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brm014 compounds  (MedChemExpress)


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    MedChemExpress brm014 compounds
    A. Schematic representation of the experimental design depicting the treatment of HepG2 cells with 10 μM <t>BRM014</t> for 1, 6, and 24 h, as well as 6 h and 24 h recovery after 24 h BRM014 treatment. B. Average profiles of DNA conversion rate around OCR with or without SWI/SNF binding sites defined by ChIP-seq, illustrating changes in chromatin accessibility following different durations of BRM014 treatment and recovery (Control 0 h-32%, 1 h-31%, 6 h-32%, 24 h-29%, R6 h-33%, R24 h-33%). C. Heatmap showing TFOS change ratio in SWI/SNF+ regions across different BRM014 treatment conditions for 134 filtered TFs in HepG2 cells. The TFs are clustered into four groups based on change ratio of TFOS across treatments. Grids color represents the dynamic change ratio compared with controls D. Butterfly graph shows flanking chromatin accessibility change ratio (left) and TFOS change ratio (right) of representative TFs in different clusters, which represent changes in flanking accessibility and TF occupancy. E. Average profiles and heatmap of overall DNA conversion rate around HNF1A binding sites in SWI/SNF+ regions (left), illustrating changes in chromatin accessibility, nucleosome position and TF occupancy after BRM014 treatment and recovery. Plot graphs of flanking chromatin accessibility, TFOS and their change ratio are shown (Right). Flanking chromatin accessibility around the TF binding motifs are calculated as the average DNA conversion rate in the 50 bp flanking regions on both sides of the motif as flanking chromatin accessibility F-H. Average profiles of DNA conversion rate around TF binding sites of HNF4A and FOSL1 (F), FOXA1 and CEBPB (G), CTCF and YY1 (H) under control, 1 h, 6 h, and 24 h BRM014 treatments, as well as 6 h and 24 h recovery after 24 h BRM014 treatment. The profiles show changes in chromatin accessibility and TF footprints across different treatment conditions. See also Figures S8, Table S4
    Brm014 Compounds, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 45 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/brm014 compounds/product/MedChemExpress
    Average 95 stars, based on 45 article reviews
    brm014 compounds - by Bioz Stars, 2026-06
    95/100 stars

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    1) Product Images from "Genome-Wide Investigation of Transcription Factor Occupancy and Dynamics Using cFOOT-seq"

    Article Title: Genome-Wide Investigation of Transcription Factor Occupancy and Dynamics Using cFOOT-seq

    Journal: bioRxiv

    doi: 10.1101/2025.07.17.664523

    A. Schematic representation of the experimental design depicting the treatment of HepG2 cells with 10 μM BRM014 for 1, 6, and 24 h, as well as 6 h and 24 h recovery after 24 h BRM014 treatment. B. Average profiles of DNA conversion rate around OCR with or without SWI/SNF binding sites defined by ChIP-seq, illustrating changes in chromatin accessibility following different durations of BRM014 treatment and recovery (Control 0 h-32%, 1 h-31%, 6 h-32%, 24 h-29%, R6 h-33%, R24 h-33%). C. Heatmap showing TFOS change ratio in SWI/SNF+ regions across different BRM014 treatment conditions for 134 filtered TFs in HepG2 cells. The TFs are clustered into four groups based on change ratio of TFOS across treatments. Grids color represents the dynamic change ratio compared with controls D. Butterfly graph shows flanking chromatin accessibility change ratio (left) and TFOS change ratio (right) of representative TFs in different clusters, which represent changes in flanking accessibility and TF occupancy. E. Average profiles and heatmap of overall DNA conversion rate around HNF1A binding sites in SWI/SNF+ regions (left), illustrating changes in chromatin accessibility, nucleosome position and TF occupancy after BRM014 treatment and recovery. Plot graphs of flanking chromatin accessibility, TFOS and their change ratio are shown (Right). Flanking chromatin accessibility around the TF binding motifs are calculated as the average DNA conversion rate in the 50 bp flanking regions on both sides of the motif as flanking chromatin accessibility F-H. Average profiles of DNA conversion rate around TF binding sites of HNF4A and FOSL1 (F), FOXA1 and CEBPB (G), CTCF and YY1 (H) under control, 1 h, 6 h, and 24 h BRM014 treatments, as well as 6 h and 24 h recovery after 24 h BRM014 treatment. The profiles show changes in chromatin accessibility and TF footprints across different treatment conditions. See also Figures S8, Table S4
    Figure Legend Snippet: A. Schematic representation of the experimental design depicting the treatment of HepG2 cells with 10 μM BRM014 for 1, 6, and 24 h, as well as 6 h and 24 h recovery after 24 h BRM014 treatment. B. Average profiles of DNA conversion rate around OCR with or without SWI/SNF binding sites defined by ChIP-seq, illustrating changes in chromatin accessibility following different durations of BRM014 treatment and recovery (Control 0 h-32%, 1 h-31%, 6 h-32%, 24 h-29%, R6 h-33%, R24 h-33%). C. Heatmap showing TFOS change ratio in SWI/SNF+ regions across different BRM014 treatment conditions for 134 filtered TFs in HepG2 cells. The TFs are clustered into four groups based on change ratio of TFOS across treatments. Grids color represents the dynamic change ratio compared with controls D. Butterfly graph shows flanking chromatin accessibility change ratio (left) and TFOS change ratio (right) of representative TFs in different clusters, which represent changes in flanking accessibility and TF occupancy. E. Average profiles and heatmap of overall DNA conversion rate around HNF1A binding sites in SWI/SNF+ regions (left), illustrating changes in chromatin accessibility, nucleosome position and TF occupancy after BRM014 treatment and recovery. Plot graphs of flanking chromatin accessibility, TFOS and their change ratio are shown (Right). Flanking chromatin accessibility around the TF binding motifs are calculated as the average DNA conversion rate in the 50 bp flanking regions on both sides of the motif as flanking chromatin accessibility F-H. Average profiles of DNA conversion rate around TF binding sites of HNF4A and FOSL1 (F), FOXA1 and CEBPB (G), CTCF and YY1 (H) under control, 1 h, 6 h, and 24 h BRM014 treatments, as well as 6 h and 24 h recovery after 24 h BRM014 treatment. The profiles show changes in chromatin accessibility and TF footprints across different treatment conditions. See also Figures S8, Table S4

    Techniques Used: Binding Assay, ChIP-sequencing, Control

    A. Heatmap showing the change ratio of flanking chromatin accessibility around TF binding sites at promoter (left) and enhancer (right) for 100 TFs in HegG2 cells. TFs are grouped into four clusters based on their change ratios at different time points following BRM014 treatment. Grids color represents the dynamic change ratio compared with controls B. Sankey diagram illustrating the correspondence between the enhancer and promoter clustering categories for each TF as defined in panel A. TFs highlighted in cluster 1 or cluster 4 in both promoter and enhancer regions represent those that are highly resistant or highly sensitive to BRM014 treatment. C. Violin plot showing the distribution of change ratios in flanking chromatin accessibility for enhancers (green) and promoters (blue) in HepG2 cells after 24 h of BRM014 treatment, with statistical significance indicated **** (p.value <0.0001). D. Sunburst plot illustrating the sensitivity of TFs to BRM014 treatment, organized by clusters and families in HepG2 cells. The inner circle categorizes TFs into highly sensitive (dark red), moderately sensitive (light red), ambiguous (gray), moderately resistant (light blue), and highly resistant (dark blue) groups. The middle circle indicates TF family classifications, with each family color-coded as shown in the legend on the bottom. Each TF is labeled around the circular plot, with colored dots representing their respective categories of BRM014 sensitivity. E. The network diagram displays the Transcription factor co-occurrence network with the enhancer regions of HepG2. Each node represents a different TF, with the color coding indicating varying levels of sensitivity or resistance. Edges between nodes indicate potential co-occurrence relationships among the TFs F. The bar graph displays the edge density in transcription factor co-occurrence network within the enhancer regions of HepG2 cells among transcription factor pairs, categorized by their sensitivity to BRM014. The categories include interactions between TF pairs that are both resistant (blue bar), one resistant and one sensitive (grey bar), and both sensitive (red bar). See also Figures S9, Table S5
    Figure Legend Snippet: A. Heatmap showing the change ratio of flanking chromatin accessibility around TF binding sites at promoter (left) and enhancer (right) for 100 TFs in HegG2 cells. TFs are grouped into four clusters based on their change ratios at different time points following BRM014 treatment. Grids color represents the dynamic change ratio compared with controls B. Sankey diagram illustrating the correspondence between the enhancer and promoter clustering categories for each TF as defined in panel A. TFs highlighted in cluster 1 or cluster 4 in both promoter and enhancer regions represent those that are highly resistant or highly sensitive to BRM014 treatment. C. Violin plot showing the distribution of change ratios in flanking chromatin accessibility for enhancers (green) and promoters (blue) in HepG2 cells after 24 h of BRM014 treatment, with statistical significance indicated **** (p.value <0.0001). D. Sunburst plot illustrating the sensitivity of TFs to BRM014 treatment, organized by clusters and families in HepG2 cells. The inner circle categorizes TFs into highly sensitive (dark red), moderately sensitive (light red), ambiguous (gray), moderately resistant (light blue), and highly resistant (dark blue) groups. The middle circle indicates TF family classifications, with each family color-coded as shown in the legend on the bottom. Each TF is labeled around the circular plot, with colored dots representing their respective categories of BRM014 sensitivity. E. The network diagram displays the Transcription factor co-occurrence network with the enhancer regions of HepG2. Each node represents a different TF, with the color coding indicating varying levels of sensitivity or resistance. Edges between nodes indicate potential co-occurrence relationships among the TFs F. The bar graph displays the edge density in transcription factor co-occurrence network within the enhancer regions of HepG2 cells among transcription factor pairs, categorized by their sensitivity to BRM014. The categories include interactions between TF pairs that are both resistant (blue bar), one resistant and one sensitive (grey bar), and both sensitive (red bar). See also Figures S9, Table S5

    Techniques Used: Binding Assay, Labeling



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    brm014 compounds  (MedChemExpress)
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    MedChemExpress brm014 compounds
    A. Schematic representation of the experimental design depicting the treatment of HepG2 cells with 10 μM <t>BRM014</t> for 1, 6, and 24 h, as well as 6 h and 24 h recovery after 24 h BRM014 treatment. B. Average profiles of DNA conversion rate around OCR with or without SWI/SNF binding sites defined by ChIP-seq, illustrating changes in chromatin accessibility following different durations of BRM014 treatment and recovery (Control 0 h-32%, 1 h-31%, 6 h-32%, 24 h-29%, R6 h-33%, R24 h-33%). C. Heatmap showing TFOS change ratio in SWI/SNF+ regions across different BRM014 treatment conditions for 134 filtered TFs in HepG2 cells. The TFs are clustered into four groups based on change ratio of TFOS across treatments. Grids color represents the dynamic change ratio compared with controls D. Butterfly graph shows flanking chromatin accessibility change ratio (left) and TFOS change ratio (right) of representative TFs in different clusters, which represent changes in flanking accessibility and TF occupancy. E. Average profiles and heatmap of overall DNA conversion rate around HNF1A binding sites in SWI/SNF+ regions (left), illustrating changes in chromatin accessibility, nucleosome position and TF occupancy after BRM014 treatment and recovery. Plot graphs of flanking chromatin accessibility, TFOS and their change ratio are shown (Right). Flanking chromatin accessibility around the TF binding motifs are calculated as the average DNA conversion rate in the 50 bp flanking regions on both sides of the motif as flanking chromatin accessibility F-H. Average profiles of DNA conversion rate around TF binding sites of HNF4A and FOSL1 (F), FOXA1 and CEBPB (G), CTCF and YY1 (H) under control, 1 h, 6 h, and 24 h BRM014 treatments, as well as 6 h and 24 h recovery after 24 h BRM014 treatment. The profiles show changes in chromatin accessibility and TF footprints across different treatment conditions. See also Figures S8, Table S4
    Brm014 Compounds, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/brm014 compounds/product/MedChemExpress
    Average 95 stars, based on 1 article reviews
    brm014 compounds - by Bioz Stars, 2026-06
    95/100 stars
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    A. Schematic representation of the experimental design depicting the treatment of HepG2 cells with 10 μM BRM014 for 1, 6, and 24 h, as well as 6 h and 24 h recovery after 24 h BRM014 treatment. B. Average profiles of DNA conversion rate around OCR with or without SWI/SNF binding sites defined by ChIP-seq, illustrating changes in chromatin accessibility following different durations of BRM014 treatment and recovery (Control 0 h-32%, 1 h-31%, 6 h-32%, 24 h-29%, R6 h-33%, R24 h-33%). C. Heatmap showing TFOS change ratio in SWI/SNF+ regions across different BRM014 treatment conditions for 134 filtered TFs in HepG2 cells. The TFs are clustered into four groups based on change ratio of TFOS across treatments. Grids color represents the dynamic change ratio compared with controls D. Butterfly graph shows flanking chromatin accessibility change ratio (left) and TFOS change ratio (right) of representative TFs in different clusters, which represent changes in flanking accessibility and TF occupancy. E. Average profiles and heatmap of overall DNA conversion rate around HNF1A binding sites in SWI/SNF+ regions (left), illustrating changes in chromatin accessibility, nucleosome position and TF occupancy after BRM014 treatment and recovery. Plot graphs of flanking chromatin accessibility, TFOS and their change ratio are shown (Right). Flanking chromatin accessibility around the TF binding motifs are calculated as the average DNA conversion rate in the 50 bp flanking regions on both sides of the motif as flanking chromatin accessibility F-H. Average profiles of DNA conversion rate around TF binding sites of HNF4A and FOSL1 (F), FOXA1 and CEBPB (G), CTCF and YY1 (H) under control, 1 h, 6 h, and 24 h BRM014 treatments, as well as 6 h and 24 h recovery after 24 h BRM014 treatment. The profiles show changes in chromatin accessibility and TF footprints across different treatment conditions. See also Figures S8, Table S4

    Journal: bioRxiv

    Article Title: Genome-Wide Investigation of Transcription Factor Occupancy and Dynamics Using cFOOT-seq

    doi: 10.1101/2025.07.17.664523

    Figure Lengend Snippet: A. Schematic representation of the experimental design depicting the treatment of HepG2 cells with 10 μM BRM014 for 1, 6, and 24 h, as well as 6 h and 24 h recovery after 24 h BRM014 treatment. B. Average profiles of DNA conversion rate around OCR with or without SWI/SNF binding sites defined by ChIP-seq, illustrating changes in chromatin accessibility following different durations of BRM014 treatment and recovery (Control 0 h-32%, 1 h-31%, 6 h-32%, 24 h-29%, R6 h-33%, R24 h-33%). C. Heatmap showing TFOS change ratio in SWI/SNF+ regions across different BRM014 treatment conditions for 134 filtered TFs in HepG2 cells. The TFs are clustered into four groups based on change ratio of TFOS across treatments. Grids color represents the dynamic change ratio compared with controls D. Butterfly graph shows flanking chromatin accessibility change ratio (left) and TFOS change ratio (right) of representative TFs in different clusters, which represent changes in flanking accessibility and TF occupancy. E. Average profiles and heatmap of overall DNA conversion rate around HNF1A binding sites in SWI/SNF+ regions (left), illustrating changes in chromatin accessibility, nucleosome position and TF occupancy after BRM014 treatment and recovery. Plot graphs of flanking chromatin accessibility, TFOS and their change ratio are shown (Right). Flanking chromatin accessibility around the TF binding motifs are calculated as the average DNA conversion rate in the 50 bp flanking regions on both sides of the motif as flanking chromatin accessibility F-H. Average profiles of DNA conversion rate around TF binding sites of HNF4A and FOSL1 (F), FOXA1 and CEBPB (G), CTCF and YY1 (H) under control, 1 h, 6 h, and 24 h BRM014 treatments, as well as 6 h and 24 h recovery after 24 h BRM014 treatment. The profiles show changes in chromatin accessibility and TF footprints across different treatment conditions. See also Figures S8, Table S4

    Article Snippet: BRM014 compounds (BRM/BRG1 ATP Inhibitor-1, MedChem Express) dissolved in dimethyl sulfoxide (DMSO) to final concentration of 10 mM.

    Techniques: Binding Assay, ChIP-sequencing, Control

    A. Heatmap showing the change ratio of flanking chromatin accessibility around TF binding sites at promoter (left) and enhancer (right) for 100 TFs in HegG2 cells. TFs are grouped into four clusters based on their change ratios at different time points following BRM014 treatment. Grids color represents the dynamic change ratio compared with controls B. Sankey diagram illustrating the correspondence between the enhancer and promoter clustering categories for each TF as defined in panel A. TFs highlighted in cluster 1 or cluster 4 in both promoter and enhancer regions represent those that are highly resistant or highly sensitive to BRM014 treatment. C. Violin plot showing the distribution of change ratios in flanking chromatin accessibility for enhancers (green) and promoters (blue) in HepG2 cells after 24 h of BRM014 treatment, with statistical significance indicated **** (p.value <0.0001). D. Sunburst plot illustrating the sensitivity of TFs to BRM014 treatment, organized by clusters and families in HepG2 cells. The inner circle categorizes TFs into highly sensitive (dark red), moderately sensitive (light red), ambiguous (gray), moderately resistant (light blue), and highly resistant (dark blue) groups. The middle circle indicates TF family classifications, with each family color-coded as shown in the legend on the bottom. Each TF is labeled around the circular plot, with colored dots representing their respective categories of BRM014 sensitivity. E. The network diagram displays the Transcription factor co-occurrence network with the enhancer regions of HepG2. Each node represents a different TF, with the color coding indicating varying levels of sensitivity or resistance. Edges between nodes indicate potential co-occurrence relationships among the TFs F. The bar graph displays the edge density in transcription factor co-occurrence network within the enhancer regions of HepG2 cells among transcription factor pairs, categorized by their sensitivity to BRM014. The categories include interactions between TF pairs that are both resistant (blue bar), one resistant and one sensitive (grey bar), and both sensitive (red bar). See also Figures S9, Table S5

    Journal: bioRxiv

    Article Title: Genome-Wide Investigation of Transcription Factor Occupancy and Dynamics Using cFOOT-seq

    doi: 10.1101/2025.07.17.664523

    Figure Lengend Snippet: A. Heatmap showing the change ratio of flanking chromatin accessibility around TF binding sites at promoter (left) and enhancer (right) for 100 TFs in HegG2 cells. TFs are grouped into four clusters based on their change ratios at different time points following BRM014 treatment. Grids color represents the dynamic change ratio compared with controls B. Sankey diagram illustrating the correspondence between the enhancer and promoter clustering categories for each TF as defined in panel A. TFs highlighted in cluster 1 or cluster 4 in both promoter and enhancer regions represent those that are highly resistant or highly sensitive to BRM014 treatment. C. Violin plot showing the distribution of change ratios in flanking chromatin accessibility for enhancers (green) and promoters (blue) in HepG2 cells after 24 h of BRM014 treatment, with statistical significance indicated **** (p.value <0.0001). D. Sunburst plot illustrating the sensitivity of TFs to BRM014 treatment, organized by clusters and families in HepG2 cells. The inner circle categorizes TFs into highly sensitive (dark red), moderately sensitive (light red), ambiguous (gray), moderately resistant (light blue), and highly resistant (dark blue) groups. The middle circle indicates TF family classifications, with each family color-coded as shown in the legend on the bottom. Each TF is labeled around the circular plot, with colored dots representing their respective categories of BRM014 sensitivity. E. The network diagram displays the Transcription factor co-occurrence network with the enhancer regions of HepG2. Each node represents a different TF, with the color coding indicating varying levels of sensitivity or resistance. Edges between nodes indicate potential co-occurrence relationships among the TFs F. The bar graph displays the edge density in transcription factor co-occurrence network within the enhancer regions of HepG2 cells among transcription factor pairs, categorized by their sensitivity to BRM014. The categories include interactions between TF pairs that are both resistant (blue bar), one resistant and one sensitive (grey bar), and both sensitive (red bar). See also Figures S9, Table S5

    Article Snippet: BRM014 compounds (BRM/BRG1 ATP Inhibitor-1, MedChem Express) dissolved in dimethyl sulfoxide (DMSO) to final concentration of 10 mM.

    Techniques: Binding Assay, Labeling