Fig 2: The graphic overview of this study. The phosphate groups transported from activated MAPK/ERK pathway and LRRK2 to HDAC3 causes the repression of H3K9ac and results in a large number of gene expression silencing in trigeminal ganglion induced by compressive stress.

Fig 3: HDAC3 activity by phosphorylation modification in TN rat model. (a) Phosphorylation of HDAC1, 2, 3, and 8 in the control, TN rat model, and TN rat model administered CBZ treatment, by WB assay. (b) Phosphorylated HDAC3 profiles in the control, TN rat model, and TN rat model administered CBZ treatment, by phosphoserine and threonine IP assay. (c) The activity of HDAC1, 2, 3, and 8 in the control, TN rat model, and TN rat model administered CBZ treatment, by enzyme-linked immunosorbent assay (ELISA); “∗” and “^” represent comparison between TN and control as well as CBZ and TN with statistical significance.

Fig 4: Overview of HDAC3 in TN rat model. (a) Overall calling peaks of HDAC3 in the rat genome of the control, TN rat model, and TN rat model administered CBZ treatment, by ChIP-seq. (b) Metagene profiles of genome-wide HDAC3 in the control, TN rat model, and TN rat model administered CBZ treatment. (c) Diagram showing intersecting genes with differential HDAC3 enrichment in the control, TN rat model, and TN rat model administered CBZ treatment. (d) Correlation analysis of DEGs with differential H3K9ac and HDAC3 enrichment in the control, TN rat model, and TN rat model administered CBZ treatment. (e) Gene-browser views of transcriptome, H3K9ac, and HDAC3 profiles of Neurod2, C2cd4c, and Sf3b4 in the control, TN rat model, and TN rat model administered CBZ treatment.

Fig 5: HDAC3 interacts with and deacetylates WISP2 in AML cells. A and B, co-IP was performed with anti-WISP2 antibody and IgG as a control, followed by immunoblotting with anti-HDAC1, anti-HDAC3, anti-HDAC6, and anti-HDAC7 antibodies in AML cells. C, the correlation between HDAC3 or HDAC1 and WISP2 expression levels from 151 AML samples analyzed by StarBase. D, Western blot analysis of HDAC3 expression in bone marrow mononuclear cells from healthy donors and AML patients. E and F, the protein and acetylation levels of WISP2 in RGFP966-treated AML cells. G and H, the protein and acetylation levels of WISP2 and the protein expression of HDAC3 in AML cells infected with HDAC3 lentivirus. Ac, acetylated lysine; AML, acute myeloid leukemia; co-IP, co-immunoprecipitation; HDAC, histone deacetylase; WISP2, Wnt-1-induced signaling protein-2.