brd4 (Cell Signaling Technology Inc)
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Brd4, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 33 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti+brd4/BRD4+(pan)+Rabbit+mAb/pmc12997339-330-23-28
Average 94 stars, based on 33 article reviews
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1) Product Images from "Nutrient-driven histone acetylation underlies energy storage and mobilization"
Article Title: Nutrient-driven histone acetylation underlies energy storage and mobilization
Journal: Molecular Metabolism
doi: 10.1016/j.molmet.2026.102344
Figure Legend Snippet: BHB-mediated HDAC inhibition shifts hepatic anabolism toward lipid oxidation. (A) Experimental design. (B) Serum gross appearance and the FFA levels ( n = 5). (C) Body weight loss of mice with the indicated treatment ( n = 5). (D and E) ChIP-seq data displaying H3K27ac (D) or BRD4 (E) occupancy at two subsets of genes: H3K27ac and BRD4 enriched at the genomic loci of fasting-induced transcripts (energy mobilization associated genes, such as Cyp4a14), but dislodged from those loci of fasting-suppressed transcripts (energy storage-associated genes, such as Pcsk9). (ref. to Hsieh et al., 2022, Mol Cell for detail method of analysis). (F and G) GO enrichment analysis of the fasting-induced H3K27ac (F) and BRD4 (G) peak-associated genes. The reads number of the ChIP-seq data for H3K27ac (log2FC > 1 and P < 0.01) or BRD4 (log2FC > 1.2 and P < 0.01) were included as the fasting-induced peaks. (H and I) Gene tracks display that fasting induced the occupancy of H3K27ac and BRD4 at the genomic loci of energy mobilization-associated genes (Cyp4a14, Pck1) (H), but reduced at those loci of energy storage-associated genes (Pcsk9, Srebf1) (I). (J) The ratio of the liver to body weight (upper panel) and the liver triglycerides levels (lower panel) of mice with the indicated treatment ( n = 5). (K-O) Body weight loss data (K), serum gross appearance and FFA levels (L), the blood glucose and BHB levels (M), the ratio of liver to body weight (N) and Liver triglycerides (O)of Brd 4 -flox or Brd4 hKO mice subjected to 24 h of fasting ( n = 5). Data are shown as the mean ± SEM. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001 by unpaired two-tailed Student’s t-test (K-O) or one-way ANOVA followed with Bonferroni’s multiple comparisons test (B, C, and J).
Techniques Used: Inhibition, ChIP-sequencing, Two Tailed Test
Figure Legend Snippet: Glucose-mediated histone acetylation promotes lipogenesis. (A-D) ChIP-seq data showed that re-feeding induced a significant redistribution of H3K27ac and BRD4 in the whole genome (A and B) with an increased occupancy at the genomic loci of lipids synthesis genes ( Srebf1 , Pcsk9 ) (C) but a decreased occupancy at those of fatty acids catabolic ( Cyp4a14 ) and gluconeogenic genes ( Pck1 ) (D). (E and F) qPCR assay showed that re-feeding induced the expression of glucose utilization ( Gck ) and lipid synthesis genes ( Pcsk9 , Hmgcr , Dgat1 , Srebf1 ) in the liver (E), while the expression was suppressed by JQ35 treatment (F) ( n = 4). (G and H) Brd 4 -flox or Brd 4 -hKO mice housed in a thermoneutral environment (30°C) feeding with high-fat diet. Hepatic Brd4 knockout suppressed body weight gain (G) without influence food intake (H) ( n = 5–6). (I-L) ITT assays (I) , liver weight (J), the liver gross appearance, HE and Oil Red O staining (K), and TG levels (L) of Brd 4 -flox or Brd 4 -hKO mice that were subjected to HFD feeding with housing at 30°C ( n = 5–6). (M) qPCR assay of lipids anabolism- ( Cd36 , Pparg , Dgat1 ) and VLDLs secretion/metabolism- ( Mttp , Apoc3 ) associated genes in the liver of Brd 4 -flox or Brd 4 -hKO mice ( n = 5–6). (N) The serum ALT levels were lower in Brd 4 -hKO than that of control mice ( n = 5–6). (O-Q) WAT weight (O) and serum TG (P) and FFA (Q) levels of Brd 4 -flox or Brd 4 -hKO mice under HFD feeding ( n = 5–6). Data are shown as the mean ± SEM. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001 by unpaired two-tailed Student’s t-test (E, F, H, J, and L-Q) or two-way ANOVA followed with Bonferroni’s multiple comparisons test (G and I).
Techniques Used: ChIP-sequencing, Expressing, Knock-Out, Staining, Control, Two Tailed Test
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