bms 582949  (MedChemExpress)

Journal: Cancer Medicine

Article Title: Carnosic Acid Mediates Production of Reactive Oxygen Species to Regulate Mitogen‐Activated Protein Kinase Pathway Phosphorylation and Induce Apoptosis in Human Breast Cancer Cells

doi: 10.1002/cam4.71446

Figure Lengend Snippet: SP600125 and BMS582949 were used to inhibit CA‐induced JNK and p38 phosphorylation. (A) T‐47D and (B) MCF‐7 cells were pre‐treated with SP600125 and BMS582949 for 2 h, followed by treatment with CA at 25 μM and 20 μM, respectively. Protein expression levels of p‐JNK, p‐p38, Bax, Bcl‐2, and PARP were measured by western blotting. (C) and (D) Relative cell viability was evaluated by MTT assays. Data are presented as mean ± SD of three independent experiments. * p < 0.05, ** p < 0.01 versus NC group.

Article Snippet: BMS‐582949 and SP600125 were purchased from Selleck (Shanghai, China).

Techniques: Phospho-proteomics, Expressing, Western Blot

Journal: Cancer Medicine

Article Title: Carnosic Acid Mediates Production of Reactive Oxygen Species to Regulate Mitogen‐Activated Protein Kinase Pathway Phosphorylation and Induce Apoptosis in Human Breast Cancer Cells

doi: 10.1002/cam4.71446

Figure Lengend Snippet: SP600125 and BMS582949 were used to inhibit CA‐induced JNK and p38 phosphorylation. (A) T‐47D and (B) MCF‐7 cells were pre‐treated with SP600125 and BMS582949 for 2 h, followed by treatment with CA at 25 μM and 20 μM, respectively. Protein expression levels of p‐JNK, p‐p38, Bax, Bcl‐2, and PARP were measured by western blotting. (C) and (D) Relative cell viability was evaluated by MTT assays. Data are presented as mean ± SD of three independent experiments. * p < 0.05, ** p < 0.01 versus NC group.

Article Snippet: BMS‐582949 and SP600125 were purchased from Selleck (Shanghai, China).

Techniques: Phospho-proteomics, Expressing, Western Blot

Journal: Frontiers in Immunology

Article Title: Macrophage migration inhibitory factor–CD74 axis drives vascular smooth muscle cell–induced M1 macrophage polarization to exacerbate intracranial aneurysm inflammation

doi: 10.3389/fimmu.2025.1682762

Figure Lengend Snippet: Hypomethylation of MIF and CD74 in dataset GSE75434 . (A-C) Methylation data quality control. (D) Genomic distribution of methylation probes. (E, F) Significantly reduced methylation levels at MIF and CD74 loci in IAs versus control arteries. ** and * indicate p-values less than 0.01 and 0.05, respectively.

Article Snippet: Experimental groups were: (1) Control VSMCs + Macrophages; (2) Secretory VSMCs + Macrophages; (3) Secretory VSMCs + Macrophages + 10 μg/mL anti-human MIF monoclonal antibody (Abcam); (4) Secretory VSMCs + Macrophages + 5 μM CD74 inhibitor BMS-582949 (MedChemExpress).

Techniques: Methylation, Control

Journal: Frontiers in Immunology

Article Title: Macrophage migration inhibitory factor–CD74 axis drives vascular smooth muscle cell–induced M1 macrophage polarization to exacerbate intracranial aneurysm inflammation

doi: 10.3389/fimmu.2025.1682762

Figure Lengend Snippet: Cell-cell communication analysis. (A) Global communication network showing interaction strength between major cell types. (B) Interaction weights for MIF ligand-receptor pairs. (C) Chord diagram highlighting MIF-CD74/CD44 signaling between VSMCs and M1-like macrophages. (D) Increased interaction strength and number between secretory VSMCs and M1-like macrophages in IAs. (E) Differential signaling pathway activity between secretory VSMCs and M1-like macrophages across conditions. (F) Heatmap showing communication probability for key pathways between secretory VSMCs and M1-like macrophages. (G) Expression patterns of key MIF axis components (Mif, Cd74, Cd44) across cell types.

Article Snippet: Experimental groups were: (1) Control VSMCs + Macrophages; (2) Secretory VSMCs + Macrophages; (3) Secretory VSMCs + Macrophages + 10 μg/mL anti-human MIF monoclonal antibody (Abcam); (4) Secretory VSMCs + Macrophages + 5 μM CD74 inhibitor BMS-582949 (MedChemExpress).

Techniques: Activity Assay, Expressing

Journal: Frontiers in Immunology

Article Title: Macrophage migration inhibitory factor–CD74 axis drives vascular smooth muscle cell–induced M1 macrophage polarization to exacerbate intracranial aneurysm inflammation

doi: 10.3389/fimmu.2025.1682762

Figure Lengend Snippet: Secretory VSMCs drive macrophage M1 polarization via the MIF-CD74 axis. (A, B) qPCR analysis of iNOS and Arg1 expression in macrophages following Transwell co-culture. Secretory VSMCs increase iNOS and decrease Arg1; anti-MIF antibody or CD74 inhibitor (BMS-582949) attenuates this effect. (C) Flow cytometry quantification of CD86 + macrophages. Secretory VSMCs increase CD86 + proportion; inhibition of MIF or CD74 reduces it. (D, E) qPCR validation of MIF knockdown efficiency in VSMCs and its effect on macrophage iNOS/Arg1 expression in co-culture. MIF knockdown reverses secretory VSMC-induced polarization. (F) Flow cytometry shows MIF knockdown reduces CD86 + macrophage proportion induced by secretory VSMCs. (G, H) qPCR analysis of macrophages treated with secretory VSMC conditioned medium (CM). CM increases iNOS and decreases Arg1; CD74 inhibition reverses this. (I) Flow cytometry shows CD74 inhibition reduces CM-induced increase in CD86 + macrophages. Data are mean ± SEM; P < 0.01, P < 0.05 versus control; ##P < 0.01, #P < 0.05 versus secretory VSMC group (One-way ANOVA with Tukey’s post hoc test).

Article Snippet: Experimental groups were: (1) Control VSMCs + Macrophages; (2) Secretory VSMCs + Macrophages; (3) Secretory VSMCs + Macrophages + 10 μg/mL anti-human MIF monoclonal antibody (Abcam); (4) Secretory VSMCs + Macrophages + 5 μM CD74 inhibitor BMS-582949 (MedChemExpress).

Techniques: Expressing, Co-Culture Assay, Flow Cytometry, Inhibition, Biomarker Discovery, Knockdown, Control

Journal: Cell Reports Methods

Article Title: RECOVER identifies synergistic drug combinations in vitro through sequential model optimization

doi: 10.1016/j.crmeth.2023.100599

Figure Lengend Snippet:

Article Snippet: BMS-582949 (hydrochloride) , MedChem Express , HY-14305A.

Techniques: Software, Recombinant