Journal: Frontiers in Immunology

Article Title: UVB-induced genotoxic stress activates the DNA damage response and innate immune pathways in sea urchin coelomocytes

doi: 10.3389/fimmu.2026.1787989

Figure Lengend Snippet: Enhanced ubiquitination and phosphorylation in UVB-treated coelomocytes was confirmed using western blot. Representative western blots showing (a) ubiquitinated, (c) phosphorylated ATM/ATR substrate, (e) phosphorylated AKT substrate, (g) phosphorylated MAPK/CDK substrate, and (i) phosphorylated PKC substrate signal in biological triplicate controls (C, white font) and UVB-treated (U, red font) samples. Beta actin loading controls are shown below. Quantification and statistical testing (one-tailed paired t-test) of western blot signals are shown in (b) , (d) , (f) , (h) , and (j) . Individual data points representing n = 6 biological replicates are overlaid as white circles. Bars represent mean values, and error bars represent ± the standard deviation of n = 6 biological replicates. NS, not significant (p > 0.05). * p ≤ 0.05, ** p ≤ 0.01. P-MAPK/CDK and P-PKC blots were run simultaneously and therefore have the same β actin loading control. Additional western blots are presented in Supplementary Figure 4 .

Article Snippet: These antibodies included phospho-ATM/ATR Substrate Motif (CST #6966), phospho-Akt Substrate Motif (CST #9614 and #10001), phospho-MAPK/CDK Substrate Motif (CST #9477 and #2325), and phospho-PKC Substrate Motif (CST #6967).

Techniques: Ubiquitin Proteomics, Phospho-proteomics, Western Blot, One-tailed Test, Standard Deviation, Control

Journal: Journal of Enzyme Inhibition and Medicinal Chemistry

Article Title: Design, synthesis and anti-breast cancer activity evaluation of 6,7-dihydro-5 H -pyrrolo[3,4- d ]pyrimidine-based PARP1/ATR dual inhibitors

doi: 10.1080/14756366.2026.2627053

Figure Lengend Snippet: Compound 38a significantly inhibits DSB repair and ATR-CHK1 signalling axis. (A) Representative images of immune-fluorescence staining of γH2AX foci in MDA-MB-231 cells treated with compounds as indicated for 24 h. Scale bar = 100 μm; (B) Western blotting of ATR/p-ATR, CHK1/p-CHK1, p53/p-p53, p21 and γH2AX in MDA-MB-231 cells exposed to different compounds as indicated for 48 h; (C) Statistical analysis of ATR/p-ATR, γH2AX, p-CHK1, p-p53 and p21 protein levels; (D) Mechanism of action of 38a in the treatment of TNBC. The data are shown as the mean ± SD of three independent experiments. NS: no significance. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: The primary antibodies used were PARP1 (1/1000 dilution, CST#9532), BCL-2(1/1000 dilution, CST#3498), Bax (1/1000 dilution, CST#5023), Caspase-3 (1/1000 dilution, CST#9662), ATR (1/1000 dilution, CST#13934), p-ATR (1/1000 dilution, CST#2853), CHK1 (1/1000 dilution, CST#2360), p-CHK1 (1/1000 dilution, CST#2348), p53 (1/1000 dilution, CST#9282), p-p53 (1/1000 dilution, CST#37909), p-21 (1/1000 dilution, CST#2947), γH2AX (1/1000 dilution, CST#9718) and Actin (1/1000 dilution, Proteintech# 66009–1-Ig).

Techniques: Fluorescence, Staining, Western Blot