bet inhibitor  (MedChemExpress)

Journal: bioRxiv

Article Title: Unraveling AMPK and BET regulation of immune checkpoint biology: implications for personalized medicine

doi: 10.64898/2026.01.26.701869

Figure Lengend Snippet: BET proteins differentially regulate TIM-3, TIGIT, PD-1 and CTLA-4 expression on both T cells and NK cells. Purified PBMCs were activated by plate-bound anti-CD3 (10 µg/ml) and soluble anti-CD28 (2 µg/ml) ex vivo at 37□ for 72h and treated with pan-BET inhibitor JQ1 (400 nM) or BRD4-selective PROTAC degrader MZ-1 (50 nM), respectively, for the last 48h of 72h. Cell surface fluorescence staining and flow cytometry analysis were performed to measure expression changes of TIM-3, TIGIT, PD-1, CTLA-4 on CD4+, CD8+ T cells and NK cells. (A-C, G-I) Representative histograms show expression shifts, comparing stimulated-only cells with stimulated plus JQ1 or plus MZ-1 inhibitors. X-axis: intensity of fluorescence signal. Y-axis: number of events (D-F, J-L) Corresponding bar graphs show mean fluorescence intensity (MFI) of markers on T and NK cells, comparing stimulated cells to stimulated plus JQ1 or plus MZ-1. Two-tailed t-test and Mann Whitney U test determined statistical significance. (N=6; ns, p>0.05; *, p<0.05; **, p<0.01; ***, p<0.001; ****, p<0.0001)

Article Snippet: Pan-BET inhibitor JQ1 (Tocris), BRD4-selective PROTAC degrader MZ-1 (Tocris), and AMPK inhibitor Compound C (Tocris) were dissolved in DMSO to final concentrations of 400 nM, 50 nM and 5 μM respectively.

Techniques: Expressing, Purification, Ex Vivo, Fluorescence, Staining, Flow Cytometry, Two Tailed Test, MANN-WHITNEY

Journal: bioRxiv

Article Title: Unraveling AMPK and BET regulation of immune checkpoint biology: implications for personalized medicine

doi: 10.64898/2026.01.26.701869

Figure Lengend Snippet: PBMCs were activated ex vivo by anti-CD3 and anti-CD28 at 37□ for 72h as above. Cell surface fluorescence staining and flow cytometry were performed to measure expression of TIM-3, TIGIT, PD-1 and CTLA-4 on both T and NK cells. Experimental groups were: stimulated plus Compound C (2.5μM), stimulated plus JQ1/MZ1 (JQ1: 400nM, MZ1: 50nM), stimulated plus Compound C and JQ1/MZ1. (A-C, G-I) Histograms combined the expression shifts of four markers in cells treated by different condition. X-axis: intensity of fluorescence signal. Y-axis: number of events. (D-F, J-L) Bar graphs show mean fluorescence intensity (MFI) of TIM-3, TIGIT, PD-1 and CTLA-4, for stimulated cells treated with Compound C, JQ1/MZ1 respectively and combined. Two-tailed t-test and Mann Whitney U test was used to measure statistical significance. (ns, p>0.05; *, p<0.05; **, p<0.01; ***, p<0.001; ****, p<0.0001)

Article Snippet: Pan-BET inhibitor JQ1 (Tocris), BRD4-selective PROTAC degrader MZ-1 (Tocris), and AMPK inhibitor Compound C (Tocris) were dissolved in DMSO to final concentrations of 400 nM, 50 nM and 5 μM respectively.

Techniques: Ex Vivo, Fluorescence, Staining, Flow Cytometry, Expressing, Two Tailed Test, MANN-WHITNEY

Journal: Frontiers in Bioengineering and Biotechnology

Article Title: Inhibition of BRD4 activates the AKT-SIRT3 signaling pathway to suppress apoptosis and attenuate hyperoxia-induced lung injury

doi: 10.3389/fbioe.2025.1674916

Figure Lengend Snippet: BRD4 inhibition mitigates HILI in mice by activating the AKT/SIRT3 signaling. SD mice were assigned to Control, HILI, and HILI + JQ1 groups. (A) BRD4, SIRT3, p-AKT, and AKT protein levels in lung tissues from each group. (B) H&E staining of lung tissues from Control and HILI mice (×30.0 magnification; scale bar = 100 µm). (C) W/D weight ratio of lung tissues from each group. (D) MDA, SOD, and GSH levels in lung tissues from each group. (E) TNF-α and IL-6 levels in BALF from each group. (F) IFN-β, NF-κB, IL-1β, and TGF-β1 expression in lung tissues from each group was detected by RT-qPCR (G) TUNEL analysis of lung sections from each group. (H) The relative protein levels of Bax, Bcl-2, and in tissues from each group. * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001.

Article Snippet: HILI mice were exposed to oxygen at a high concentration of (≥95%; 5.0 L/min) for 72 h. For BRD4 inhibition in vivo , a BET bromodomain inhibitor JQ1 (Selleck Chemicals) was administrated to HILI mice.

Techniques: Inhibition, Control, Staining, Expressing, Quantitative RT-PCR, TUNEL Assay