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Image Search Results
Journal: BMC Biology
Article Title: Identification of Epinastine as CD96/PVR inhibitor for cancer immunotherapy
doi: 10.1186/s12915-025-02132-y
Figure Lengend Snippet: Virtual screening of small molecules from the FDA-approved drug library. A Crystal structure of CD96 in complex with PVR (PDB Code: 6ARQ), with the binding interface highlighted in blue. B Detailed depiction of amino acids involved in the CD96/PVR interaction, with residues shown in stick representation. C Relationship between molecular weight and S-value for selected small molecules. Red indicates molecules with molecular weights between 250 and 700 and S-values of -5 or less. D-F Results of further screening of small molecules interacting with the CD96/PVR binding interface. G Distribution of S-values for the final 15 selected small molecules
Article Snippet: 1729 small molecules were obtained from
Techniques: Drug discovery, Binding Assay, Molecular Weight
Journal: Cell communication and signaling : CCS
Article Title: BMX, a specific HDAC8 inhibitor, with TMZ for advanced CRC therapy: a novel synergic effect to elicit p53-, β-catenin- and MGMT-dependent apoptotic cell death.
doi: 10.1186/s12964-022-01007-x
Figure Lengend Snippet: Fig. 1 BMX, TMZ, oxaliplatin (Oxp) and doxorubicin (Dox) combination inhibited cell proliferation in CRC cells. (A) The proliferation of BMX, TMZ, Oxp, Dox, BMX plus TMZ, BMX plus Oxp or BMX plus Dox in HT29, HCT116 and RKO cells with various drug concentration. (B) Colony formation capability assay with different treatments of BMX, TMZ, Oxp, BMX plus TMZ, and BMX plus Oxp in HT29, HCT116 and RKO cells; the colonies were counted for quantification. (C) Cell cycle analysis after 48 h treatment with different concentrations of BMX alone or BMX combined with TMZ in HT29, HCT116, and RKO cells and the proportion of cells in each cell cycle phase. SubG1, cell with polyploid chromosome; > 4 N, polyploid cell. (D) Apoptosis analysis after 48 h treatment with different concentrations of BMX alone or BMX combined with TMZ and the apoptotic rate of cells in HT29, HCT116, and RKO cells. All results are shown as mean ± s.d. from three independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001 versus control (HT29 cells); #p < 0.05, ##p < 0.01, ###p < 0.001 vs. control (HCT116 cells); †p < 0.05, ††p < 0.01, †††p < 0.001 versus control (RKO cells)
Article Snippet: The
Techniques: Concentration Assay, Cell Cycle Assay, Control
Journal: Cell communication and signaling : CCS
Article Title: BMX, a specific HDAC8 inhibitor, with TMZ for advanced CRC therapy: a novel synergic effect to elicit p53-, β-catenin- and MGMT-dependent apoptotic cell death.
doi: 10.1186/s12964-022-01007-x
Figure Lengend Snippet: Fig. 5 BMX, VPA, SAHA, TMZ, Oxp, and Dox combination inhibited cell proliferation in CRC cells. (A) HDAC8 mRNA expression levels stimulated with BMX (5 µM), VPA (4 mM), SAHA (2 µM) with or without TMZ were determined using qRT-PCR assays. (B) HT29, HCT116, and RKO cells were treated with BMX with or without TMZ for 48 h. Then, cells were harvested for detection of acetyl-histone H3 (Lys9/Lys14), acetyl-histone H4 (Lys8), and HDAC8 by Western blot analysis. (C) The proliferation of BMX, VPA, SAHA with or without TMZ, Oxp (5 µM) and Dox (1 µM) in HT29, HCT116, and RKO cells with treatment durations were assayed using the CCK-8 method. (D) Colony formation capability assay with different treatments of BMX, VPA, SAHA with or without TMZ, Oxp and Dox in HT29, HCT116, and RKO cells; the colonies were counted for quantification. All results are shown as mean ± s.d. from three independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001 versus control (HT29 cells); #p < 0.05, ##p < 0.01, ###p < 0.001 versus control (HCT116 cells); †p < 0.05, ††p < 0.01, †††p < 0.001 versus control (RKO cells)
Article Snippet: The
Techniques: Expressing, Quantitative RT-PCR, Western Blot, CCK-8 Assay, Control
Journal: Cell communication and signaling : CCS
Article Title: BMX, a specific HDAC8 inhibitor, with TMZ for advanced CRC therapy: a novel synergic effect to elicit p53-, β-catenin- and MGMT-dependent apoptotic cell death.
doi: 10.1186/s12964-022-01007-x
Figure Lengend Snippet: Fig. 7 Autophagy expression levels stimulated with BMX and PCI-34051 in the presence or absence of TMZ. (A) HT29, HCT116, and RKO cells were treated with BMX and PCI-34051 with or without TMZ for 48 h. Then, cells were harvested for detection of acetyl-histone H3 (Lys9/Lys14), acetyl-histone H4 (Lys8), and HDAC8 by Western blot analysis. (B) The proliferation of BMX and PCI-34051 with or without TMZ in HT29, HCT116, and RKO cells. (C) Colony formation capability assay with different treatments of BMX and PCI-34051 with or without TMZ in HT29, HCT116, and RKO cells; the colonies were counted for quantification. (D, E) Expressions of cleaved caspase 3, cleaved PARP, LC3 and p62 proteins in HT29, HCT116, and RKO cells treated with BMX and PCI-34051 with or without TMZ for 48 h. All results are shown as mean ± s.d. from three independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001 versus control (HT29 cells); #p < 0.05, ##p < 0.01, ###p < 0.001 versus control (HCT116 cells); †p < 0.05, ††p < 0.01, †††p < 0.001 versus control (RKO cells)
Article Snippet: The
Techniques: Expressing, Western Blot, Control
Journal: Journal of Extracellular Vesicles
Article Title: Calcified apoptotic vesicles from PROCR + fibroblasts initiate heterotopic ossification
doi: 10.1002/jev2.12425
Figure Lengend Snippet: Single‐cell RNA‐sequencing (scRNA‐seq) analysis identifies novel apoptotic‐preferential PROCR + fibroblasts in the early stage of HO. (a) The workflow depicting the collection and processing of specimens of sham and HO tendons for scRNA‐seq. (b) Dimension reduction presentation (via tSNE) of combined single‐cell transcriptome data from Achilles tendons of rats from the sham and HO groups after 1 and 3 weeks ( n = 14402). Each dot represents a single cell and is labelled with corresponding cell categories and is coloured according to its cell type identity. Clusters were generated using a resolution of 0.2 before subclustering into major cell types according to the Methods. The Seurat 3 R‐Package segregation grouped the cells into 6 distinct cell clusters. (c and d) Quantitative analysis of clusters based on the combined single‐cell transcriptome data in (b). (e) tSNE of fibroblast clusters (F1–F5). (f) Apoptosis score analyses of fibroblasts based on (e). (g) Bioinformatic analysis of PROCR + cell populations based on (e). (h) Representation analysis of GO categories showing different functions for PROCR + cells. (i) Representation analysis of KEGG categories showing different functions for PROCR + cells.
Article Snippet: To inhibit
Techniques: Single Cell, RNA Sequencing, Generated