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atr kinase inhibitor ve 821  (MedChemExpress)


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    MedChemExpress atr kinase inhibitor ve 821
    Atr Kinase Inhibitor Ve 821, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 53 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/atr kinase inhibitor ve 821/product/MedChemExpress
    Average 95 stars, based on 53 article reviews
    atr kinase inhibitor ve 821 - by Bioz Stars, 2026-02
    95/100 stars

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    atr kinase inhibitor ve 821  (MedChemExpress)
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    ATR signaling contributes to cGAS/STING pathway activation in TRF1-deficient MEFs. MEFs were treated with OHT, followed by the ATR inhibitor VE-821 for 24 hours. (A) Detection of micronuclei in MEFs treated with mock (ctr) or ATR inhibitor <t>(ATRi).</t> Cells were fixed and stained with DAPI. Scale bar, 10 μm. Quantification shows the percentage of cells with micronuclei; approximately 100 cells were counted per group. (B-C) Measurement of cellular 2’3’-cGAMP (B) and IFNβ in culture medium (C) by ELISA, with normalization to total protein concentration in the cell pellet. (D) Il6 and Ifnb mRNA levels in OHT-treated MEFs exposed to mock (-) or VE-821 (ATRi), assessed by RT-qPCR. P values were calculated using Student’s t-test (A-C) and one-way ANOVA (D). Data are presented as mean ± SD from three independent experiments for panels B and C, as representative data from one of three independent biological experiments for D.
    Atr Inhibitor Ve 821, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATR signaling contributes to cGAS/STING pathway activation in TRF1-deficient MEFs. MEFs were treated with OHT, followed by the ATR inhibitor VE-821 for 24 hours. (A) Detection of micronuclei in MEFs treated with mock (ctr) or ATR inhibitor <t>(ATRi).</t> Cells were fixed and stained with DAPI. Scale bar, 10 μm. Quantification shows the percentage of cells with micronuclei; approximately 100 cells were counted per group. (B-C) Measurement of cellular 2’3’-cGAMP (B) and IFNβ in culture medium (C) by ELISA, with normalization to total protein concentration in the cell pellet. (D) Il6 and Ifnb mRNA levels in OHT-treated MEFs exposed to mock (-) or VE-821 (ATRi), assessed by RT-qPCR. P values were calculated using Student’s t-test (A-C) and one-way ANOVA (D). Data are presented as mean ± SD from three independent experiments for panels B and C, as representative data from one of three independent biological experiments for D.
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    ATR signaling contributes to cGAS/STING pathway activation in TRF1-deficient MEFs. MEFs were treated with OHT, followed by the ATR inhibitor VE-821 for 24 hours. (A) Detection of micronuclei in MEFs treated with mock (ctr) or ATR inhibitor <t>(ATRi).</t> Cells were fixed and stained with DAPI. Scale bar, 10 μm. Quantification shows the percentage of cells with micronuclei; approximately 100 cells were counted per group. (B-C) Measurement of cellular 2’3’-cGAMP (B) and IFNβ in culture medium (C) by ELISA, with normalization to total protein concentration in the cell pellet. (D) Il6 and Ifnb mRNA levels in OHT-treated MEFs exposed to mock (-) or VE-821 (ATRi), assessed by RT-qPCR. P values were calculated using Student’s t-test (A-C) and one-way ANOVA (D). Data are presented as mean ± SD from three independent experiments for panels B and C, as representative data from one of three independent biological experiments for D.
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    ATR signaling contributes to cGAS/STING pathway activation in TRF1-deficient MEFs. MEFs were treated with OHT, followed by the ATR inhibitor VE-821 for 24 hours. (A) Detection of micronuclei in MEFs treated with mock (ctr) or ATR inhibitor <t>(ATRi).</t> Cells were fixed and stained with DAPI. Scale bar, 10 μm. Quantification shows the percentage of cells with micronuclei; approximately 100 cells were counted per group. (B-C) Measurement of cellular 2’3’-cGAMP (B) and IFNβ in culture medium (C) by ELISA, with normalization to total protein concentration in the cell pellet. (D) Il6 and Ifnb mRNA levels in OHT-treated MEFs exposed to mock (-) or VE-821 (ATRi), assessed by RT-qPCR. P values were calculated using Student’s t-test (A-C) and one-way ANOVA (D). Data are presented as mean ± SD from three independent experiments for panels B and C, as representative data from one of three independent biological experiments for D.
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    ATR signaling contributes to cGAS/STING pathway activation in TRF1-deficient MEFs. MEFs were treated with OHT, followed by the ATR inhibitor VE-821 for 24 hours. (A) Detection of micronuclei in MEFs treated with mock (ctr) or ATR inhibitor (ATRi). Cells were fixed and stained with DAPI. Scale bar, 10 μm. Quantification shows the percentage of cells with micronuclei; approximately 100 cells were counted per group. (B-C) Measurement of cellular 2’3’-cGAMP (B) and IFNβ in culture medium (C) by ELISA, with normalization to total protein concentration in the cell pellet. (D) Il6 and Ifnb mRNA levels in OHT-treated MEFs exposed to mock (-) or VE-821 (ATRi), assessed by RT-qPCR. P values were calculated using Student’s t-test (A-C) and one-way ANOVA (D). Data are presented as mean ± SD from three independent experiments for panels B and C, as representative data from one of three independent biological experiments for D.

    Journal: bioRxiv

    Article Title: sTelomere replication stress-induced DNA damage response triggers inflammatory signaling via canonical and non-canonical STING pathways

    doi: 10.1101/2025.07.11.664434

    Figure Lengend Snippet: ATR signaling contributes to cGAS/STING pathway activation in TRF1-deficient MEFs. MEFs were treated with OHT, followed by the ATR inhibitor VE-821 for 24 hours. (A) Detection of micronuclei in MEFs treated with mock (ctr) or ATR inhibitor (ATRi). Cells were fixed and stained with DAPI. Scale bar, 10 μm. Quantification shows the percentage of cells with micronuclei; approximately 100 cells were counted per group. (B-C) Measurement of cellular 2’3’-cGAMP (B) and IFNβ in culture medium (C) by ELISA, with normalization to total protein concentration in the cell pellet. (D) Il6 and Ifnb mRNA levels in OHT-treated MEFs exposed to mock (-) or VE-821 (ATRi), assessed by RT-qPCR. P values were calculated using Student’s t-test (A-C) and one-way ANOVA (D). Data are presented as mean ± SD from three independent experiments for panels B and C, as representative data from one of three independent biological experiments for D.

    Article Snippet: The following chemicals were used for cell treatments in the experiments: ATM inhibitor KU-55933 (Abcam, 120637, 10 μM), ATR inhibitor VE-821 (Selleck, S8007, 2.5 μM); cGAS inhibitor RU.521 (Invivogen, inh-ru521, 10 μM), STING-specific inhibitor H-151 (MedChem Express, HY-112693, 7.5 μM), STING ER exit inhibitor Brefeldin A (BFA; Thermo Fisher Scientific, 00-4506-51, 3.0 μg/mL), proteasome inhibitor MG132 (Millipore Sigma, M7449, 5 μM), lysosome inhibitor Bafilomycin A1 (Baf A1; Millipore Sigma, 19-148, 100 nM), and replication stress inducer Aphidicolin (Millipore Sigma, 178273, 0.2 μM).

    Techniques: Activation Assay, Staining, Enzyme-linked Immunosorbent Assay, Protein Concentration, Quantitative RT-PCR