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Genome-wide acetylated histone 3 lysine 9 (H3K9ac) in HDAC3-depleted liver rescued with deacectylase-dead HDAC3 mutants

ABSTRACT: We found that several deacetylase-dead HDAC3 mutants were able to rescue the metabolic phenotype of HDAC3-depleted livers. Here we profile the histone acetylation in the presence of different HDAC3 mutants in mouse liver.

ORGANISM(S): Mus musculus

PROVIDER: GSE49365 | GEO | 2013/11/25

SECONDARY ACCESSION(S): PRJNA213727

REPOSITORIES: GEO

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Genome-wide acetylated histone 3 lysine 9 (H3K9ac) in HDAC3-depleted liver rescued with deacectylase-dead HDAC3 mutants

Project description:We found that several deacetylase-dead HDAC3 mutants were able to rescue the metabolic phenotype of HDAC3-depleted livers. Here we profile the histone acetylation in the presence of different HDAC3 mutants in mouse liver. Deacetylase-dead HDAC3 mutants, including HAHA, KA, YF and HEBI, were introduced into HDAC3-depleted (Cre) mouse livers by virus along with wild-type (WT) HDAC3 as a control. Livers were harvested at 5 pm (ZT 10) and subjected to ChIP with anti-H3K9ac antibodies followed by deep sequencing.

2013-11-25 | E-GEOD-49365 | biostudies-arrayexpress

Gene expression profiling of HDAC3-depleted mouse liver rescued with wild-type exogenous HDAC3

Project description:We have shown that intravenous injection of HDAC3 floxed mice with adeno-associated virus (AAV) expressing Cre depletes hepatic HDAC3, upregulates lipogenic gene expression, and causes fatty liver. When AAV-Flag-HDAC3 wild-type (WT) is co-injected along with AAV-Cre, the exogenous HDAC3 is expressed at endogenous levels and can completely rescue fatty liver phenotype. Here we profile transcriptome of the rescued WT livers in comparison with HDAC3-depleted (KO) livers. 4-months old C57BL/6 male mice were co-injected with AAV-Cre or AAV-Cre plus AAV-Flag-HDAC3. Mice were fed ad libitum and harvested at 5 pm (ZT10) at 2-weeks post-injection. Liver total RNA was extracted and hybridized to Affymetrix Mouse Gene 1.0ST array.

2013-11-25 | E-GEOD-49386 | biostudies-arrayexpress

Gene expression profiling of HDAC3-depleted mouse liver rescued with wild-type exogenous HDAC3

2013-11-25 | GSE49386 | GEO

Gene expression in mouse liver depleted of HDAC3

Project description:Liver-specific depletion of HDAC3 leads to liver steatosis (fatty liver), suggesting disregulation of lipid metabolism. This is correlated with changes in lipid metabolic gene expression. Livers depleted of HDAC3 were removed from 12 week old male HDAC3 fl/fl mice (loxP sites flanking exon 4 to 7 of the HDAC3 gene encoding the catalytic domain of HDAC3) one week after the injection of AAV2/8-Tbg-Cre virus. Livers from the HDAC3 fl/fl mice injected with AAV2/8-Tbg-GFP were used as normal controls. mRNA was extracted from 100mg mouse liver samples and hybridized to Affymetrix microarrays. For each group (HDAC3 depleted liver and normal liver), we have 5 samples from different mice.

2011-03-11 | E-GEOD-25937 | biostudies-arrayexpress

Gene expression in mouse liver depleted of HDAC3

2011-03-11 | GSE25937 | GEO

DEAD

Project description:DEAD

| PRJEB12645 | ENA

Changes of H3K9ac and H3K27ac recruitment in pachytene spermatocytes and round spermatids from testes-specific HDAC3-depleted mice and genome-wide maps of HDAC3,NCOR and Sox30 in wild-type and Sox30 KO testes

Project description:We reported changes in the recruitment of H3K9ac and H3K27ac in HDAC3-depleted mouse testes in the late meiotic and early haploid stages. We also investigated genome-wide occupancy of HDAC3, NCOR and Sox30 to the mouse testes from wild-type and Sox30 KO mice.

2021-05-26 | GSE153063 | GEO

Transcriptional repression by HDAC3 mediates T cell exclusion from Kras mutant lung tumors [H3K9Ac ChIP-seq]

Project description:Histone Deacetylase 3 (HDAC3) function in vivo is nuanced and directed in a tissue specific fashion. The importance of HDAC3 in Kras mutant lung tumors has recently been identified, but HDAC3 function in this context remains to be fully elucidated. Here, we identified HDAC3 as a lung tumor cell-intrinsic transcriptional regulator of the tumor immune microenvironment. In Kras mutant lung cancer cells, we found that HDAC3 is a direct transcriptional repressor of a cassette of secreted chemokines, including Cxcl10. Genetic and pharmacological inhibition of HDAC3 robustly upregulated this gene set in human and mouse Kras, LKB1 (KL) and Kras, p53 (KP) mutant lung cancer cells through an NF-kB/p65-dependent mechanism. Using genetic engineered mouse models, we found that HDAC3 inactivation in vivo induced expression of this gene set selectively in lung tumors, and resulted in enhanced T-cell recruitment at least in part via Cxcl10. Furthermore, we found that inhibition of HDAC3 in the presence of Kras pathway inhibitors dissociated Cxcl10 expression from that of immunosuppressive chemokines, and that combination treatment of entinostat with trametinib enhanced T-cell recruitment into lung tumors in vivo. Finally, we showed that T-cells contribute to in vivo tumor growth control in the presence of entinostat and trametinib combination treatment. Together, our findings reveal that HDAC3 is a druggable endogenous repressor of T-cell recruitment into Kras mutant lung tumors.

2024-10-10 | GSE277927 | GEO

Diurnal changes of HDAC3, Rev-erbα, NCoR and Pol II recruitment to the mouse liver genome and of H3K9Ac

Project description:We reported a diurnal changes in the recruitment of HDAC3, Rev-erbα, NCoR and Pol II to the mouse liver genome as well as H3K9 acetylation in vivo at ZT10 and ZT22. ChIP-Seq profiling of HDAC3, Rev-erbα, NCoR and Pol II binding and H3K9Ac in mouse liver harvested at 2 different times (ZT10 and ZT22) of the day

2011-03-11 | E-GEOD-26345 | biostudies-arrayexpress

Discovery of a Highly Potent and Selective HDAC3 and HDAC8 PROTAC Dual Degrader

Project description:HDAC3 and HDAC8 are members of class I deacetylases involved in several biological mechanisms and represent a highly sought-after therapeutic target for drug development. It is historically challenging to develop selective deacetylase inhibitors due to their conserved catalytic domains. HDAC3 also has deacetylase-independent activity, which cannot be blocked by conventional enzymatic inhibitors. Recent advances in proteolysis-targeting chimeras (PROTACs) provides an opportunity to eliminate the whole protein selectively, abolishing both enzymatic and scaffolding functions. Here, we report a novel HDAC3/8 dual degrader YX968 that induces highly potent, rapid and selective degradation of both HDAC3 and HDAC8 without trigging pan-HDAC inhibitory effects. Unbiased quantitative proteomics experiments further confirmed its high selectivity. This dual-specific degrader specifically ablates cellular pathways attributed to HDAC3 and HDAC8 and exhibits high potency in killing cancer cells. YX968 represents a new probe for dissecting the complex biological functions of HDAC3 and HDAC8.

2023-07-18 | PXD040941 | Pride

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