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p chk2 thr68  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc p chk2 thr68
    P Chk2 Thr68, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1461 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/p-chk2+antibody/Phospho-Chk2+(Thr68)+Antibody/pm41912510-363-95-99
    Average 96 stars, based on 1461 article reviews
    p chk2 thr68 - by Bioz Stars, 2026-09
    96/100 stars

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    Related Articles

    Blocking Assay:

    Article Title: Suppression of fumarate hydratase activity increases the efficacy of cisplatin-mediated chemotherapy in gastric cancer.
    Article Snippet: Antibodies specific for the following proteins were used in this study were as follow: p-ATM, p-Chk1, p-Chk2, cleaved-PARP, cleaved-caspase 3, Vinculin (all from Cell Signaling Technology, Beverly, MA, USA), Lamin B1, FH, ATM, Chk1, Chk2, γ-H2AX (all from Abcam, Cambridge, UK), GAPDH (Sigma-Aldrich, St Louis, USA), DNA-PK (Affinity Biosciences, Cincinnati, OH, USA) and Ki-67 (Zhongshan Golden Bridge Biotech, Beijing, China).

    Article Title: ARID1A Deficiency Impairs the DNA Damage Checkpoint and Sensitizes Cells to PARP Inhibitors
    Article Snippet: Anti-ATRIP (1:1,000), p-ATM (1:500), p-Chk1 (1:500), p-Chk2 (1:500), GFP (1:1,000) and p-H3 (1:500) were purchased from Cell Signaling Technology.

    Article Title: Potential role of PRKCSH in lung cancer: bioinformatics analysis and a case study of Nano ZnO.
    Article Snippet: PRKCSH defi ciency promoted G2/M arrest in response to zinc oxide nanoparticle (Nano ZnO) treatment in lung cancer cells.. With regard to the mechanism, PRKCSH defi ciency may induce STAT6 translocation to the nucleus to activate p53 expression.. Activated p53 contributed to Nano-ZnOinduced G2/M arrest in lung cancer cells.

    Article Title: Sirt3 Promoted DNA Damage Repair and Radioresistance Through ATM-Chk2 in Non-small Cell Lung Cancer Cells
    Article Snippet: The proteins were incubated with Sirt3 (1:1000), p-ATM (1:1000), p-ATR (1:1000), p-Chk1 (1:1000), p-Chk2 (1:1000), γ-H2AX (1:1000) and β-tublin (1:1000) (Cell Signal Tech, Danvers, MA, USA) at 4°C overnight in a shaker incubator.

    Article Title: Natural bioactive gallic acid shows potential anticancer effects by inhibiting the proliferation and invasiveness behavior in human embryonic carcinoma cells
    Article Snippet: Cell Signaling Technology, Inc. supplied: p27 Kip1 (cat. no. 3686), p-EGFR (cat. no. 3777), EGFR (cat. no. 4267), phosphorylated (p-)JAK2 (cat. no. 3776), JAK2 (cat. no. 3230), p-STAT5 (cat. no. 9351), pCHK1 (cat. no. 2348), p-CHK2 (cat. no. 2197), p-ATM (cat. no. 5883), p-Histone (cat. no. 9718) and p-BRCA1 (cat. no. 9009).

    Article Title: Sirt3 Promoted DNA Damage Repair and Radioresistance Through ATM-Chk2 in Non-small Cell Lung Cancer Cells
    Article Snippet: At indicated time points, lung tissues were isolated and subjected to sectioning, then the samples were stained with H&E, terminal transferase-mediated dUTP nick end labeling (TUNEL), Ki67 (1:400), Sirt3 (1:200), p-ATM (1:100), p-Chk2 (1:200), and γ-H2AX (1:200) (Cell Signal Tech, Danvers, MA, USA) staining.

    Article Title: Inactivation of the ATMIN/ATM pathway protects against glioblastoma formation
    Article Snippet: The following antibodies were used: p53, Pdgfra, p-Pdgfra, p-Chk2, p-Akt, Akt (all Cell Signaling); Myc-9E10 (CRUK); Smc1 (Abcam); p-Smc1, Chk2, Tubulin (all Merck); p-Kap1, Kap1 (both Bethyl Labs); Atm (Santa Cruz), p-Atm (Epitomics), p-p53, Actin, GAPDH, HRP-conjugated goat anti-mouse/rabbit IgG (all Sigma).

    Article Title: FTO regulates osteoclast development by modulating the proliferation and apoptosis of osteoclast precursors in inflammatory conditions.
    Article Snippet: Periodontitis is an oral inflammatory disease that causes alveolar bone destruction by activating osteoclast.. FTO, a crucial demethylase of N6-methyladenosine(m6A), exerts essential function in maintaining bone homeostasis.. However, the effects of FTO on periodontitis-related bone destruction remain unknown.

    Incubation:

    Article Title: Suppression of fumarate hydratase activity increases the efficacy of cisplatin-mediated chemotherapy in gastric cancer.
    Article Snippet: Antibodies specific for the following proteins were used in this study were as follow: p-ATM, p-Chk1, p-Chk2, cleaved-PARP, cleaved-caspase 3, Vinculin (all from Cell Signaling Technology, Beverly, MA, USA), Lamin B1, FH, ATM, Chk1, Chk2, γ-H2AX (all from Abcam, Cambridge, UK), GAPDH (Sigma-Aldrich, St Louis, USA), DNA-PK (Affinity Biosciences, Cincinnati, OH, USA) and Ki-67 (Zhongshan Golden Bridge Biotech, Beijing, China).

    Article Title: ARID1A Deficiency Impairs the DNA Damage Checkpoint and Sensitizes Cells to PARP Inhibitors
    Article Snippet: Anti-ATRIP (1:1,000), p-ATM (1:500), p-Chk1 (1:500), p-Chk2 (1:500), GFP (1:1,000) and p-H3 (1:500) were purchased from Cell Signaling Technology.

    Article Title: Potential role of PRKCSH in lung cancer: bioinformatics analysis and a case study of Nano ZnO.
    Article Snippet: PRKCSH defi ciency promoted G2/M arrest in response to zinc oxide nanoparticle (Nano ZnO) treatment in lung cancer cells.. With regard to the mechanism, PRKCSH defi ciency may induce STAT6 translocation to the nucleus to activate p53 expression.. Activated p53 contributed to Nano-ZnOinduced G2/M arrest in lung cancer cells.

    Article Title: Sirt3 Promoted DNA Damage Repair and Radioresistance Through ATM-Chk2 in Non-small Cell Lung Cancer Cells
    Article Snippet: The proteins were incubated with Sirt3 (1:1000), p-ATM (1:1000), p-ATR (1:1000), p-Chk1 (1:1000), p-Chk2 (1:1000), γ-H2AX (1:1000) and β-tublin (1:1000) (Cell Signal Tech, Danvers, MA, USA) at 4°C overnight in a shaker incubator.

    Article Title: Natural bioactive gallic acid shows potential anticancer effects by inhibiting the proliferation and invasiveness behavior in human embryonic carcinoma cells
    Article Snippet: Cell Signaling Technology, Inc. supplied: p27 Kip1 (cat. no. 3686), p-EGFR (cat. no. 3777), EGFR (cat. no. 4267), phosphorylated (p-)JAK2 (cat. no. 3776), JAK2 (cat. no. 3230), p-STAT5 (cat. no. 9351), pCHK1 (cat. no. 2348), p-CHK2 (cat. no. 2197), p-ATM (cat. no. 5883), p-Histone (cat. no. 9718) and p-BRCA1 (cat. no. 9009).

    Article Title: Sirt3 Promoted DNA Damage Repair and Radioresistance Through ATM-Chk2 in Non-small Cell Lung Cancer Cells
    Article Snippet: At indicated time points, lung tissues were isolated and subjected to sectioning, then the samples were stained with H&E, terminal transferase-mediated dUTP nick end labeling (TUNEL), Ki67 (1:400), Sirt3 (1:200), p-ATM (1:100), p-Chk2 (1:200), and γ-H2AX (1:200) (Cell Signal Tech, Danvers, MA, USA) staining.

    Article Title: Inactivation of the ATMIN/ATM pathway protects against glioblastoma formation
    Article Snippet: The following antibodies were used: p53, Pdgfra, p-Pdgfra, p-Chk2, p-Akt, Akt (all Cell Signaling); Myc-9E10 (CRUK); Smc1 (Abcam); p-Smc1, Chk2, Tubulin (all Merck); p-Kap1, Kap1 (both Bethyl Labs); Atm (Santa Cruz), p-Atm (Epitomics), p-p53, Actin, GAPDH, HRP-conjugated goat anti-mouse/rabbit IgG (all Sigma).

    Article Title: FTO regulates osteoclast development by modulating the proliferation and apoptosis of osteoclast precursors in inflammatory conditions.
    Article Snippet: Periodontitis is an oral inflammatory disease that causes alveolar bone destruction by activating osteoclast.. FTO, a crucial demethylase of N6-methyladenosine(m6A), exerts essential function in maintaining bone homeostasis.. However, the effects of FTO on periodontitis-related bone destruction remain unknown.

    Isolation:

    Article Title: Suppression of fumarate hydratase activity increases the efficacy of cisplatin-mediated chemotherapy in gastric cancer.
    Article Snippet: Antibodies specific for the following proteins were used in this study were as follow: p-ATM, p-Chk1, p-Chk2, cleaved-PARP, cleaved-caspase 3, Vinculin (all from Cell Signaling Technology, Beverly, MA, USA), Lamin B1, FH, ATM, Chk1, Chk2, γ-H2AX (all from Abcam, Cambridge, UK), GAPDH (Sigma-Aldrich, St Louis, USA), DNA-PK (Affinity Biosciences, Cincinnati, OH, USA) and Ki-67 (Zhongshan Golden Bridge Biotech, Beijing, China).

    Article Title: ARID1A Deficiency Impairs the DNA Damage Checkpoint and Sensitizes Cells to PARP Inhibitors
    Article Snippet: Anti-ATRIP (1:1,000), p-ATM (1:500), p-Chk1 (1:500), p-Chk2 (1:500), GFP (1:1,000) and p-H3 (1:500) were purchased from Cell Signaling Technology.

    Article Title: Potential role of PRKCSH in lung cancer: bioinformatics analysis and a case study of Nano ZnO.
    Article Snippet: PRKCSH defi ciency promoted G2/M arrest in response to zinc oxide nanoparticle (Nano ZnO) treatment in lung cancer cells.. With regard to the mechanism, PRKCSH defi ciency may induce STAT6 translocation to the nucleus to activate p53 expression.. Activated p53 contributed to Nano-ZnOinduced G2/M arrest in lung cancer cells.

    Article Title: Sirt3 Promoted DNA Damage Repair and Radioresistance Through ATM-Chk2 in Non-small Cell Lung Cancer Cells
    Article Snippet: The proteins were incubated with Sirt3 (1:1000), p-ATM (1:1000), p-ATR (1:1000), p-Chk1 (1:1000), p-Chk2 (1:1000), γ-H2AX (1:1000) and β-tublin (1:1000) (Cell Signal Tech, Danvers, MA, USA) at 4°C overnight in a shaker incubator.

    Article Title: Natural bioactive gallic acid shows potential anticancer effects by inhibiting the proliferation and invasiveness behavior in human embryonic carcinoma cells
    Article Snippet: Cell Signaling Technology, Inc. supplied: p27 Kip1 (cat. no. 3686), p-EGFR (cat. no. 3777), EGFR (cat. no. 4267), phosphorylated (p-)JAK2 (cat. no. 3776), JAK2 (cat. no. 3230), p-STAT5 (cat. no. 9351), pCHK1 (cat. no. 2348), p-CHK2 (cat. no. 2197), p-ATM (cat. no. 5883), p-Histone (cat. no. 9718) and p-BRCA1 (cat. no. 9009).

    Article Title: Sirt3 Promoted DNA Damage Repair and Radioresistance Through ATM-Chk2 in Non-small Cell Lung Cancer Cells
    Article Snippet: At indicated time points, lung tissues were isolated and subjected to sectioning, then the samples were stained with H&E, terminal transferase-mediated dUTP nick end labeling (TUNEL), Ki67 (1:400), Sirt3 (1:200), p-ATM (1:100), p-Chk2 (1:200), and γ-H2AX (1:200) (Cell Signal Tech, Danvers, MA, USA) staining.

    Article Title: Inactivation of the ATMIN/ATM pathway protects against glioblastoma formation
    Article Snippet: The following antibodies were used: p53, Pdgfra, p-Pdgfra, p-Chk2, p-Akt, Akt (all Cell Signaling); Myc-9E10 (CRUK); Smc1 (Abcam); p-Smc1, Chk2, Tubulin (all Merck); p-Kap1, Kap1 (both Bethyl Labs); Atm (Santa Cruz), p-Atm (Epitomics), p-p53, Actin, GAPDH, HRP-conjugated goat anti-mouse/rabbit IgG (all Sigma).

    Article Title: FTO regulates osteoclast development by modulating the proliferation and apoptosis of osteoclast precursors in inflammatory conditions.
    Article Snippet: Periodontitis is an oral inflammatory disease that causes alveolar bone destruction by activating osteoclast.. FTO, a crucial demethylase of N6-methyladenosine(m6A), exerts essential function in maintaining bone homeostasis.. However, the effects of FTO on periodontitis-related bone destruction remain unknown.

    Staining:

    Article Title: Suppression of fumarate hydratase activity increases the efficacy of cisplatin-mediated chemotherapy in gastric cancer.
    Article Snippet: Antibodies specific for the following proteins were used in this study were as follow: p-ATM, p-Chk1, p-Chk2, cleaved-PARP, cleaved-caspase 3, Vinculin (all from Cell Signaling Technology, Beverly, MA, USA), Lamin B1, FH, ATM, Chk1, Chk2, γ-H2AX (all from Abcam, Cambridge, UK), GAPDH (Sigma-Aldrich, St Louis, USA), DNA-PK (Affinity Biosciences, Cincinnati, OH, USA) and Ki-67 (Zhongshan Golden Bridge Biotech, Beijing, China).

    Article Title: ARID1A Deficiency Impairs the DNA Damage Checkpoint and Sensitizes Cells to PARP Inhibitors
    Article Snippet: Anti-ATRIP (1:1,000), p-ATM (1:500), p-Chk1 (1:500), p-Chk2 (1:500), GFP (1:1,000) and p-H3 (1:500) were purchased from Cell Signaling Technology.

    Article Title: Potential role of PRKCSH in lung cancer: bioinformatics analysis and a case study of Nano ZnO.
    Article Snippet: PRKCSH defi ciency promoted G2/M arrest in response to zinc oxide nanoparticle (Nano ZnO) treatment in lung cancer cells.. With regard to the mechanism, PRKCSH defi ciency may induce STAT6 translocation to the nucleus to activate p53 expression.. Activated p53 contributed to Nano-ZnOinduced G2/M arrest in lung cancer cells.

    Article Title: Sirt3 Promoted DNA Damage Repair and Radioresistance Through ATM-Chk2 in Non-small Cell Lung Cancer Cells
    Article Snippet: The proteins were incubated with Sirt3 (1:1000), p-ATM (1:1000), p-ATR (1:1000), p-Chk1 (1:1000), p-Chk2 (1:1000), γ-H2AX (1:1000) and β-tublin (1:1000) (Cell Signal Tech, Danvers, MA, USA) at 4°C overnight in a shaker incubator.

    Article Title: Natural bioactive gallic acid shows potential anticancer effects by inhibiting the proliferation and invasiveness behavior in human embryonic carcinoma cells
    Article Snippet: Cell Signaling Technology, Inc. supplied: p27 Kip1 (cat. no. 3686), p-EGFR (cat. no. 3777), EGFR (cat. no. 4267), phosphorylated (p-)JAK2 (cat. no. 3776), JAK2 (cat. no. 3230), p-STAT5 (cat. no. 9351), pCHK1 (cat. no. 2348), p-CHK2 (cat. no. 2197), p-ATM (cat. no. 5883), p-Histone (cat. no. 9718) and p-BRCA1 (cat. no. 9009).

    Article Title: Sirt3 Promoted DNA Damage Repair and Radioresistance Through ATM-Chk2 in Non-small Cell Lung Cancer Cells
    Article Snippet: At indicated time points, lung tissues were isolated and subjected to sectioning, then the samples were stained with H&E, terminal transferase-mediated dUTP nick end labeling (TUNEL), Ki67 (1:400), Sirt3 (1:200), p-ATM (1:100), p-Chk2 (1:200), and γ-H2AX (1:200) (Cell Signal Tech, Danvers, MA, USA) staining.

    Article Title: Inactivation of the ATMIN/ATM pathway protects against glioblastoma formation
    Article Snippet: The following antibodies were used: p53, Pdgfra, p-Pdgfra, p-Chk2, p-Akt, Akt (all Cell Signaling); Myc-9E10 (CRUK); Smc1 (Abcam); p-Smc1, Chk2, Tubulin (all Merck); p-Kap1, Kap1 (both Bethyl Labs); Atm (Santa Cruz), p-Atm (Epitomics), p-p53, Actin, GAPDH, HRP-conjugated goat anti-mouse/rabbit IgG (all Sigma).

    Article Title: FTO regulates osteoclast development by modulating the proliferation and apoptosis of osteoclast precursors in inflammatory conditions.
    Article Snippet: Periodontitis is an oral inflammatory disease that causes alveolar bone destruction by activating osteoclast.. FTO, a crucial demethylase of N6-methyladenosine(m6A), exerts essential function in maintaining bone homeostasis.. However, the effects of FTO on periodontitis-related bone destruction remain unknown.

    End Labeling:

    Article Title: Suppression of fumarate hydratase activity increases the efficacy of cisplatin-mediated chemotherapy in gastric cancer.
    Article Snippet: Antibodies specific for the following proteins were used in this study were as follow: p-ATM, p-Chk1, p-Chk2, cleaved-PARP, cleaved-caspase 3, Vinculin (all from Cell Signaling Technology, Beverly, MA, USA), Lamin B1, FH, ATM, Chk1, Chk2, γ-H2AX (all from Abcam, Cambridge, UK), GAPDH (Sigma-Aldrich, St Louis, USA), DNA-PK (Affinity Biosciences, Cincinnati, OH, USA) and Ki-67 (Zhongshan Golden Bridge Biotech, Beijing, China).

    Article Title: ARID1A Deficiency Impairs the DNA Damage Checkpoint and Sensitizes Cells to PARP Inhibitors
    Article Snippet: Anti-ATRIP (1:1,000), p-ATM (1:500), p-Chk1 (1:500), p-Chk2 (1:500), GFP (1:1,000) and p-H3 (1:500) were purchased from Cell Signaling Technology.

    Article Title: Potential role of PRKCSH in lung cancer: bioinformatics analysis and a case study of Nano ZnO.
    Article Snippet: PRKCSH defi ciency promoted G2/M arrest in response to zinc oxide nanoparticle (Nano ZnO) treatment in lung cancer cells.. With regard to the mechanism, PRKCSH defi ciency may induce STAT6 translocation to the nucleus to activate p53 expression.. Activated p53 contributed to Nano-ZnOinduced G2/M arrest in lung cancer cells.

    Article Title: Sirt3 Promoted DNA Damage Repair and Radioresistance Through ATM-Chk2 in Non-small Cell Lung Cancer Cells
    Article Snippet: The proteins were incubated with Sirt3 (1:1000), p-ATM (1:1000), p-ATR (1:1000), p-Chk1 (1:1000), p-Chk2 (1:1000), γ-H2AX (1:1000) and β-tublin (1:1000) (Cell Signal Tech, Danvers, MA, USA) at 4°C overnight in a shaker incubator.

    Article Title: Natural bioactive gallic acid shows potential anticancer effects by inhibiting the proliferation and invasiveness behavior in human embryonic carcinoma cells
    Article Snippet: Cell Signaling Technology, Inc. supplied: p27 Kip1 (cat. no. 3686), p-EGFR (cat. no. 3777), EGFR (cat. no. 4267), phosphorylated (p-)JAK2 (cat. no. 3776), JAK2 (cat. no. 3230), p-STAT5 (cat. no. 9351), pCHK1 (cat. no. 2348), p-CHK2 (cat. no. 2197), p-ATM (cat. no. 5883), p-Histone (cat. no. 9718) and p-BRCA1 (cat. no. 9009).

    Article Title: Sirt3 Promoted DNA Damage Repair and Radioresistance Through ATM-Chk2 in Non-small Cell Lung Cancer Cells
    Article Snippet: At indicated time points, lung tissues were isolated and subjected to sectioning, then the samples were stained with H&E, terminal transferase-mediated dUTP nick end labeling (TUNEL), Ki67 (1:400), Sirt3 (1:200), p-ATM (1:100), p-Chk2 (1:200), and γ-H2AX (1:200) (Cell Signal Tech, Danvers, MA, USA) staining.

    Article Title: Inactivation of the ATMIN/ATM pathway protects against glioblastoma formation
    Article Snippet: The following antibodies were used: p53, Pdgfra, p-Pdgfra, p-Chk2, p-Akt, Akt (all Cell Signaling); Myc-9E10 (CRUK); Smc1 (Abcam); p-Smc1, Chk2, Tubulin (all Merck); p-Kap1, Kap1 (both Bethyl Labs); Atm (Santa Cruz), p-Atm (Epitomics), p-p53, Actin, GAPDH, HRP-conjugated goat anti-mouse/rabbit IgG (all Sigma).

    Article Title: FTO regulates osteoclast development by modulating the proliferation and apoptosis of osteoclast precursors in inflammatory conditions.
    Article Snippet: Periodontitis is an oral inflammatory disease that causes alveolar bone destruction by activating osteoclast.. FTO, a crucial demethylase of N6-methyladenosine(m6A), exerts essential function in maintaining bone homeostasis.. However, the effects of FTO on periodontitis-related bone destruction remain unknown.

    TUNEL Assay:

    Article Title: Suppression of fumarate hydratase activity increases the efficacy of cisplatin-mediated chemotherapy in gastric cancer.
    Article Snippet: Antibodies specific for the following proteins were used in this study were as follow: p-ATM, p-Chk1, p-Chk2, cleaved-PARP, cleaved-caspase 3, Vinculin (all from Cell Signaling Technology, Beverly, MA, USA), Lamin B1, FH, ATM, Chk1, Chk2, γ-H2AX (all from Abcam, Cambridge, UK), GAPDH (Sigma-Aldrich, St Louis, USA), DNA-PK (Affinity Biosciences, Cincinnati, OH, USA) and Ki-67 (Zhongshan Golden Bridge Biotech, Beijing, China).

    Article Title: ARID1A Deficiency Impairs the DNA Damage Checkpoint and Sensitizes Cells to PARP Inhibitors
    Article Snippet: Anti-ATRIP (1:1,000), p-ATM (1:500), p-Chk1 (1:500), p-Chk2 (1:500), GFP (1:1,000) and p-H3 (1:500) were purchased from Cell Signaling Technology.

    Article Title: Potential role of PRKCSH in lung cancer: bioinformatics analysis and a case study of Nano ZnO.
    Article Snippet: PRKCSH defi ciency promoted G2/M arrest in response to zinc oxide nanoparticle (Nano ZnO) treatment in lung cancer cells.. With regard to the mechanism, PRKCSH defi ciency may induce STAT6 translocation to the nucleus to activate p53 expression.. Activated p53 contributed to Nano-ZnOinduced G2/M arrest in lung cancer cells.

    Article Title: Sirt3 Promoted DNA Damage Repair and Radioresistance Through ATM-Chk2 in Non-small Cell Lung Cancer Cells
    Article Snippet: The proteins were incubated with Sirt3 (1:1000), p-ATM (1:1000), p-ATR (1:1000), p-Chk1 (1:1000), p-Chk2 (1:1000), γ-H2AX (1:1000) and β-tublin (1:1000) (Cell Signal Tech, Danvers, MA, USA) at 4°C overnight in a shaker incubator.

    Article Title: Natural bioactive gallic acid shows potential anticancer effects by inhibiting the proliferation and invasiveness behavior in human embryonic carcinoma cells
    Article Snippet: Cell Signaling Technology, Inc. supplied: p27 Kip1 (cat. no. 3686), p-EGFR (cat. no. 3777), EGFR (cat. no. 4267), phosphorylated (p-)JAK2 (cat. no. 3776), JAK2 (cat. no. 3230), p-STAT5 (cat. no. 9351), pCHK1 (cat. no. 2348), p-CHK2 (cat. no. 2197), p-ATM (cat. no. 5883), p-Histone (cat. no. 9718) and p-BRCA1 (cat. no. 9009).

    Article Title: Sirt3 Promoted DNA Damage Repair and Radioresistance Through ATM-Chk2 in Non-small Cell Lung Cancer Cells
    Article Snippet: At indicated time points, lung tissues were isolated and subjected to sectioning, then the samples were stained with H&E, terminal transferase-mediated dUTP nick end labeling (TUNEL), Ki67 (1:400), Sirt3 (1:200), p-ATM (1:100), p-Chk2 (1:200), and γ-H2AX (1:200) (Cell Signal Tech, Danvers, MA, USA) staining.

    Article Title: Inactivation of the ATMIN/ATM pathway protects against glioblastoma formation
    Article Snippet: The following antibodies were used: p53, Pdgfra, p-Pdgfra, p-Chk2, p-Akt, Akt (all Cell Signaling); Myc-9E10 (CRUK); Smc1 (Abcam); p-Smc1, Chk2, Tubulin (all Merck); p-Kap1, Kap1 (both Bethyl Labs); Atm (Santa Cruz), p-Atm (Epitomics), p-p53, Actin, GAPDH, HRP-conjugated goat anti-mouse/rabbit IgG (all Sigma).

    Article Title: FTO regulates osteoclast development by modulating the proliferation and apoptosis of osteoclast precursors in inflammatory conditions.
    Article Snippet: Periodontitis is an oral inflammatory disease that causes alveolar bone destruction by activating osteoclast.. FTO, a crucial demethylase of N6-methyladenosine(m6A), exerts essential function in maintaining bone homeostasis.. However, the effects of FTO on periodontitis-related bone destruction remain unknown.



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    ( A ) HCT116 SIRT2 WT and KO cells were treated with 6 Gy IR, harvested after 4 hours, run on SDS-PAGE, and probed with the indicated antibodies. The image shown is representative of data from 3 separate experiments conducted independently. ( B ) Quantitation of IR-induced phosphorylation of KAP1 and <t>CHK2</t> relative to total KAP1 and CHK2 protein levels. Data are represented as the mean ± SD from 3 independent experiments. ** P < 0.01 and *** P < 0.001, by 2-tail Student’s t test. ( C ) HCT116 SIRT2 KO cells expressing SFB-MRE11 WT, K393Q, and K393R were treated with or without 6 Gy IR, harvested after 4 hours, run on SDS-PAGE, and probed with the indicated antibodies. Shown is a representative image of 3 independent experiments. ( D and E ) Quantitation of phosphorylation of KAP1 and CHK2 relative to total KAP1 and CHK2 protein levels. Data are presented as the mean ± SD of 3 independent experiments. Statistical significance was determined using 1-way ANOVA followed by Dunnett’s post hoc test for multiple comparisons. **** P < 0.0001.
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    ( A ) HCT116 SIRT2 WT and KO cells were treated with 6 Gy IR, harvested after 4 hours, run on SDS-PAGE, and probed with the indicated antibodies. The image shown is representative of data from 3 separate experiments conducted independently. ( B ) Quantitation of IR-induced phosphorylation of KAP1 and <t>CHK2</t> relative to total KAP1 and CHK2 protein levels. Data are represented as the mean ± SD from 3 independent experiments. ** P < 0.01 and *** P < 0.001, by 2-tail Student’s t test. ( C ) HCT116 SIRT2 KO cells expressing SFB-MRE11 WT, K393Q, and K393R were treated with or without 6 Gy IR, harvested after 4 hours, run on SDS-PAGE, and probed with the indicated antibodies. Shown is a representative image of 3 independent experiments. ( D and E ) Quantitation of phosphorylation of KAP1 and CHK2 relative to total KAP1 and CHK2 protein levels. Data are presented as the mean ± SD of 3 independent experiments. Statistical significance was determined using 1-way ANOVA followed by Dunnett’s post hoc test for multiple comparisons. **** P < 0.0001.
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    Proteintech p chk2 thr68
    ( A ) HCT116 SIRT2 WT and KO cells were treated with 6 Gy IR, harvested after 4 hours, run on SDS-PAGE, and probed with the indicated antibodies. The image shown is representative of data from 3 separate experiments conducted independently. ( B ) Quantitation of IR-induced phosphorylation of KAP1 and <t>CHK2</t> relative to total KAP1 and CHK2 protein levels. Data are represented as the mean ± SD from 3 independent experiments. ** P < 0.01 and *** P < 0.001, by 2-tail Student’s t test. ( C ) HCT116 SIRT2 KO cells expressing SFB-MRE11 WT, K393Q, and K393R were treated with or without 6 Gy IR, harvested after 4 hours, run on SDS-PAGE, and probed with the indicated antibodies. Shown is a representative image of 3 independent experiments. ( D and E ) Quantitation of phosphorylation of KAP1 and CHK2 relative to total KAP1 and CHK2 protein levels. Data are presented as the mean ± SD of 3 independent experiments. Statistical significance was determined using 1-way ANOVA followed by Dunnett’s post hoc test for multiple comparisons. **** P < 0.0001.
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    ( A ) HCT116 SIRT2 WT and KO cells were treated with 6 Gy IR, harvested after 4 hours, run on SDS-PAGE, and probed with the indicated antibodies. The image shown is representative of data from 3 separate experiments conducted independently. ( B ) Quantitation of IR-induced phosphorylation of KAP1 and <t>CHK2</t> relative to total KAP1 and CHK2 protein levels. Data are represented as the mean ± SD from 3 independent experiments. ** P < 0.01 and *** P < 0.001, by 2-tail Student’s t test. ( C ) HCT116 SIRT2 KO cells expressing SFB-MRE11 WT, K393Q, and K393R were treated with or without 6 Gy IR, harvested after 4 hours, run on SDS-PAGE, and probed with the indicated antibodies. Shown is a representative image of 3 independent experiments. ( D and E ) Quantitation of phosphorylation of KAP1 and CHK2 relative to total KAP1 and CHK2 protein levels. Data are presented as the mean ± SD of 3 independent experiments. Statistical significance was determined using 1-way ANOVA followed by Dunnett’s post hoc test for multiple comparisons. **** P < 0.0001.
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    ( A ) HCT116 SIRT2 WT and KO cells were treated with 6 Gy IR, harvested after 4 hours, run on SDS-PAGE, and probed with the indicated antibodies. The image shown is representative of data from 3 separate experiments conducted independently. ( B ) Quantitation of IR-induced phosphorylation of KAP1 and <t>CHK2</t> relative to total KAP1 and CHK2 protein levels. Data are represented as the mean ± SD from 3 independent experiments. ** P < 0.01 and *** P < 0.001, by 2-tail Student’s t test. ( C ) HCT116 SIRT2 KO cells expressing SFB-MRE11 WT, K393Q, and K393R were treated with or without 6 Gy IR, harvested after 4 hours, run on SDS-PAGE, and probed with the indicated antibodies. Shown is a representative image of 3 independent experiments. ( D and E ) Quantitation of phosphorylation of KAP1 and CHK2 relative to total KAP1 and CHK2 protein levels. Data are presented as the mean ± SD of 3 independent experiments. Statistical significance was determined using 1-way ANOVA followed by Dunnett’s post hoc test for multiple comparisons. **** P < 0.0001.
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    ( A ) HCT116 SIRT2 WT and KO cells were treated with 6 Gy IR, harvested after 4 hours, run on SDS-PAGE, and probed with the indicated antibodies. The image shown is representative of data from 3 separate experiments conducted independently. ( B ) Quantitation of IR-induced phosphorylation of KAP1 and <t>CHK2</t> relative to total KAP1 and CHK2 protein levels. Data are represented as the mean ± SD from 3 independent experiments. ** P < 0.01 and *** P < 0.001, by 2-tail Student’s t test. ( C ) HCT116 SIRT2 KO cells expressing SFB-MRE11 WT, K393Q, and K393R were treated with or without 6 Gy IR, harvested after 4 hours, run on SDS-PAGE, and probed with the indicated antibodies. Shown is a representative image of 3 independent experiments. ( D and E ) Quantitation of phosphorylation of KAP1 and CHK2 relative to total KAP1 and CHK2 protein levels. Data are presented as the mean ± SD of 3 independent experiments. Statistical significance was determined using 1-way ANOVA followed by Dunnett’s post hoc test for multiple comparisons. **** P < 0.0001.
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    Image Search Results


    ( A ) HCT116 SIRT2 WT and KO cells were treated with 6 Gy IR, harvested after 4 hours, run on SDS-PAGE, and probed with the indicated antibodies. The image shown is representative of data from 3 separate experiments conducted independently. ( B ) Quantitation of IR-induced phosphorylation of KAP1 and CHK2 relative to total KAP1 and CHK2 protein levels. Data are represented as the mean ± SD from 3 independent experiments. ** P < 0.01 and *** P < 0.001, by 2-tail Student’s t test. ( C ) HCT116 SIRT2 KO cells expressing SFB-MRE11 WT, K393Q, and K393R were treated with or without 6 Gy IR, harvested after 4 hours, run on SDS-PAGE, and probed with the indicated antibodies. Shown is a representative image of 3 independent experiments. ( D and E ) Quantitation of phosphorylation of KAP1 and CHK2 relative to total KAP1 and CHK2 protein levels. Data are presented as the mean ± SD of 3 independent experiments. Statistical significance was determined using 1-way ANOVA followed by Dunnett’s post hoc test for multiple comparisons. **** P < 0.0001.

    Journal: The Journal of Clinical Investigation

    Article Title: MRE11 deacetylation by SIRT2 promotes DNA binding to facilitate DNA end resection and ATM-dependent signaling

    doi: 10.1172/JCI186711

    Figure Lengend Snippet: ( A ) HCT116 SIRT2 WT and KO cells were treated with 6 Gy IR, harvested after 4 hours, run on SDS-PAGE, and probed with the indicated antibodies. The image shown is representative of data from 3 separate experiments conducted independently. ( B ) Quantitation of IR-induced phosphorylation of KAP1 and CHK2 relative to total KAP1 and CHK2 protein levels. Data are represented as the mean ± SD from 3 independent experiments. ** P < 0.01 and *** P < 0.001, by 2-tail Student’s t test. ( C ) HCT116 SIRT2 KO cells expressing SFB-MRE11 WT, K393Q, and K393R were treated with or without 6 Gy IR, harvested after 4 hours, run on SDS-PAGE, and probed with the indicated antibodies. Shown is a representative image of 3 independent experiments. ( D and E ) Quantitation of phosphorylation of KAP1 and CHK2 relative to total KAP1 and CHK2 protein levels. Data are presented as the mean ± SD of 3 independent experiments. Statistical significance was determined using 1-way ANOVA followed by Dunnett’s post hoc test for multiple comparisons. **** P < 0.0001.

    Article Snippet: The antibodies used in this study included SIRT2 (MilliporeSigma, 09-843; Santa Cruz Biotechnology, sc-20966), GAPDH (Santa Cruz, sc-47724), Flag (Santa Cruz Biotechnology, sc-51590), GFP (Abcam, Ab6556), pan acetyl-Lys (Santa Cruz Biotechnology, sc-8649), RPA70 (Cell Signaling Technology, 2267), P-CHK2 T68 (Cell Signaling Technology, 2661S), CHK2 (Santa Cruz Biotechnology, sc-7898), P-KAP1 (Invitrogen, Thermo Fisher Scientific, MA1-2023), and KAP1 (Bethyl Laboratories, A300-767A).

    Techniques: SDS Page, Quantitation Assay, Phospho-proteomics, Expressing

    (Step 1) DNA damage results in DSBs. (Step 2) SIRT2 deacetylates MRE11 at K393 in response to DNA damage. (Step 3) MRE11 K393 deacetylation by SIRT2 facilitates its recruitment and binding to DNA at DSBs. (Step 4) MRE11-RAD50-NBS1 assembles and promotes DNA end resection and ATM-dependent phosphorylation of downstream substrates, including CHK2 and KAP1.

    Journal: The Journal of Clinical Investigation

    Article Title: MRE11 deacetylation by SIRT2 promotes DNA binding to facilitate DNA end resection and ATM-dependent signaling

    doi: 10.1172/JCI186711

    Figure Lengend Snippet: (Step 1) DNA damage results in DSBs. (Step 2) SIRT2 deacetylates MRE11 at K393 in response to DNA damage. (Step 3) MRE11 K393 deacetylation by SIRT2 facilitates its recruitment and binding to DNA at DSBs. (Step 4) MRE11-RAD50-NBS1 assembles and promotes DNA end resection and ATM-dependent phosphorylation of downstream substrates, including CHK2 and KAP1.

    Article Snippet: The antibodies used in this study included SIRT2 (MilliporeSigma, 09-843; Santa Cruz Biotechnology, sc-20966), GAPDH (Santa Cruz, sc-47724), Flag (Santa Cruz Biotechnology, sc-51590), GFP (Abcam, Ab6556), pan acetyl-Lys (Santa Cruz Biotechnology, sc-8649), RPA70 (Cell Signaling Technology, 2267), P-CHK2 T68 (Cell Signaling Technology, 2661S), CHK2 (Santa Cruz Biotechnology, sc-7898), P-KAP1 (Invitrogen, Thermo Fisher Scientific, MA1-2023), and KAP1 (Bethyl Laboratories, A300-767A).

    Techniques: Binding Assay, Phospho-proteomics