rabbit anti atm antibody  (Bioss)

Journal: Clinical and Translational Radiation Oncology

Article Title: MonoHER selectively enhances the radiotherapy response in p53 wild-type breast cancer via stabilization of p53

doi: 10.1016/j.ctro.2026.101147

Figure Lengend Snippet: Different protein expression of p-ATM, p- p 53 and p53 in breast cancer cells treated with combination of monoHER (M) and radiation (RT). Representative Western blots of p-ATM, p-p53 and p53 in MCF7 (A), T47D (E) and MCF10A (H) cells. Quantification of p-ATM (B), p-p53 (C) and p53 (D) protein expression in MCF7 cells. Quantification of p-ATM (E), p-p53 (F) and p53 (G) protein expression in T47D cells. Quantification of p-ATM (I), p-p53 (J) and p53 (K) protein expression in MCF10A cells. Data are presented as mean ± SEM from three independent experiments. *p < 0.05, **p < 0.01.

Article Snippet: Membranes were blocked in 5% non-fat milk in TBST for 1 h at RT and incubated overnight at 4°C with primary antibodies against p-ATM (1:2000; Cell Signaling Technology, 5883), p-p53 (1:1000; Cell Signaling Technology, 9284) and p53 (1:1000; Cell Signaling Technology, 9282). α-Tubulin (1:1000, Sigma Aldrich, T7451) or Vinculin (1:1000, Sigma Aldrich, V9131) were used as loading controls.

Techniques: Expressing, Western Blot

Journal: Clinical and Translational Radiation Oncology

Article Title: MonoHER selectively enhances the radiotherapy response in p53 wild-type breast cancer via stabilization of p53

doi: 10.1016/j.ctro.2026.101147

Figure Lengend Snippet: Monoher interacts with p53. Biomolecular interactions of monoHER with wild-type p53 (A) and mutant p53 (B). Docking scores are indicated at the bottom of the image. Representative Western blots and quantification (E) of the CETSA experiment with cell lysates of MCF7 cells, which were treated with DMEM (C) or monoHER (D). Data are presented as mean ± SEM from three independent experiments.

Article Snippet: Membranes were blocked in 5% non-fat milk in TBST for 1 h at RT and incubated overnight at 4°C with primary antibodies against p-ATM (1:2000; Cell Signaling Technology, 5883), p-p53 (1:1000; Cell Signaling Technology, 9284) and p53 (1:1000; Cell Signaling Technology, 9282). α-Tubulin (1:1000, Sigma Aldrich, T7451) or Vinculin (1:1000, Sigma Aldrich, V9131) were used as loading controls.

Techniques: Mutagenesis, Western Blot

Journal: Cell Death Discovery

Article Title: ATGL sensitizes hepatocellular carcinoma cells to genotoxic drugs by modulating p53 acetylation/phosphorylation status

doi: 10.1038/s41420-026-03048-4

Figure Lengend Snippet: A – D HepG2 cells were transfected with empty vector (Vehicle) or ATGL-overexpressing construct (ATGL-OE) and, after 24 h, treated with 50 µM etoposide for 6 h with or without recovery (Rec) with fresh medium for 2 h. Western blot analysis of Ac-p53 Lys-382, p-p53 Ser-15, p53 and γH2AX levels was performed. E , F HepG2 cells were transfected with empty vector (Vehicle) or ATGL-overexpressing construct (ATGL-OE) and, after 24 h, treated with 50 µM etoposide or 2 µM doxorubicin for 6 h. The proliferation was assayed via the Trypan blue direct counting procedure. G , H HepG2 cells were treated with 50 µM etoposide for 6 h with or without 25 µM ATGListatin (ATGLi) for 24 h. HepG2 cells were treated with 50 µM etoposide for 6 h. I – K Western blot analysis of p21 and Puma levels was performed. HepG2 cells were treated with 1 µM GW7647 for 24 h. L , M Proliferation was assayed by the Trypan blue direct counting procedure. N – P Western blot analysis of p21 and Puma levels was performed. The images are representative of three independent experiments that yielded similar results. β-Actin and ATGL were used as loading and transfection controls, respectively. The data are presented as the means ± SDs from three independent experiments. Statistical significance was determined by one-way ANOVA with Tukey’s post hoc test; * p < 0.05, ** p < 0.01, *** p < 0.001 vs CTRL or as indicated by brackets.

Article Snippet: The following primary antibodies were used: β-Actin (Cell Signaling Technology, cat. number #4970S, diluted 1:1000), γH2AX Ser-139 (Cell Signaling Technology, cat. number #9718, diluted 1:1000), ATGL (Cell Signaling Technology, cat. number 2138S, diluted 1:1000), pATM Ser-1981 (Cell Signaling Technology, cat. number #5883, diluted 1:1000), ATM (Cell Signaling Technology, cat. number #2873, diluted 1:1000), p21 (Cell Signaling Technology, cat. number #2947, diluted 1:1000), PPARα (Santa Cruz Biotechnology, cat. number sc-398394, diluted 1:1000), Puma (Cell Signaling Technology, cat. number #4976, diluted 1:1000), Ac-p53 Lys-382 (Cell Signaling Technology, cat. number #2525S, diluted 1:1000), p-p53 Ser-15 (Cell Signaling Technology, cat. number #9284S, diluted 1:1000), and p53 (Sigma-Aldrich, cat. number #P5813, diluted 1:1000).

Techniques: Transfection, Plasmid Preparation, Construct, Western Blot

Journal: Cell Death Discovery

Article Title: ATGL sensitizes hepatocellular carcinoma cells to genotoxic drugs by modulating p53 acetylation/phosphorylation status

doi: 10.1038/s41420-026-03048-4

Figure Lengend Snippet: A Boxplot showing significantly reduced PNPLA2 expression in primary HCC tissues (primary tumor; n = 371) compared with solid tumor-adjacent non-tumoral liver tissues (solid tissue normal; n = 50) samples based on TCGA data. B Boxplot of Z-score–normalized ATGL expression from TCGA-LIHC RNA-seq data based on TP53 mutation status (wild type n = 263 and mutant n = 111). C Visualization of the PPAR signaling pathway, reporting normalized enrichment score (NES) and adjusted p -value. D Bar plot showing the most significantly enriched transcription factors after a transcription factor enrichment analysis performed using TRRUST transcription factors 2019 database on differentially expressed genes (DEGs) in ATGL-high versus ATGL-low HCC samples. Adjusted p -value was reported. Scatter plot showing the correlation between E PNPLA2 and PPARα ( PPARA ); between F PNPLA2 and EP300 ; between G PPARA and EP300 ; between H PNPLA2 and Puma ( BBC3 ); between I PNPLA2 and p21 ( CDKN1A ) mRNA expression levels in HCC samples from the TCGA-LIHC cohort analyzed using GEPIA. Gene expression values are reported as log2-transformed TPM. Each dot represents an individual tumor sample.

Article Snippet: The following primary antibodies were used: β-Actin (Cell Signaling Technology, cat. number #4970S, diluted 1:1000), γH2AX Ser-139 (Cell Signaling Technology, cat. number #9718, diluted 1:1000), ATGL (Cell Signaling Technology, cat. number 2138S, diluted 1:1000), pATM Ser-1981 (Cell Signaling Technology, cat. number #5883, diluted 1:1000), ATM (Cell Signaling Technology, cat. number #2873, diluted 1:1000), p21 (Cell Signaling Technology, cat. number #2947, diluted 1:1000), PPARα (Santa Cruz Biotechnology, cat. number sc-398394, diluted 1:1000), Puma (Cell Signaling Technology, cat. number #4976, diluted 1:1000), Ac-p53 Lys-382 (Cell Signaling Technology, cat. number #2525S, diluted 1:1000), p-p53 Ser-15 (Cell Signaling Technology, cat. number #9284S, diluted 1:1000), and p53 (Sigma-Aldrich, cat. number #P5813, diluted 1:1000).

Techniques: Expressing, RNA Sequencing, Mutagenesis, Gene Expression, Transformation Assay