Journal: Clinical and Translational Medicine

Article Title: ROS‐ATM‐CBP axis‐mediated PARP1 lactylation aggravates doxorubicin‐induced cardiotoxicity

doi: 10.1002/ctm2.70745

Figure Lengend Snippet: ROS‐ATM‐CBP signalling pathway activates PARP1 lactylation. (A, B) Intracellular ROS and lactate levels in HL‐1 cells treated with 1 µM doxorubicin for 0, 2 and 4 h. (C) Representative immunoprecipitation, western blots and quantification for detecting PARP1 lactylation. HL‐1 cells were stimulated by doxorubicin (1 µM for 0, 2 and 4 h), and the cells were lysed and immunoprecipitated using an anti‐PARP1 antibody, followed by detection of Pan‐KLA. (D) Schematic of the effect of SIRT1 activation on the lactylation level of PARP1 in mice. DOX (5 mg/kg) or the same volume of saline was administered intraperitoneally once weekly. One week before the DOX treatment, mice were pre‐treated with resveratrol (SIRT1 activator, 10 mg/kg/day) via daily intraperitoneal injections. (E) The SIRT1 activity was detected. (F–H) Representative immunoprecipitation, western blots and quantification for detecting PARP1 lactylation and protein expression of SIRT1. (I) Schematic of the effect of CBP inhibition on the lactylation level of PARP1 in mice. DOX (5 mg/kg) or the same volume of saline was administered intraperitoneally once weekly. One week before the DOX treatment, mice were pre‐treated with SGC‐CBP30 (CBP inhibitor, 15 mg/kg/day) via daily intraperitoneal injections. (J) The CBP activity was detected. (K–M) Representative immunoprecipitation, western blots and quantification for detecting PARP1 lactylation and protein expression of CBP. (A–C) Based on the central limit theorem, the data were considered to be normally distributed. Relative protein levels were calculated as fold changes vs the first group. Data are presented as mean ± SD. Statistical significance was assessed by one‐way ANOVA with Tukey multiple comparisons test ( P values adjusted for 3 comparisons). (D–M) Relative protein levels were calculated as fold changes vs. the first group. Data are presented as mean ± SD. Statistical significance was assessed by two‐way ANOVA with Bonferroni multiple comparisons test ( p ‐values adjusted for 9 comparisons). ns p > .05, * p < .05, ** p < .01, *** p < .001.

Article Snippet: ATM inhibitor (KU‐55933; #HY‐12016; 10 μM; 2 h); LDHA inhibitor (Galloflavin; #HY‐W040118; 10 −5 M; 24 h) and CBP activator (CTB; #HY‐134964; 10 −4 M; 24 h) were obtained from MedChemExpress.

Techniques: Immunoprecipitation, Western Blot, Activation Assay, Saline, Activity Assay, Expressing, Inhibition

Journal: Clinical and Translational Medicine

Article Title: ROS‐ATM‐CBP axis‐mediated PARP1 lactylation aggravates doxorubicin‐induced cardiotoxicity

doi: 10.1002/ctm2.70745

Figure Lengend Snippet: Model showing the molecular signalling cascade of CBP‐PARP1 lactylation–PARylation axis. The schematic depicts how oxidative stress‐induced ROS activates the ATM‐CBP‐PARP1 signalling pathway via a lactylation–PARylation cascade to promote cardiomyocyte apoptosis.

Article Snippet: ATM inhibitor (KU‐55933; #HY‐12016; 10 μM; 2 h); LDHA inhibitor (Galloflavin; #HY‐W040118; 10 −5 M; 24 h) and CBP activator (CTB; #HY‐134964; 10 −4 M; 24 h) were obtained from MedChemExpress.

Techniques:

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

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

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