KAT3B/p300 Antibody - #AF5360

Fig. 7 |Hyperoside inhibits the EMT and metastasis of HCC by targeting YY1 complex.(a) Detailed binding mode of YY1, p65, and p300. (b) Prediction score of docking between small-molecule drugs and YY1 complex. (c) The structure of hyperoside (left). Predicted binding modes of hyperoside (green) and YY1/p65/p300 complex (right). (d) Co-IP of endogenous YY1, p65, and p300 was performed in PLC-PRF-5 cells treated with 120 µM hyperoside.

Fig. 4 From: Musashi-2 potentiates colorectal cancer immune infiltration by regulating the post-translational modifications of HMGB1 to promote DCs maturation and migration MSI2 interacts with P300 to promote K29-HMGB1 acetylation, translocation and extracellular release. A Western blot analysis of acetyllysine in stable SW620 and LOVO cells. B Identification of lysine acetylation at K29 and K30 of HMGB1 by 4D label-free acetylome sequencing in stable SW620 cells. C Four gene clusters (Q1-Q4) based on the fold difference were identified in stable SW620 cells. D KEGG pathway enrichment analysis of the gene clusters (Q1-Q4) by BP and MF. E The DEGs identified by proteomics in stable SW620 and LOVO cells were subjected to KEGG pathway enrichment analysis using the DAVID bioinformatics tool. F Acetyl-K29-HMGB1 expression in the extracellular supernatant of stable SW620 and LOVO cells treated with or without 10 μg/mL LPS for 8 h. G Representative IFC images showing aberrant low expression of Acetyl-K29-HMGB1 in SW620 and LOVO cells with stable MSI2 knockdown. Scale bars, 100 μm. H-I Ectopic nucleocytoplasmic translocation of Acetyl-K29-HMGB1 in stable SW620 and LOVO cells in the absence (H) or presence (I) of LPS (10 μg/mL) for 8 h. J Acetyl-K29-HMGB1 and HMGB1 protein levels in HEK 293 T, SW620 and LOVO cells treated with TSA (1 μM) or (and) NAM (10 mM) for 12 h. K IP of HMGB1 and acetyllysine in stable SW620 and LOVO cells. L Positive correlations between MSI2 expression and KATs and KDACs expression in TCGA CRC database. M Heatmap of MSI2 and KAT/KDACs protein expression in stable SW620 cells as determined by 4D label-free proteomics. N MSI2, HDAC1, HDAC2, SIRT1 and EP300 mRNA expression was measured by qRT–PCR in stable SW620 and LOVO cells cultured in the presence of LPS (10 μg/mL) for 8 h. O Endogenous Co-immunoprecipitation of MSI2 and EP300 in SW620 and LOVO cells. P Representative IFC images of MSI2 and EP300 cytoplasmic localization in SW620 and LOVO cells. Scale bars, 10 μm. Q Representative IHC images of P300 from CAC mice and statistical analysis for P300 average IHC staining density. Scale bars, 100 μm. R Western blot analysis of EP300, HMGB1, K29-HMGB1 and NF-κB gene expression in CAC mice and stable CRC cells. These results are presented as the mean ± SD values; ns: not significant, **p 

Fig. 2.| A. The mRNA expression level of IQGAP1 in myeloma cell lines among different group (Sp1-siRNA: p＜0.0001; p300-siRNA: p = 0.0003；pcDNA3.1-Sp1: p＜0.0001; pcDNA3.1- p300: p＜0.0001). B. The mRNA expression level of Sp1 in myeloma cell lines among different group (Sp1-siRNA: p = 0.0014; pcDNA3.1-Sp1:p = 0.0001; pcDNA3.1- p300: p = 0.0006). C. The mRNA expression level of p300 in myeloma cell lines among different group (p300-siRNA: p = 0.0012; pcDNA3.1-Sp1: p = 0.0003; pcDNA3.1- p300: p = 0.0002). D. The protein level of Sp1, p300, IQGAP1, ERK1/2 and p-ERK1/2 in myeloma cell lines among different group.

FIGURE 5 Effects of β-PAE on AQP3 expression and cAMP/PKA/CREB signaling pathway-related proteins. (A,B) AQP3 expression; (C,D) VIP, VIPR2, cAMP and PKA expression; (E,F) MEK1/2, p-MEK1/2, ERK, p-ERK, p-p38, p38, MSK1, p-MSK1, CREB, p-CREB, and P300/CBP expression. Data are shown as mean ± SD (n = 3). # p < 0.05, ## p < 0.01 versus control group; * p < 0.05, ** p < 0.01 versus 5-FU group.

FIGURE 5| Altered P300 and HDAC1 affect ERS in cells in ADLI. (a) The mRNA content of P300, HDAC1, GRP78, and CHOP in different groups after treatment with C646 and MS‐275 for 6 hr. (b) Western blot analysis and (c) gray value detection of P300, HDAC1, GRP78, and CHOP in different groups. Means ± SEM were calculated from six independent experiments. A one‐way ANOVA with SNK‐q test was performed.*p < 0.05 compared with the levels in the control group.