brm brg1 atpase swi snf inhibitor brm014  (MedChemExpress)

Journal: bioRxiv

Article Title: A Conserved Chromatin-Driven Checkpoint Defines Late Macrophage Maturation Independent of Tissue Specialization

doi: 10.64898/2026.07.01.735834

Figure Lengend Snippet: A) Genomic Locus Overlap Enrichment Analysis (LOLA) of differentially accessible regions (DARs) between day 13 and day 11, stratified according to the four clusters defined in A) (open promoter, n = 477 DARs; open distal, n = 368 DARs; closed promoter, n = 309 DARs; closed distal, n = 1,008 DARs). Enrichment was performed against the database of transcriptional regulators peaks from ReMap2022. Statistical significance was assessed using Fisher’s exact test implemented in LOLA (FDR-adjusted p < 0.05). The x-axis represents the odds ratio, and adjusted FDR values are indicated in the labels (ns, grey; FDR < 0.05, light blue; FDR < 0.005, blue; FDR < 0,0005 dark blue). The background universe corresponds to all accessible regions detected in the ATAC-Seq dataset. B) Functional enrichment analysis of the nearest associated genes to the defined DARs using ChEA gene sets. , Enrichment was assessed using a one-sided hypergeometric test with false discovery rate correction (Benjamini–Hochberg). The x-axis shows the number of enriched genes, and adjusted P values are indicated in the labels. The background gene universe corresponds to all genes associated with peak detected in the ATAC-seq dataset. C) Heatmap of differentially expressed genes (DEGs) induced by BAF inhibition, identified by comparing BAF inhibitor–treated samples (BRM/BRG1 ATP Inhibitor-1 - BRM014; 0.016, 0.08, and 0.4 µM; pink gradient from light to dark) to untreated controls. The inhibitor was applied at day 12 and RNA was collected at day 13 (DESeq2 with apeglm LFC shrinkage; adjusted p < 0.05; |fold change| > 1.5). Expression values are scaled by row (turquoise to yellow).

Article Snippet: On day 12, cells were treated for 24 h with the BRM/BRG1 ATPase (SWI/SNF) inhibitor BRM014 (MedChemExpress, cat. no. HY-119374) at final concentrations of 400, 80, or 16 nM, with PBS-treated wells included as controls.

Techniques: Functional Assay, Inhibition, Expressing

Journal: bioRxiv

Article Title: Chromatin modifiers KMT2D, BAF, and p300 are required for de novo binding of transcription factors on enhancers

doi: 10.64898/2026.01.29.702555

Figure Lengend Snippet: (A) Schematic of the 4-OHT-inducible MyoD-ER system. (B) MyoD expression in preadipocytes and C2C12 myoblasts was determined using RNA-Seq (n = 1). RPKM values indicate gene expression levels. (C) Western blot (WB) analysis of nuclear extracts from preadipocytes expressing MyoD-ER-T7 and treated with 4-OHT. Antibodies used were indicated on the right. BRG1 was used as a loading control. (D-I) MyoD-ER-T7 expressing preadipocytes were treated with 4-OHT for 1 hour (h), followed by CUT&RUN analysis. (D) Bar chart showing ARID1A (an exclusive subunit of BAF), KMT2D, and p300 binding status on induced MyoD sites. (E) Box plots displaying the normalized MyoD read counts in subgroups defined in (D). (F) Bar chart showing ARID1A (BAF), KMT2D, and p300 binding on 38,732 MyoD + enhancers defined in (D) prior to 4-OHT treatment. (G-H) Box plots showing the normalized MyoD read counts (G) and HOMER de novo motif analysis (H) on BAF-KMT2D-p300 prebound or de novo sites defined in (F). Statistical significance was determined using a two-sided, unpaired Mann Whitney test. (I) Genome browser view of MyoD binding sites around Maged1 and Cap2 loci.

Article Snippet: BRG1 Inhibitor BRM014 (#HY-119374) and 5Ph-IAA (#HY-134653) were from MedChemExpress (MCE) and used at 1μM.

Techniques: Expressing, RNA Sequencing, Gene Expression, Western Blot, Control, Binding Assay, MANN-WHITNEY

Journal: bioRxiv

Article Title: Chromatin modifiers KMT2D, BAF, and p300 are required for de novo binding of transcription factors on enhancers

doi: 10.64898/2026.01.29.702555

Figure Lengend Snippet: (A) Sanger sequencing results verifying the integration of 132-bp AID sequence after the start codon (ATG) of Kmt2d . (B) Breeding scheme for generating Kmt2c f/f ; Kmt2d AID/AID ; Cre-ER mice. (C) Diagram illustrating the workflow to generate Kmt2c -/- ; Kmt2d AID/AID preadipocytes expressing OsTIR1-F74G-Myc and MyoD-ER-T7. (D) WB of nuclear extracts confirming KMT2C knockout. Antibodies used were indicated on the right. BRG1 was a loading control. (E) WB of nuclear extracts confirming the depletion of KMT2D in Kmt2d AID/AID ; MyoD-ER-T7 preadipocytes upon 5Ph-IAA treatment for various time durations. Antibodies used were indicated on the right. RbBP5 was a loading control.

Article Snippet: BRG1 Inhibitor BRM014 (#HY-119374) and 5Ph-IAA (#HY-134653) were from MedChemExpress (MCE) and used at 1μM.

Techniques: Sequencing, Expressing, Knock-Out, Control

Journal: bioRxiv

Article Title: Chromatin modifiers KMT2D, BAF, and p300 are required for de novo binding of transcription factors on enhancers

doi: 10.64898/2026.01.29.702555

Figure Lengend Snippet: Kmt2d AID/AID ; MyoD-ER-T7 preadipocytes were pretreated with BRG1 inhibitor BRM014 (BRG1i) for 1h, and then 4-OHT was added for 1h to induce MyoD nuclear translocation. Cells were harvested for WB, CUT&RUN, and ATAC-seq. (A) WB of nuclear extracts for KMT2D, p300, and BAF subunits BRG1 and ARID1A. (B) Pie chart illustrating BAF binding status on 38,732 MyoD + enhancers. (C) Heat maps for CUT&RUN of ARID1A (BAF), T7 (MyoD), KMT2D, and p300 on BAF pre-bound and de novo BAF binding sites. (D-E) Chromatin accessibility determined by ATAC-seq signals on MyoD + enhancers. Chromatin accessibility status on BAF prebound sites (D) or de novo BAF binding sites (E) is shown in pie charts ( upper panels ). Average profiles of normalized ATAC-seq reads on constitutively open and MyoD-dependent opening sites are shown in lower panels .

Article Snippet: BRG1 Inhibitor BRM014 (#HY-119374) and 5Ph-IAA (#HY-134653) were from MedChemExpress (MCE) and used at 1μM.

Techniques: Translocation Assay, Binding Assay

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

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