindo, Kumamoto, Japan) and cell counting.

Incubation:

Article Title: Oridonin Enhances Radiation-Induced Cell Death by Promoting DNA Damage in Non-Small Cell Lung Cancer Cells
Article Snippet: .. The sections were incubated with anti-cleaved caspase-3 (1:100, #9661, Cell Signaling Technology, Inc.), anti-γ-H2AX (1:100, 05-636, Merck KGaA), or anti-Ki-67 (1:200, DRM004, Acris Antibodies, Herford, Germany) antibodies at 4 °C overnight and then washed with PBS containing 0.05% Triton X-100. .. The sections were incubated with horseradish peroxidase-conjugated secondary antibody for 30 min and counterstained with hematoxylin.

other:

Article Title: BRG1 Promotes chromatin remodeling around DNA damage sites
Article Snippet: Anti-γ H2AX (05-636) and anti-H2A (07-146) antibodies were obtained from Merck Millipore (CA).

Immunofluorescence:

Article Title: Targeting integrins with RGD-conjugated gold nanoparticles in radiotherapy decreases the invasive activity of breast cancer cells
Article Snippet: .. The following primary antibodies were used for immunofluorescence staining: anti-α5-integrin (Cell Signaling Technology), anti-αv-integrin (Cell Signaling Technology), anti-LAMP1 (Cell Signaling Technology), anti-EEA1 (Cell Signaling Technology), anti-Rab5 (Cell Signaling Technology), anti-Rab7 (Cell Signaling Technology), anti-Rab9 (Cell Signaling Technology) and anti-γ-H2AX (Merck Millipore). .. Cell viability assay Cell viability and cytotoxicity were examined by the Cell Counting Kit-8 (CCK-8; Dojindo, Kumamoto, Japan) and cell counting.

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  • 92
    Merck KGaA anti γ h2ax antibody
    Induction of <t>γ-H2AX</t> following Olaparib treatment. Induction of γ-H2AX foci was assessed 24 48 hrs after treatment with 10 μM Olaparib. γ-H2AX levels were quantified using flow cytometry and are depicted as Mean Fluorescent Intensity (MFI) normalised to vehicle for each cell line. Data are representative of at least 3 independent experiments (ANOVA and Tukey post test, * P
    Anti γ H2ax Antibody, supplied by Merck KGaA, used in various techniques. Bioz Stars score: 92/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti γ h2ax antibody/product/Merck KGaA
    Average 92 stars, based on 2 article reviews
    Price from $9.99 to $1999.99
    anti γ h2ax antibody - by Bioz Stars, 2020-09
    92/100 stars
      Buy from Supplier

    88
    Merck KGaA monoclonal antibodies against γ h2ax
    The yield of <t>γ-H2AX</t> foci in Chinese hamster V79 cells exposed to γ-rays at high (400 mGy/min), medium (10 mGy/min) and low (1 mGy/min) dose rates.
    Monoclonal Antibodies Against γ H2ax, supplied by Merck KGaA, used in various techniques. Bioz Stars score: 88/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/monoclonal antibodies against γ h2ax/product/Merck KGaA
    Average 88 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    monoclonal antibodies against γ h2ax - by Bioz Stars, 2020-09
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    88
    Merck KGaA monoclonal anti s139 γ h2ax
    Nuclear delocalization of pS27-Ku70 following irradiation stress A. In situ immunofluorescence monitoring of pS27-Ku70 and pS2056-DNA-PKcs in resistant CLL cells left untreated (NT) or at 30min after a 10 Gy dose of IR. Nuclei were counterstained with Hoechst 33342. B. Simultaneous immunofluorescence labeling was proceeded following prextraction/RNase treatment procedure described in Method section. ZR75.1 cell line was irradiated at 4 Gy and following 30min of post-irradiation culture, simulataneusly labelled with anti-pS27-Ku70 (red) and <t>anti-γ-H2AX</t> (green). Hoechst H33342 was used for chromosomal DNA staining.
    Monoclonal Anti S139 γ H2ax, supplied by Merck KGaA, used in various techniques. Bioz Stars score: 88/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/monoclonal anti s139 γ h2ax/product/Merck KGaA
    Average 88 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    monoclonal anti s139 γ h2ax - by Bioz Stars, 2020-09
    88/100 stars
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    90
    Merck KGaA mouse monoclonal anti γ h2ax antibody
    TERT inhibition by BIBR increases DNA damage in TERT-positive cells. ( a ) TERT-positive 4134/Late, 4134/TERT+, BL41 and BL41/B95.8 cells and TERT-negative 4134/TERT- and U2OS cells exposed for 24 h to BIBR or to DMSO as control, were stained with <t>γ</t> H2AX to evaluate DNA damage and analyzed by flow cytometry. Panels from one representative experiment are shown. ( b ) Levels of γ H2AX MFI in BIBR- and DMSO-treated cells. Significant differences between values in BIBR-treated versus DMSO-treated cells are shown: * P
    Mouse Monoclonal Anti γ H2ax Antibody, supplied by Merck KGaA, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mouse monoclonal anti γ h2ax antibody/product/Merck KGaA
    Average 90 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    mouse monoclonal anti γ h2ax antibody - by Bioz Stars, 2020-09
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    Image Search Results


    Induction of γ-H2AX following Olaparib treatment. Induction of γ-H2AX foci was assessed 24 48 hrs after treatment with 10 μM Olaparib. γ-H2AX levels were quantified using flow cytometry and are depicted as Mean Fluorescent Intensity (MFI) normalised to vehicle for each cell line. Data are representative of at least 3 independent experiments (ANOVA and Tukey post test, * P

    Journal: PLoS ONE

    Article Title: Sensitivity to inhibition of DNA repair by Olaparib in novel oropharyngeal cancer cell lines infected with Human Papillomavirus

    doi: 10.1371/journal.pone.0207934

    Figure Lengend Snippet: Induction of γ-H2AX following Olaparib treatment. Induction of γ-H2AX foci was assessed 24 48 hrs after treatment with 10 μM Olaparib. γ-H2AX levels were quantified using flow cytometry and are depicted as Mean Fluorescent Intensity (MFI) normalised to vehicle for each cell line. Data are representative of at least 3 independent experiments (ANOVA and Tukey post test, * P

    Article Snippet: Cell cycle and γ-H2AX Cell cycle distribution and levels of γ-H2AX (to quantify DNA DSB) were determined in prepared nuclei by flow cytometry using DAPI (Sigma-Aldrich, UK) and anti-γ-H2AX antibody (clone JBW301) fluorescein isothiocyanate (FITC) conjugate (Merck-Millipore, Watford, UK; catalogue 16-202A) using published methodology [ ].

    Techniques: Flow Cytometry, Cytometry

    The yield of γ-H2AX foci in Chinese hamster V79 cells exposed to γ-rays at high (400 mGy/min), medium (10 mGy/min) and low (1 mGy/min) dose rates.

    Journal: International Journal of Molecular Sciences

    Article Title: Changes in the Number of Double-Strand DNA Breaks in Chinese Hamster V79 Cells Exposed to ?-Radiation with Different Dose Rates

    doi: 10.3390/ijms140713719

    Figure Lengend Snippet: The yield of γ-H2AX foci in Chinese hamster V79 cells exposed to γ-rays at high (400 mGy/min), medium (10 mGy/min) and low (1 mGy/min) dose rates.

    Article Snippet: Slides were incubated with monoclonal antibodies against γ-H2AX (Anti-phospho-Histone H2AX Rabbit Monoclonal, Merck-Millipore, Darmstadt, Germany) at 4 °C over night.

    Techniques:

    Nuclear delocalization of pS27-Ku70 following irradiation stress A. In situ immunofluorescence monitoring of pS27-Ku70 and pS2056-DNA-PKcs in resistant CLL cells left untreated (NT) or at 30min after a 10 Gy dose of IR. Nuclei were counterstained with Hoechst 33342. B. Simultaneous immunofluorescence labeling was proceeded following prextraction/RNase treatment procedure described in Method section. ZR75.1 cell line was irradiated at 4 Gy and following 30min of post-irradiation culture, simulataneusly labelled with anti-pS27-Ku70 (red) and anti-γ-H2AX (green). Hoechst H33342 was used for chromosomal DNA staining.

    Journal: Oncotarget

    Article Title: A new phosphorylated form of Ku70 identified in resistant leukemic cells confers fast but unfaithful dna repair in cancer cell lines

    doi:

    Figure Lengend Snippet: Nuclear delocalization of pS27-Ku70 following irradiation stress A. In situ immunofluorescence monitoring of pS27-Ku70 and pS2056-DNA-PKcs in resistant CLL cells left untreated (NT) or at 30min after a 10 Gy dose of IR. Nuclei were counterstained with Hoechst 33342. B. Simultaneous immunofluorescence labeling was proceeded following prextraction/RNase treatment procedure described in Method section. ZR75.1 cell line was irradiated at 4 Gy and following 30min of post-irradiation culture, simulataneusly labelled with anti-pS27-Ku70 (red) and anti-γ-H2AX (green). Hoechst H33342 was used for chromosomal DNA staining.

    Article Snippet: Monoclonal anti-S139-γ-H2AX (clone JBW103) antibody was from Upstate (Merck-Millipore, France).

    Techniques: Irradiation, In Situ, Immunofluorescence, Labeling, Staining

    Function of the phosphorylated form of Ku70 in cell cycle checkpoint control, DNA repair and genomic stability ZR75.1 breast cancer cells express either wt-Ku70 (S27-S33-Ku70) or mutated Ku70 (A27-A33-K70 or E27-E33-Ku70). A. pS27-Ku70 expression was monitored using a pS27-Ku70 antibody. B. The cell cycle was assayed at different timepoints after IR (4Gy) in S27-S33-Ku70- (blue) and A27-A33-Ku70- (red) expressing cells E27-E33-Ku70 expressing cells shown cell cycle profile similar to S27-S33-Ku70 (not shown). The cell cycle profiles shown are of untreated cells (a), and of post-irradiated cells at 12 h (b), 24 h (c) and 48 h (d). C. Cell incorporation of ethynyl deoxyuridine (EdU) in S phase. Untreated (NT) or 12 h post-irradiated (4Gy) cells are shown. Cells expressed S27-S33-Ku70 (a, b) or A27-A33-Ku70 (c, d). D. Role of phospho-Ku70 in cell growth and proliferation following irradiation stress. The cell index (i.e. cell growth, proliferation and membrane potential) following IR (4 Gy) was defined using an xCELLigence® living cells’ real-time follow-up system (see Methods section). Full lines represent untreated cells and dashed lines indicate irradiated cells. A27-A33-Ku70- (red), S27-S33-Ku70- (blue) and E27-E33-Ku70- (green) expressing cells were evaluated. The cell index is given in arbitrary units (AU). E. Western blot analysis of γ-H2AX protein level following 2Gy irradiation. Cells expressing S27-S33-Ku70, A27-A33-Ku70 were untreated (NT) or harvested after indicated time post-irradiation. After PAGE of total protein extracts and transfer, the membranes were probed with anti-phospho-S139-H2AX and anti-β-actin antibodies. F. Kinetic of DNA damage-induced γ-H2AX, foci formation in untreated (NT) or irradiated (2Gy) cells expressing wild-type S27-S33-Ku70, mutated A27-A33-Ku70 or E27-E33-Ku70 at indicated time post-irradiation. G. γ-H2AX immunostaining results were analyzed in untreated and post-irradiated cells at the indicated timepoints in A27-A33-Ku70- (red), S27-S33-Ku70- (blue) and E27-E33-Ku70- (green) expressing cells. Cells exhibiting at least 5 foci per nuclei were included in this analysis. Counts were performed on at least 200 cells per condition and results are depicted as box plot distribution values [minimum (min), maximum (max), median, 25th and 75th percentiles (25th and 75th perc.)] of the number of foci obtained for each tested condition. Statistical analysis: a Wilcoxon rank test was performed. *** p

    Journal: Oncotarget

    Article Title: A new phosphorylated form of Ku70 identified in resistant leukemic cells confers fast but unfaithful dna repair in cancer cell lines

    doi:

    Figure Lengend Snippet: Function of the phosphorylated form of Ku70 in cell cycle checkpoint control, DNA repair and genomic stability ZR75.1 breast cancer cells express either wt-Ku70 (S27-S33-Ku70) or mutated Ku70 (A27-A33-K70 or E27-E33-Ku70). A. pS27-Ku70 expression was monitored using a pS27-Ku70 antibody. B. The cell cycle was assayed at different timepoints after IR (4Gy) in S27-S33-Ku70- (blue) and A27-A33-Ku70- (red) expressing cells E27-E33-Ku70 expressing cells shown cell cycle profile similar to S27-S33-Ku70 (not shown). The cell cycle profiles shown are of untreated cells (a), and of post-irradiated cells at 12 h (b), 24 h (c) and 48 h (d). C. Cell incorporation of ethynyl deoxyuridine (EdU) in S phase. Untreated (NT) or 12 h post-irradiated (4Gy) cells are shown. Cells expressed S27-S33-Ku70 (a, b) or A27-A33-Ku70 (c, d). D. Role of phospho-Ku70 in cell growth and proliferation following irradiation stress. The cell index (i.e. cell growth, proliferation and membrane potential) following IR (4 Gy) was defined using an xCELLigence® living cells’ real-time follow-up system (see Methods section). Full lines represent untreated cells and dashed lines indicate irradiated cells. A27-A33-Ku70- (red), S27-S33-Ku70- (blue) and E27-E33-Ku70- (green) expressing cells were evaluated. The cell index is given in arbitrary units (AU). E. Western blot analysis of γ-H2AX protein level following 2Gy irradiation. Cells expressing S27-S33-Ku70, A27-A33-Ku70 were untreated (NT) or harvested after indicated time post-irradiation. After PAGE of total protein extracts and transfer, the membranes were probed with anti-phospho-S139-H2AX and anti-β-actin antibodies. F. Kinetic of DNA damage-induced γ-H2AX, foci formation in untreated (NT) or irradiated (2Gy) cells expressing wild-type S27-S33-Ku70, mutated A27-A33-Ku70 or E27-E33-Ku70 at indicated time post-irradiation. G. γ-H2AX immunostaining results were analyzed in untreated and post-irradiated cells at the indicated timepoints in A27-A33-Ku70- (red), S27-S33-Ku70- (blue) and E27-E33-Ku70- (green) expressing cells. Cells exhibiting at least 5 foci per nuclei were included in this analysis. Counts were performed on at least 200 cells per condition and results are depicted as box plot distribution values [minimum (min), maximum (max), median, 25th and 75th percentiles (25th and 75th perc.)] of the number of foci obtained for each tested condition. Statistical analysis: a Wilcoxon rank test was performed. *** p

    Article Snippet: Monoclonal anti-S139-γ-H2AX (clone JBW103) antibody was from Upstate (Merck-Millipore, France).

    Techniques: Expressing, Irradiation, Western Blot, Polyacrylamide Gel Electrophoresis, Immunostaining

    TERT inhibition by BIBR increases DNA damage in TERT-positive cells. ( a ) TERT-positive 4134/Late, 4134/TERT+, BL41 and BL41/B95.8 cells and TERT-negative 4134/TERT- and U2OS cells exposed for 24 h to BIBR or to DMSO as control, were stained with γ H2AX to evaluate DNA damage and analyzed by flow cytometry. Panels from one representative experiment are shown. ( b ) Levels of γ H2AX MFI in BIBR- and DMSO-treated cells. Significant differences between values in BIBR-treated versus DMSO-treated cells are shown: * P

    Journal: Cell Death & Disease

    Article Title: Short-term inhibition of TERT induces telomere length-independent cell cycle arrest and apoptotic response in EBV-immortalized and transformed B cells

    doi: 10.1038/cddis.2016.425

    Figure Lengend Snippet: TERT inhibition by BIBR increases DNA damage in TERT-positive cells. ( a ) TERT-positive 4134/Late, 4134/TERT+, BL41 and BL41/B95.8 cells and TERT-negative 4134/TERT- and U2OS cells exposed for 24 h to BIBR or to DMSO as control, were stained with γ H2AX to evaluate DNA damage and analyzed by flow cytometry. Panels from one representative experiment are shown. ( b ) Levels of γ H2AX MFI in BIBR- and DMSO-treated cells. Significant differences between values in BIBR-treated versus DMSO-treated cells are shown: * P

    Article Snippet: To visualize DNA damage foci, slides were incubated for 1 h with a mouse monoclonal anti-γ H2AX antibody (1 : 1000, Merck Millipore, Darmstadt, Germany) in PBG buffer, followed by Alexa Fluor 488 anti-mouse secondary antibody (Thermo Fisher Scientific) in PBG buffer.

    Techniques: Inhibition, Staining, Flow Cytometry, Cytometry