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Inhibition of ATM restores NSCLC cells to IFN-γ by inducing DNA damage response (A) Cell viability of A549 (left panel) or PC-9 (right panel) treated with IFN-γ (1000 ng/ml) <t>and/or</t> <t>KU-55933</t> (10 μM) for 24 h are shown. Data are presented as mean ± SD. * p < 0.05. (B) Expression of γH2AX and b-Actin (loading control) in A549 (left panel) or PC-9 (right panel) cells treated with IFN-γ (1000 ng/ml) and/or KU-55933 (10 μM) for 24 h are shown.
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Inhibition of ATM restores NSCLC cells to IFN-γ by inducing DNA damage response (A) Cell viability of A549 (left panel) or PC-9 (right panel) treated with IFN-γ (1000 ng/ml) <t>and/or</t> <t>KU-55933</t> (10 μM) for 24 h are shown. Data are presented as mean ± SD. * p < 0.05. (B) Expression of γH2AX and b-Actin (loading control) in A549 (left panel) or PC-9 (right panel) cells treated with IFN-γ (1000 ng/ml) and/or KU-55933 (10 μM) for 24 h are shown.
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Inhibition of ATM restores NSCLC cells to IFN-γ by inducing DNA damage response (A) Cell viability of A549 (left panel) or PC-9 (right panel) treated with IFN-γ (1000 ng/ml) <t>and/or</t> <t>KU-55933</t> (10 μM) for 24 h are shown. Data are presented as mean ± SD. * p < 0.05. (B) Expression of γH2AX and b-Actin (loading control) in A549 (left panel) or PC-9 (right panel) cells treated with IFN-γ (1000 ng/ml) and/or KU-55933 (10 μM) for 24 h are shown.
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Inhibition of ATM restores NSCLC cells to IFN-γ by inducing DNA damage response (A) Cell viability of A549 (left panel) or PC-9 (right panel) treated with IFN-γ (1000 ng/ml) <t>and/or</t> <t>KU-55933</t> (10 μM) for 24 h are shown. Data are presented as mean ± SD. * p < 0.05. (B) Expression of γH2AX and b-Actin (loading control) in A549 (left panel) or PC-9 (right panel) cells treated with IFN-γ (1000 ng/ml) and/or KU-55933 (10 μM) for 24 h are shown.
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Inhibition of ATM restores NSCLC cells to IFN-γ by inducing DNA damage response (A) Cell viability of A549 (left panel) or PC-9 (right panel) treated with IFN-γ (1000 ng/ml) <t>and/or</t> <t>KU-55933</t> (10 μM) for 24 h are shown. Data are presented as mean ± SD. * p < 0.05. (B) Expression of γH2AX and b-Actin (loading control) in A549 (left panel) or PC-9 (right panel) cells treated with IFN-γ (1000 ng/ml) and/or KU-55933 (10 μM) for 24 h are shown.
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Inhibition of ATM restores NSCLC cells to IFN-γ by inducing DNA damage response (A) Cell viability of A549 (left panel) or PC-9 (right panel) treated with IFN-γ (1000 ng/ml) <t>and/or</t> <t>KU-55933</t> (10 μM) for 24 h are shown. Data are presented as mean ± SD. * p < 0.05. (B) Expression of γH2AX and b-Actin (loading control) in A549 (left panel) or PC-9 (right panel) cells treated with IFN-γ (1000 ng/ml) and/or KU-55933 (10 μM) for 24 h are shown.
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Inhibition of ATM restores NSCLC cells to IFN-γ by inducing DNA damage response (A) Cell viability of A549 (left panel) or PC-9 (right panel) treated with IFN-γ (1000 ng/ml) <t>and/or</t> <t>KU-55933</t> (10 μM) for 24 h are shown. Data are presented as mean ± SD. * p < 0.05. (B) Expression of γH2AX and b-Actin (loading control) in A549 (left panel) or PC-9 (right panel) cells treated with IFN-γ (1000 ng/ml) and/or KU-55933 (10 μM) for 24 h are shown.
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Inhibition of ATM restores NSCLC cells to IFN-γ by inducing DNA damage response (A) Cell viability of A549 (left panel) or PC-9 (right panel) treated with IFN-γ (1000 ng/ml) <t>and/or</t> <t>KU-55933</t> (10 μM) for 24 h are shown. Data are presented as mean ± SD. * p < 0.05. (B) Expression of γH2AX and b-Actin (loading control) in A549 (left panel) or PC-9 (right panel) cells treated with IFN-γ (1000 ng/ml) and/or KU-55933 (10 μM) for 24 h are shown.
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Cell Signaling Technology Inc p atm
Knocking down SKA2-induced cell-cycle arrest and apoptosis through <t>the</t> <t>SKA2/ROS/ATM</t> axis in GC cell lines (A) Western blotting analysis of γ-H2AX (Ser139), ATM, p -ATM (Ser1981), p -Chk2 (Thr68), and SKA2 expression in SNU638 and NUGC3 SKA2-knockdown cell lines. (B) Western blotting analysis of SKA2 overexpression in SNU638 and NUGC3 SKA2-knockdown cell lines using antibodies against γ-H2AX (Ser139), ATM, p -ATM (Ser1981), p -Chk2 (Thr68), and SKA2. (C) Western blotting analysis of KU-55933 treatment in SNU638 and NUGC3 SKA2-knockdown cell lines using antibodies against cyclin D1, cyclin A2, cyclin B1, p -Chk2 (Thr68), PARP, Cleaved-Caspase3, JNK, p -JNK (Thr183/Tyr185), ATM, p -ATM (Ser1981), and SKA2. (D) Western blotting analysis of BML-277 treatment in SNU638 and NUGC3 SKA2-knockdown cell lines using antibodies against cyclin D1, cyclin A2, cyclin B1, p -Chk2 (Thr68), and SKA2. (E) Western blotting analysis of P38, p-P38 (Thr180/Tyr182), ERK, p -ERK1/2 (Thr202/Tyr204), JNK, p -JNK (Thr183/Tyr185), and SKA2 expression in SNU638 and NUGC3 SKA2-knockdown cell lines. (F) Western blotting analysis of the rescue effect of SKA2 overexpression on MAPK pathway markers (ERK, p -ERK1/2, JNK, and p -JNK) in SNU638 and NUGC3 SKA2-knockdown cell lines. (G) Western blotting analysis of JNK-IN-8 treatment in SNU638 SKA2-knockdown cell lines using antibodies against PARP, cleaved-caspase3, JNK, p -JNK (Thr183/Tyr185), and SKA2. α-Tubulin was used as the internal control for all blots. Representative blotting images are shown from 3 independent experiments.
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Image Search Results


Inhibition of ATM restores NSCLC cells to IFN-γ by inducing DNA damage response (A) Cell viability of A549 (left panel) or PC-9 (right panel) treated with IFN-γ (1000 ng/ml) and/or KU-55933 (10 μM) for 24 h are shown. Data are presented as mean ± SD. * p < 0.05. (B) Expression of γH2AX and b-Actin (loading control) in A549 (left panel) or PC-9 (right panel) cells treated with IFN-γ (1000 ng/ml) and/or KU-55933 (10 μM) for 24 h are shown.

Journal: Biochemistry and Biophysics Reports

Article Title: ATM inhibition restores IFN-γ sensitivity and induces ferroptosis in NSCLC via DNA damage response

doi: 10.1016/j.bbrep.2026.102568

Figure Lengend Snippet: Inhibition of ATM restores NSCLC cells to IFN-γ by inducing DNA damage response (A) Cell viability of A549 (left panel) or PC-9 (right panel) treated with IFN-γ (1000 ng/ml) and/or KU-55933 (10 μM) for 24 h are shown. Data are presented as mean ± SD. * p < 0.05. (B) Expression of γH2AX and b-Actin (loading control) in A549 (left panel) or PC-9 (right panel) cells treated with IFN-γ (1000 ng/ml) and/or KU-55933 (10 μM) for 24 h are shown.

Article Snippet: IFN-γ was purchased from Biolegend, and ATM inhibitor KU-55933 was purchased from MedChem Express.

Techniques: Inhibition, Expressing, Control

Inhibition of ATM in combination with IFN-γ induce ferroptosis in NSCLCs Cell viability of A549 (A) or PC-9 (B) treated with the indicated combination of IFN-γ (1000 ng/ml), KU-55933 (10 μM), Ferrostatin-1 (5 μM), and Liproxstatin-1 (5 μM) for 24 h are shown. Data are presented as mean ± SD. * p < 0.05.

Journal: Biochemistry and Biophysics Reports

Article Title: ATM inhibition restores IFN-γ sensitivity and induces ferroptosis in NSCLC via DNA damage response

doi: 10.1016/j.bbrep.2026.102568

Figure Lengend Snippet: Inhibition of ATM in combination with IFN-γ induce ferroptosis in NSCLCs Cell viability of A549 (A) or PC-9 (B) treated with the indicated combination of IFN-γ (1000 ng/ml), KU-55933 (10 μM), Ferrostatin-1 (5 μM), and Liproxstatin-1 (5 μM) for 24 h are shown. Data are presented as mean ± SD. * p < 0.05.

Article Snippet: IFN-γ was purchased from Biolegend, and ATM inhibitor KU-55933 was purchased from MedChem Express.

Techniques: Inhibition

ATM inhibition in combination with IFN-γ alters glutathione metabolism in NSCLC Cells were treated with IFN-γ (1000 ng/mL) and/or KU-55933 (10 μM) for 24 h, and then the intracellular levels of GSH and GSSG were quantified. The results of total glutathione (A), GSH (B), GSSG (C), and GSH/GSSG ratio (D) are shown. * p < 0.05.

Journal: Biochemistry and Biophysics Reports

Article Title: ATM inhibition restores IFN-γ sensitivity and induces ferroptosis in NSCLC via DNA damage response

doi: 10.1016/j.bbrep.2026.102568

Figure Lengend Snippet: ATM inhibition in combination with IFN-γ alters glutathione metabolism in NSCLC Cells were treated with IFN-γ (1000 ng/mL) and/or KU-55933 (10 μM) for 24 h, and then the intracellular levels of GSH and GSSG were quantified. The results of total glutathione (A), GSH (B), GSSG (C), and GSH/GSSG ratio (D) are shown. * p < 0.05.

Article Snippet: IFN-γ was purchased from Biolegend, and ATM inhibitor KU-55933 was purchased from MedChem Express.

Techniques: Inhibition

Knocking down SKA2-induced cell-cycle arrest and apoptosis through the SKA2/ROS/ATM axis in GC cell lines (A) Western blotting analysis of γ-H2AX (Ser139), ATM, p -ATM (Ser1981), p -Chk2 (Thr68), and SKA2 expression in SNU638 and NUGC3 SKA2-knockdown cell lines. (B) Western blotting analysis of SKA2 overexpression in SNU638 and NUGC3 SKA2-knockdown cell lines using antibodies against γ-H2AX (Ser139), ATM, p -ATM (Ser1981), p -Chk2 (Thr68), and SKA2. (C) Western blotting analysis of KU-55933 treatment in SNU638 and NUGC3 SKA2-knockdown cell lines using antibodies against cyclin D1, cyclin A2, cyclin B1, p -Chk2 (Thr68), PARP, Cleaved-Caspase3, JNK, p -JNK (Thr183/Tyr185), ATM, p -ATM (Ser1981), and SKA2. (D) Western blotting analysis of BML-277 treatment in SNU638 and NUGC3 SKA2-knockdown cell lines using antibodies against cyclin D1, cyclin A2, cyclin B1, p -Chk2 (Thr68), and SKA2. (E) Western blotting analysis of P38, p-P38 (Thr180/Tyr182), ERK, p -ERK1/2 (Thr202/Tyr204), JNK, p -JNK (Thr183/Tyr185), and SKA2 expression in SNU638 and NUGC3 SKA2-knockdown cell lines. (F) Western blotting analysis of the rescue effect of SKA2 overexpression on MAPK pathway markers (ERK, p -ERK1/2, JNK, and p -JNK) in SNU638 and NUGC3 SKA2-knockdown cell lines. (G) Western blotting analysis of JNK-IN-8 treatment in SNU638 SKA2-knockdown cell lines using antibodies against PARP, cleaved-caspase3, JNK, p -JNK (Thr183/Tyr185), and SKA2. α-Tubulin was used as the internal control for all blots. Representative blotting images are shown from 3 independent experiments.

Journal: iScience

Article Title: SKA2 promotes gastric cancer progression by regulating glutathione metabolism

doi: 10.1016/j.isci.2026.115202

Figure Lengend Snippet: Knocking down SKA2-induced cell-cycle arrest and apoptosis through the SKA2/ROS/ATM axis in GC cell lines (A) Western blotting analysis of γ-H2AX (Ser139), ATM, p -ATM (Ser1981), p -Chk2 (Thr68), and SKA2 expression in SNU638 and NUGC3 SKA2-knockdown cell lines. (B) Western blotting analysis of SKA2 overexpression in SNU638 and NUGC3 SKA2-knockdown cell lines using antibodies against γ-H2AX (Ser139), ATM, p -ATM (Ser1981), p -Chk2 (Thr68), and SKA2. (C) Western blotting analysis of KU-55933 treatment in SNU638 and NUGC3 SKA2-knockdown cell lines using antibodies against cyclin D1, cyclin A2, cyclin B1, p -Chk2 (Thr68), PARP, Cleaved-Caspase3, JNK, p -JNK (Thr183/Tyr185), ATM, p -ATM (Ser1981), and SKA2. (D) Western blotting analysis of BML-277 treatment in SNU638 and NUGC3 SKA2-knockdown cell lines using antibodies against cyclin D1, cyclin A2, cyclin B1, p -Chk2 (Thr68), and SKA2. (E) Western blotting analysis of P38, p-P38 (Thr180/Tyr182), ERK, p -ERK1/2 (Thr202/Tyr204), JNK, p -JNK (Thr183/Tyr185), and SKA2 expression in SNU638 and NUGC3 SKA2-knockdown cell lines. (F) Western blotting analysis of the rescue effect of SKA2 overexpression on MAPK pathway markers (ERK, p -ERK1/2, JNK, and p -JNK) in SNU638 and NUGC3 SKA2-knockdown cell lines. (G) Western blotting analysis of JNK-IN-8 treatment in SNU638 SKA2-knockdown cell lines using antibodies against PARP, cleaved-caspase3, JNK, p -JNK (Thr183/Tyr185), and SKA2. α-Tubulin was used as the internal control for all blots. Representative blotting images are shown from 3 independent experiments.

Article Snippet: p-ATM , Cell Signaling Technology , Cat# 5883; RRID: AB_10835213.

Techniques: Western Blot, Expressing, Knockdown, Over Expression, Control