GEO DataSets

Analysis of hearts of 6 week old mutants deleted for histone deacetylase 3 (HDAC3). HDAC3 deletion occurred 7 days after birth. These MCH3-KO mutants are viable on normal chow but a high fat diet is lethal. The results underscore the impact gene-diet interactions may have on cardiovascular health.

Organism:

Mus musculus

Type:

Expression profiling by array, count, 2 genotype/variation sets

Platform:

GPL6246

Series:

GSE31251

8 Samples

Download data: CEL

(Submitter supplied) Gene expression changes in the heart of MCH3-KO mouse (HDAC3 f/f, Muscle Creatine Kinase-Cre) versus control WT mouse (HDAC3 f/f). Histone deacetylases (HDACs) play important roles in cardiac development and function. We show here that mice deficient of HDAC3 in heart and skeletabl muscle are relatively normal on normal chow, but develop hypertrophic cardiomyopathy and heart failure that leads to death on high-fat diet. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS4886

Platform:

GPL6246

8 Samples

Download data: CEL

(Submitter supplied) Histone deacetylase 3 (Hdac3) is the enzymatic component of transcriptional repression complexes recruited by the nuclear hormone receptors. Inactivation of Hdac3 in cancer cell lines triggered apoptosis, and removal of Hdac3 in the germ-line of mice caused embryonic lethality. Therefore, we conditionally deleted the Hdac3 allele in the mouse liver. These mice developed hepatomegaly, which was the result of hepatocyte hypertrophy, and these morphological changes coincided with significant imbalances between carbohydrate and lipid metabolism. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL2995

12 Samples

Download data: XLS

(Submitter supplied) Histone deacetylase 3 (Hdac3) regulates the expression of lipid metabolism genes in multiple tissues, however its role in regulating lipid metabolism in the intestinal epithelium is unknown. Here we demonstrate that intestine-specific deletion of Hdac3 (Hdac3IKO) protects mice from diet induced obesity. Intestinal epithelial cells (IECs) from Hdac3IKO mice display co-ordinate induction of genes and proteins involved in mitochondrial and peroxisomal b-oxidation, have an increased rate of fatty acid oxidation, and undergo marked remodelling of their lipidome, particularly a reduction in long chain triglycerides. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL27602

6 Samples

Download data: IDAT, TXT

(Submitter supplied) Analysis of whole heart samples from Hdac3-Isl1KO embryos at embryonic day E9.5. Results provide insights into the role of Hdac3 in second heart field-derived cardiac cells. We used microarray to investigate the gene expression program affected by Hdac3 during cardiac development and identified patterns of differentially-expressed genes and pathways during this process.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL16570

6 Samples

Download data: CEL

(Submitter supplied) We address whether the functions of HDAC3 in skeletal muscle require its enzyme activity. By mutating the NCoR/SMRT corepressors in a knock-in mouse model named NS-DADm, we ablated the enzymatic activity of HDAC3 without affecting its protein levels. Compared to the control mice, skeletal muscles from NS-DADm mice showed lower force generation, enhanced fatigue resistance, enhanced fatty acid oxidation, reduced glucose uptake during exercise, upregulated expression of metabolic genes involved in branched-chain amino acids (BCAAs) catabolism, and aging-associated reduction in muscle mass, without changes in the muscle fiber type composition or mitochondrial protein content. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL21493

6 Samples

Download data: XLSX

(Submitter supplied) We address the function of HDAC3 in skeletal muscle metabolism

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing; Other

Platform:

GPL13112

14 Samples

Download data: BED, BIGWIG, TXT

(Submitter supplied) We report the genomic regions enriched for Rev-erb(beta) binding in WT mouse liver, in addition to the false positive regions enriched by ChIP for Rev-erb(alpha) in Rev-erb(alpha) KO liver. In conjunction with previously published data for Rev-erb(alpha) in GSE26345 (GSM647029, GSM647033, and GSM647034), we report the common and subtype specific cistromes for Rev-erb using a quantitative analysis method.

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing; Third-party reanalysis

Platforms:

GPL11002 GPL13112

3 Samples

Download data: BED, TXT

(Submitter supplied) 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.

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL9250

18 Samples

Download data: SAM

(Submitter supplied) 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. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6246

10 Samples

Download data: CEL, CHP

(Submitter supplied) Global gene expression analysis reveals that Med1 regulates many genes involved in energy metabolism, calcium signaling, and oxidative phosphorylation in myocardium.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL13112

2 Samples

Download data: TXT

(Submitter supplied) Histone deacetylases (HDAC) are enzymes that modify key residues in histones to regulate chromatin architecture, and play a vital role in cell survival, cell cycle progression, and tumorigenesis. To understand the function of Hdac3, a critical component of the N-CoR/SMRT repression complex, a conditional allele of Hdac3 was engineered. Given the vital role of HDAC3 in normal cells and in the generation and treatment of various cancers, a conditional deletion of Hdac3 was engineered in mice. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL2995

10 Samples

Download data: TXT

(Submitter supplied) Mice deficient for Hdac3 in mesenchymal progenitor cell (under the PRX1 promoter) die perinataly and exhibit severly short limbs. Here we analyzed the differentiational gene expression in the limbs of these mice. We observed that limbs from the CKO mice have higher expression of genes responsible for matrix degradation. In addition, we identified significant upregulation of FGF21 expression in CKO limbs.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL13112

6 Samples

Download data: TSV

(Submitter supplied) BACKGROUND: Histone deacetylase 4 (HDAC4) has been proposed as a target for the treatment of Amyotrophic Lateral Sclerosis (ALS) because it mediates nerve-skeletal muscle interaction and since its expression in skeletal muscle correlates with the severity of the disease. However, our recent studies on the skeletal muscle response upon long-term denervation highlighted the importance of HDAC4 in maintaining muscle integrity. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL17021

4 Samples

Download data: TSV, XLSX

(Submitter supplied) Histone deacetylase 3 (HDAC3) is an epigenome-modifying enzyme that is required for normal mouse development and tissue-specific functions. In vitro, HDAC3 protein itself has minimal enzyme activity, but gains its histone deacetylation function from stable association with the conserved deacetylase activation domain (DAD) contained in nuclear receptor corepressors NCOR1 and SMRT. Here we show that HDAC3 enzyme activity is undetectable in mice bearing point mutations in the DAD of both NCOR1 and SMRT (NS-DADm), despite normal levels of HDAC3 protein. more...

Organism:

Mus musculus

Type:

Expression profiling by array; Genome binding/occupancy profiling by high throughput sequencing

Platforms:

GPL11002 GPL6246

11 Samples

Download data: BED, CEL

(Submitter supplied) We report the genomic regions enriched in Histone Deacetylase 3 (HDAC3) in mouse livers. We also report the change of HDAC3 occupancy upon DAD mutations in NCOR and SMRT.

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL11002

3 Samples

Download data: BED

(Submitter supplied) We report the hepatic gene expression changes in NCOR and SMRT DADm-mutated mice.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6246

8 Samples

Download data: CEL

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL21103

15 Samples

Download data: BEDGRAPH, TXT, XLSX

(Submitter supplied) Tissue-resident macrophages (TRMs) play central roles in local tissue development and immunity. However, how to control TRM ontogeny and maintenance remains unclear. We performed transcriptional and histone modification analyses of alveolar macrophages in mice with myeloid-specific (Csf1rCre) deletion of HDAC3 using bulk RNA-seq, single-cell RNA-seq and ChIP-seq. We report that HDAC3 deficiency results in metabolic disorders and increased cell death of the fetal lung TRMs, which is partially regulated through directly targeting PPAR-γ. more...

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL21103

7 Samples

Download data: BEDGRAPH, XLSX

(Submitter supplied) Tissue-resident macrophages (TRMs) play central roles in local tissue development and immunity. However, how to control TRM ontogeny and maintenance remains unclear. We performed transcriptional and histone modification analyses of alveolar macrophages in mice with myeloid-specific (Csf1rCre) deletion of HDAC3 using bulk RNA-seq, single-cell RNA-seq and ChIP-seq. We report that HDAC3 deficiency results in metabolic disorders and increased cell death of the fetal lung TRMs, which is partially regulated through directly targeting PPAR-γ. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL21103

2 Samples

Download data: TXT