Review

total atm antibody #2873 (Cell Signaling Technology Inc)

Cell Signaling Technology Inc is a verified supplier

Cell Signaling Technology Inc manufactures this product

About

News

Press Release

Team

Advisors

Partners

Contact

Bioz Stars

Bioz vStars

Buy from Supplier

Structured Review

Cell Signaling Technology Inc total atm antibody #2873

BCAT1–depletion induces a dysfunctional DNA damage response following etoposide treatment. ( A ) Schematic representations of the plasmids encoding full-length (WT) and truncation mutants of XRCC6 (top). vWA: von Willebrand A domain; SAP: SAF-A/B, Acinus, and PIAS domain. HEK 293T cells stably expressing epitope-tagged BCAT1 were transfected with the indicated plasmid. Cell lysates were subjected to IP with anti-FLAG beads followed by immunoblot analysis with the indicated antibodies. The arrows indicate expected positions of the respective proteins, and asterisks (*) indicate non–specific bands. ( B ) Schematic representations of the plasmids encoding full-length (WT) and truncation mutants of BCAT1 (top). N: Branched–chain amino acid aminotransferase-like N-terminal domain; AT–IV: aminotransferase class IV domain; C: Branched-chain amino acid aminotransferase-like C–terminal domain. HEK 293T cells were transfected with HA–tagged XRCC6 and the indicated BCAT1 mutant plasmids. Cell lysates were subjected to IP with anti-HA beads followed by immunoblot analysis with the indicated antibodies. The arrows indicate expected positions of the respective proteins, and asterisks (*) indicate non-specific bands. ( C – E ) CCRF–CEM T-ALL cells transduced with shCTRL or sh BCAT1 were treated with 1 µM etoposide for the indicated time. Subsequently, whole cell lysates were collected and analyzed by immunoblotting for proteins implicated in ( C , D ) the activation of the DNA damage response (pDNA-PKcs, pATM, <t>pCHK1,</t> pCHK2, pTP53); ( E ) DNA damage (γH2AX) and apoptosis (cleaved PARP-1). Total DNA–PKcs and ATM are shown as loading controls ( C ). Total CHK2, total TP53, and GADPH are shown as loading controls ( D , E ). Phospho-protein/protein ratios are shown (top) in each panel. A graphical representation of the phospho-protein/protein ratios is also shown for selected proteins (right panels).

Total Atm Antibody #2873, supplied by Cell Signaling Technology Inc, 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/product/atm(total)+2873/atm+2873+antibody/pmc11676169-149-49-69
Average 90 stars, based on 1 article reviews

total atm antibody #2873 - by Bioz Stars, 2026-09

90/100 stars

Images

1) Product Images from "BCAT1 Associates with DNA Repair Proteins KU70 and KU80 and Contributes to Regulate DNA Repair in T-Cell Acute Lymphoblastic Leukemia (T-ALL)"

Article Title: BCAT1 Associates with DNA Repair Proteins KU70 and KU80 and Contributes to Regulate DNA Repair in T-Cell Acute Lymphoblastic Leukemia (T-ALL)

Journal: International Journal of Molecular Sciences

doi: 10.3390/ijms252413571

Figure Legend Snippet: BCAT1–depletion induces a dysfunctional DNA damage response following etoposide treatment. ( A ) Schematic representations of the plasmids encoding full-length (WT) and truncation mutants of XRCC6 (top). vWA: von Willebrand A domain; SAP: SAF-A/B, Acinus, and PIAS domain. HEK 293T cells stably expressing epitope-tagged BCAT1 were transfected with the indicated plasmid. Cell lysates were subjected to IP with anti-FLAG beads followed by immunoblot analysis with the indicated antibodies. The arrows indicate expected positions of the respective proteins, and asterisks (*) indicate non–specific bands. ( B ) Schematic representations of the plasmids encoding full-length (WT) and truncation mutants of BCAT1 (top). N: Branched–chain amino acid aminotransferase-like N-terminal domain; AT–IV: aminotransferase class IV domain; C: Branched-chain amino acid aminotransferase-like C–terminal domain. HEK 293T cells were transfected with HA–tagged XRCC6 and the indicated BCAT1 mutant plasmids. Cell lysates were subjected to IP with anti-HA beads followed by immunoblot analysis with the indicated antibodies. The arrows indicate expected positions of the respective proteins, and asterisks (*) indicate non-specific bands. ( C – E ) CCRF–CEM T-ALL cells transduced with shCTRL or sh BCAT1 were treated with 1 µM etoposide for the indicated time. Subsequently, whole cell lysates were collected and analyzed by immunoblotting for proteins implicated in ( C , D ) the activation of the DNA damage response (pDNA-PKcs, pATM, pCHK1, pCHK2, pTP53); ( E ) DNA damage (γH2AX) and apoptosis (cleaved PARP-1). Total DNA–PKcs and ATM are shown as loading controls ( C ). Total CHK2, total TP53, and GADPH are shown as loading controls ( D , E ). Phospho-protein/protein ratios are shown (top) in each panel. A graphical representation of the phospho-protein/protein ratios is also shown for selected proteins (right panels).

Techniques Used: Stable Transfection, Expressing, Transfection, Plasmid Preparation, Western Blot, Mutagenesis, Transduction, Activation Assay

Western Blot:

Article Title: Platinum-Induced Ubiquitination of Phosphorylated H2AX by RING1A is Mediated by Replication Protein A in Ovarian Cancer
Article Snippet: This media with lentiviral particles harvested on day 4 and day 5 was filtered using 0.45 μm filter and concentrated using Spin-X concentrator (Corning, #431490). .. Antibodies For western blot of endogenous proteins, anti-γH2AX (Cell Signaling Technology (CST), MA #9718, 1:1000), anti-Actin B (CST, MA #4970, 1:1000), anti-p-ATM S1981 (CST, MA #13050, 1:1000), anti-total ATM (CST, MA #2873, 1:1000), anti-total H2AX (CST, MA #2595, 1:1000), anti-RING1A (CST, MA #13069, 1:1000), anti-RING1B (Santa Cruz (SC), CA sc-101109, 1:1000), anti-H2AK119ub1 (CST, MA #8240,1:1000), anti-XPC (SC, CA sc-74410, 1:1000), anti-lamin B (SC, CA sc-6216, 1:1000; SC, CA sc-374015, 1:1000), anti-XPA (SC, CA sc-28353, 1:1000), anti-pRPA32 S33 (Bethyl Laboratories, TX A300–246A-M, 1:1000), anti-RPA32 (CST, MA #2208,1:1000), anti-phospho-Chk1 S345 (CST, MA #2348, 1:1000) and anti-total Chk1 (CST, MA #2360, 1:1000) antibodies were used. .. For immunofluorescence, anti- γH2AX (CST,MA #9718, 1:100), anti-RING1A (Abcam, CA ab175149, 1:100), anti-RPA32 (CST, MA #2208, 1:100), anti-Rad51 (Novus biological, CO NB100–148, 1:100), anti-H2AK119ub1 (Millipore Sigma, MA 05–678,1:100) and secondary Alexa Conjugate (CST, MA rat #4416, 1:1000, mouse #8890, 1:500, rabbit #4412, 1:1000 and, rabbit #8889,1:500) antibodies were used.

Article Title: Platinum-Induced Ubiquitination of Phosphorylated H2AX by RING1A Is Mediated by Replication Protein A in Ovarian Cancer
Article Snippet: This media with lentiviral particles harvested on day 4 and day 5 was filtered using 0.45 μm filter and concentrated using Spin-X concentrator (Corning, #431490). .. For western blot of endogenous proteins, anti-H2AX (Cell Signaling Technology (CST), MA #9718, 1:1000), anti-Actin B (CST, MA #4970, 1:1000), anti-p-ATM S1981 (CST, MA #13050, 1:1000), anti-total ATM (CST, MA #2873, 1:1000), anti-total H2AX (CST, MA #2595, 1:1000), anti-RING1A (CST, MA #13069, 1:1000), anti-RING1B (Santa Cruz (SC), CA sc-101109, 1:1000), anti-H2AK119ub1 (CST, MA #8240,1:1000), antiXPC ( SC, CA sc-74410, 1:1000), anti-lamin B (SC, CA sc-6216, 1:1000 ; SC, CA sc374015, 1:1000), anti-XPA (SC, CA sc-28353, 1:1000), anti-pRPA32 S33 (Bethyl Laboratories, TX A300-246A-M, 1:1000), anti-RPA32 (CST, MA #2208,1:1000), antiphospho-Chk1 S345 (CST, MA #2348, 1:1000) and anti-total Chk1 (CST, MA #2360, 1:1000) antibodies were used. .. For immunofluorescence, anti- H2AX (CST,MA #9718, on August 18, 2020.

Article Title: Platinum-Induced Ubiquitination of Phosphorylated H2AX by RING1A is Mediated by Replication Protein A in Ovarian Cancer
Article Snippet: This media with lentiviral particles harvested on day 4 and day 5 was filtered using 0.45 μm filter and concentrated using Spin-X concentrator (Corning, #431490). .. For western blot of endogenous proteins, anti-γH2AX (Cell Signaling Technology (CST), MA #9718, 1:1000), anti-Actin B (CST, MA #4970, 1:1000), anti-p-ATM S1981 (CST, MA #13050, 1:1000), anti-total ATM (CST, MA #2873, 1:1000), anti-total H2AX (CST, MA #2595, 1:1000), anti-RING1A (CST, MA #13069, 1:1000), anti-RING1B (Santa Cruz (SC), CA sc-101109, 1:1000), anti-H2AK119ub1 (CST, MA #8240,1:1000), anti-XPC (SC, CA sc-74410, 1:1000), anti-lamin B (SC, CA sc-6216, 1:1000; SC, CA sc-374015, 1:1000), anti-XPA (SC, CA sc-28353, 1:1000), anti-pRPA32 S33 (Bethyl Laboratories, TX A300–246A-M, 1:1000), anti-RPA32 (CST, MA #2208,1:1000), anti-phospho-Chk1 S345 (CST, MA #2348, 1:1000) and anti-total Chk1 (CST, MA #2360, 1:1000) antibodies were used. .. For immunofluorescence, anti- γH2AX (CST,MA #9718, 1:100), anti-RING1A (Abcam, CA ab175149, 1:100), anti-RPA32 (CST, MA #2208, 1:100), anti-Rad51 (Novus biological, CO NB100–148, 1:100), anti-H2AK119ub1 (Millipore Sigma, MA 05–678,1:100) and secondary Alexa Conjugate (CST, MA rat #4416, 1:1000, mouse #8890, 1:500, rabbit #4412, 1:1000 and, rabbit #8889,1:500) antibodies were used.

other:

Article Title: Net39 protects muscle nuclei from mechanical stress during the pathogenesis of Emery-Dreifuss muscular dystrophy
Article Snippet: The following antibodies were used: GAPDH (MilliporeSigma, MAB374), α-tubulin (MilliporeSigma, T6199), NET39 (MilliporeSigma, HPA070252), MEF2C (Cell Signaling Technology, 5030), MYOD (Santa Cruz Biotechnology Inc., sc-377460), MYOG (Santa Cruz Biotechnology Inc., sc-12732 X), vinculin (VCL) (MilliporeSigma, V9131), HRP-conjugated streptavidin (Thermo Fisher, N100), γH2A.X (MilliporeSigma, 05-636), total ATM (Cell Signaling Technology, 2873T), and phosphorylated ATM (Ser1981) (Santa Cruz Biotechnology Inc., sc-47739).

Article Title: Ku–DNA binding inhibitors modulate the DNA damage response in response to DNA double-strand breaks
Article Snippet: Membranes were blocked for 1 h in 1× TBS with 0.5% Tween and 2% non-fat dried milk and probed with the following primary antibodies against phospho-DNA PKcs (S2056) (Cat: ab124918, Abcam), phospho-DNA PKcs (T2609) (Cat: ab4194, Abcam), total DNA-PKcs (Cat: sc-5282, Santa Cruz Biotechnology), γ-H2AX pS139 (Cat: 613401, BioLegend), phospho-ATM (Ser1981) (Cat: ab81292, Abcam), total ATM (Cat: 2873, Cell Signaling), phospho-p53 (S15) (Cat: 9284 S, Cell signaling), phospho-Chk1 (Ser345) (Cat: 2348, Cell signaling), phospho-Chk2 (Thr68) (Cat: 2661, Cell Signaling) and GAPDH (Cat: MA-15738, Thermo Fisher), diluted in TBST with 2% BSA and 0.02% NaN 3 .

Image Search Results

Journal: International Journal of Molecular Sciences

Article Title: BCAT1 Associates with DNA Repair Proteins KU70 and KU80 and Contributes to Regulate DNA Repair in T-Cell Acute Lymphoblastic Leukemia (T-ALL)

doi: 10.3390/ijms252413571

Figure Lengend Snippet: BCAT1–depletion induces a dysfunctional DNA damage response following etoposide treatment. ( A ) Schematic representations of the plasmids encoding full-length (WT) and truncation mutants of XRCC6 (top). vWA: von Willebrand A domain; SAP: SAF-A/B, Acinus, and PIAS domain. HEK 293T cells stably expressing epitope-tagged BCAT1 were transfected with the indicated plasmid. Cell lysates were subjected to IP with anti-FLAG beads followed by immunoblot analysis with the indicated antibodies. The arrows indicate expected positions of the respective proteins, and asterisks (*) indicate non–specific bands. ( B ) Schematic representations of the plasmids encoding full-length (WT) and truncation mutants of BCAT1 (top). N: Branched–chain amino acid aminotransferase-like N-terminal domain; AT–IV: aminotransferase class IV domain; C: Branched-chain amino acid aminotransferase-like C–terminal domain. HEK 293T cells were transfected with HA–tagged XRCC6 and the indicated BCAT1 mutant plasmids. Cell lysates were subjected to IP with anti-HA beads followed by immunoblot analysis with the indicated antibodies. The arrows indicate expected positions of the respective proteins, and asterisks (*) indicate non-specific bands. ( C – E ) CCRF–CEM T-ALL cells transduced with shCTRL or sh BCAT1 were treated with 1 µM etoposide for the indicated time. Subsequently, whole cell lysates were collected and analyzed by immunoblotting for proteins implicated in ( C , D ) the activation of the DNA damage response (pDNA-PKcs, pATM, pCHK1, pCHK2, pTP53); ( E ) DNA damage (γH2AX) and apoptosis (cleaved PARP-1). Total DNA–PKcs and ATM are shown as loading controls ( C ). Total CHK2, total TP53, and GADPH are shown as loading controls ( D , E ). Phospho-protein/protein ratios are shown (top) in each panel. A graphical representation of the phospho-protein/protein ratios is also shown for selected proteins (right panels).

Article Snippet: Antibodies against tubulin (TU-02; sc-8035), c-myc (9E10; sc-40), and p53 (DO-1; sc-126) were from Santa Cruz Biotechnology (Dallas, TX, USA); antibodies recognizing FLAG epitope (#14793), BCAT1 (#88785), KU-80 (#2180), KU-70 (#4588), phosphorylated H2AX (pS139; #9718), phosphorylated DNA-PKcs (pS2056; #68716), total DNA-PKcs (#12311), phosphorylated ATM (pS1981; #5883), total ATM (#2873), phosphorylated CHK1 (pS345; #2348), phosphorylated CHK2 (pT68; #2197), total CHK2 (#6334), phosphorylated TP53 (pS15; #12571), and GADPH (#5174) were from Cell Signaling Technology (Danvers, MA, USA).

Techniques: Stable Transfection, Expressing, Transfection, Plasmid Preparation, Western Blot, Mutagenesis, Transduction, Activation Assay

Impact of novel Ku–DNA binding inhibitors on the ATM DDR pathway in NSCLC cells. ( A ) Schematic representation of treatments used in this assay. NSCLC cells were pre-incubated with 20 μM Ku-DBi 245 and 1 h 10 μM bleomycin 10 μM NU-7441 or vehicle. Cells were fixed for IF detection 0.25, 0.5, 1 or 6h after treatments were ended, and proteins were extracted for Western blot immunodetection. ( B ) IF staining of ATM p(S1981) (green) and γ-H2AX (pS139) (red) following treatments. Sb: 10 μm. ( C ) Quantification of integrated fluorescence intensity of γH2AX foci and ( D ) ATM (pS1981). Data are presented as the mean and SEM of triplicate determinations. ( E ) H460 cells were pre-treated with 20 μM Ku-DBi 245 or vehicle. DNA damage was induced by bleomycin treatment and cells were processed for immunodetection at 0.5h after treatment was ended. ( F ) Western blot analysis from A549 cells extracts. **** P <0.0001, * P <0.05 as calculated by one-way ANOVA with multiple comparisons test.

Journal: NAR Cancer

Article Title: Ku–DNA binding inhibitors modulate the DNA damage response in response to DNA double-strand breaks

doi: 10.1093/narcan/zcad003

Figure Lengend Snippet: Impact of novel Ku–DNA binding inhibitors on the ATM DDR pathway in NSCLC cells. ( A ) Schematic representation of treatments used in this assay. NSCLC cells were pre-incubated with 20 μM Ku-DBi 245 and 1 h 10 μM bleomycin 10 μM NU-7441 or vehicle. Cells were fixed for IF detection 0.25, 0.5, 1 or 6h after treatments were ended, and proteins were extracted for Western blot immunodetection. ( B ) IF staining of ATM p(S1981) (green) and γ-H2AX (pS139) (red) following treatments. Sb: 10 μm. ( C ) Quantification of integrated fluorescence intensity of γH2AX foci and ( D ) ATM (pS1981). Data are presented as the mean and SEM of triplicate determinations. ( E ) H460 cells were pre-treated with 20 μM Ku-DBi 245 or vehicle. DNA damage was induced by bleomycin treatment and cells were processed for immunodetection at 0.5h after treatment was ended. ( F ) Western blot analysis from A549 cells extracts. **** P <0.0001, * P <0.05 as calculated by one-way ANOVA with multiple comparisons test.

Article Snippet: Membranes were blocked for 1 h in 1× TBS with 0.5% Tween and 2% non-fat dried milk and probed with the following primary antibodies against phospho-DNA PKcs (S2056) (Cat: ab124918, Abcam), phospho-DNA PKcs (T2609) (Cat: ab4194, Abcam), total DNA-PKcs (Cat: sc-5282, Santa Cruz Biotechnology), γ-H2AX pS139 (Cat: 613401, BioLegend), phospho-ATM (Ser1981) (Cat: ab81292, Abcam), total ATM (Cat: 2873, Cell Signaling), phospho-p53 (S15) (Cat: 9284 S, Cell signaling), phospho-Chk1 (Ser345) (Cat: 2348, Cell signaling), phospho-Chk2 (Thr68) (Cat: 2661, Cell Signaling) and GAPDH (Cat: MA-15738, Thermo Fisher), diluted in TBST with 2% BSA and 0.02% NaN 3 .

Techniques: Binding Assay, Incubation, Western Blot, Immunodetection, Staining, Fluorescence

Ku-DBi's differentially impact on NSCLC cell lines carrying different ATM, p53 and BRCA1 genetic status. ( A ) Effect of Ku-DBi 245 as a single agent in cells carrying mutations for ATM, p53 and BRCA1. H460 (ATM wt, p53 wt), A549 (ATM wt, p53 wt) and H1299 (ATM wt, p53 deficient) (i), and H23 (ATM deficient, p53 mutated) or BRCA1 mutation MDA-436 (ATM wt, p53 mutated) (ii) were treated with increasing concentrations Ku-DBi 245 for 72 h and cellular viability was determined by CCK-8 assay. Data are presented as the mean and SEM of triplicate determinations. ( B ) H460, H1299 and H23 cells were treated with 20 μM Ku-DBi or vehicle and increasing concentrations of the AZD0156 ATM inhibitor. Cells were incubated for 72 h and cellular viability was determined by CCK-8 assay. Data are presented as the mean and SEM of triplicate determinations. ( C ) H23 cells were pre-incubated with 20 μM Ku-DBi, 30 nM AZD0156 , 1 μM bleomycin or vehicle or combinations. Cells were incubated for 72 h after which cell viability was determined by CCK-8 assay. Data are presented as the mean and SEM of triplicate determinations. **** P < 0.0001 as calculated by one-way ANOVA with Tukey's multiple comparisons test.

Journal: NAR Cancer

Article Title: Ku–DNA binding inhibitors modulate the DNA damage response in response to DNA double-strand breaks

doi: 10.1093/narcan/zcad003

Figure Lengend Snippet: Ku-DBi's differentially impact on NSCLC cell lines carrying different ATM, p53 and BRCA1 genetic status. ( A ) Effect of Ku-DBi 245 as a single agent in cells carrying mutations for ATM, p53 and BRCA1. H460 (ATM wt, p53 wt), A549 (ATM wt, p53 wt) and H1299 (ATM wt, p53 deficient) (i), and H23 (ATM deficient, p53 mutated) or BRCA1 mutation MDA-436 (ATM wt, p53 mutated) (ii) were treated with increasing concentrations Ku-DBi 245 for 72 h and cellular viability was determined by CCK-8 assay. Data are presented as the mean and SEM of triplicate determinations. ( B ) H460, H1299 and H23 cells were treated with 20 μM Ku-DBi or vehicle and increasing concentrations of the AZD0156 ATM inhibitor. Cells were incubated for 72 h and cellular viability was determined by CCK-8 assay. Data are presented as the mean and SEM of triplicate determinations. ( C ) H23 cells were pre-incubated with 20 μM Ku-DBi, 30 nM AZD0156 , 1 μM bleomycin or vehicle or combinations. Cells were incubated for 72 h after which cell viability was determined by CCK-8 assay. Data are presented as the mean and SEM of triplicate determinations. **** P < 0.0001 as calculated by one-way ANOVA with Tukey's multiple comparisons test.

Techniques: Mutagenesis, CCK-8 Assay, Incubation

Review

total atm antibody #2873 (Cell Signaling Technology Inc)

Structured Review

Images

1) Product Images from "BCAT1 Associates with DNA Repair Proteins KU70 and KU80 and Contributes to Regulate DNA Repair in T-Cell Acute Lymphoblastic Leukemia (T-ALL)"

Related Articles

Western Blot:

other:

Similar Products

Image Search Results