ChIP-seq analysis about Hdac4/5 samples
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE178130 | GEO | 2022/09/05
REPOSITORIES: GEO
Similar Datasets
Project description:To identify whether Dot1l or Npm1 were enriched in MERVL directly, we performed Dot1l and Npm1 ChIP-seq in wildtype ESCs. We conclude that Dot1l and Npm1 binding were enriched on MERVL-int region, suggesting a direct regulatory role of Dot1l and Npm1 on MERVL expression.
2023-07-18 | GSE201848 | GEO
Project description:Transcriptional alterations are characteristic of persistent pain states but the key regulators remain elusive. Using a conditional knockout (cKO) strategy in mice we sought to determine whether loss of the transcriptional co-repressor histone deacetylase four (HDAC4) would have implications for sensory neuron transcription and nociception. HDAC4 was found to be largely dispensable for transcriptional regulation of naïve sensory neurons but was required for transcriptional responses after injury, with Calca and Trpv1 expression consistently downregulated in HDAC4 cKO compared to littermate controls (0.2-0.44 fold). This downregulation corresponded to reduced sensitivity to capsaicin in vitro (76% +/- 4.4% wildtype capsaicin responders vs 56.9% +/- 4.7% cKO responders) and to reduced thermal hypersensitivity in the complete Freund’s adjuvant model of inflammatory pain (1.3-1.4 fold improvement). These data indicate that HDAC4 is a novel inflammatory pain mediator and may be a good therapeutic target, capable of orchestrating the regulation of multiple downstream effectors. Total RNA was extracted from HDAC4 cKO and HDAC4 fl/fl naïve adult lumbar dorsal root ganglia (n=3/group). mRNA expression was compared using Affymetrix Mouse Gene Arrays (Mouse Gene 2.0ST) run on a GeneChip Fluidics Station 450. Chips were scanned on an Affymetrix GeneChip Scanner.
2015-04-23 | E-GEOD-62405 | biostudies-arrayexpress
Project description:Transcriptional alterations are characteristic of persistent pain states but the key regulators remain elusive. Using a conditional knockout (cKO) strategy in mice we sought to determine whether loss of the transcriptional co-repressor histone deacetylase four (HDAC4) would have implications for sensory neuron transcription and nociception. HDAC4 was found to be largely dispensable for transcriptional regulation of naïve sensory neurons but was required for transcriptional responses after injury, with Calca and Trpv1 expression consistently downregulated in HDAC4 cKO compared to littermate controls (0.2-0.44 fold). This downregulation corresponded to reduced sensitivity to capsaicin in vitro (76% +/- 4.4% wildtype capsaicin responders vs 56.9% +/- 4.7% cKO responders) and to reduced thermal hypersensitivity in the complete Freund’s adjuvant model of inflammatory pain (1.3-1.4 fold improvement). These data indicate that HDAC4 is a novel inflammatory pain mediator and may be a good therapeutic target, capable of orchestrating the regulation of multiple downstream effectors.
2015-04-23 | GSE62405 | GEO
Project description:Access to DNA is the first level of control in regulating gene transcription, a control that is also critical for maintaining DNA integrity. Cellular senescence is characterized by profound transcriptional rearrangements and accumulation of DNA lesions. Here, we discovered an epigenetic complex between HDAC4 and HDAC1/HDAC2 that is involved in the erase of H2BK120 acetylation. The HDAC4/HDAC1/HDAC2 complex modulates the efficiency of DNA repair by homologous recombination, through dynamic deacetylation of H2BK120. Deficiency of HDAC4 leads to accumulation of H2BK120ac, impaired recruitment of BRCA1 and CtIP to the site of lesions, accumulation of damaged DNA and senescence. In senescent cells this complex is disassembled because of increased proteasomal degradation of HDAC4. Forced expression of HDAC4 during RAS-induced senescence reduces the genomic spread of γH2AX and affects H2BK120ac levels, which are increased in DNA-damaged regions accumulated during RAS-induced senescence. In summary, degradation of HDAC4 during senescence causes the accumulation of damaged DNA and contributes to the activation of the transcriptional program controlled by super-enhancers that maintains senescence.
2024-10-17 | PXD051316 | Pride
Project description:Hdac4 has been found to modulate symptoms in Huntington's Disease (HD) mouse models through an uknown mechanism unrelated to any enzymatic activity. We investigated the protein-protein interactions to gain insight into the role of Hdac4 in HD.
2019-05-01 | PXD011845 | Pride
Project description:To explore the downstream genes of HDAC4, we performed RNA-seq to screen after knocking down HDAC4 in 5-8F cells, a nasopharyngeal carcinoma cell line.
2022-01-28 | GSE125744 | GEO
Project description:HDACs play crucial role in epigenetic modulation through deacetylation of histone and non-histone substrates in critical process of normal development and cancer. Moreover, HDAC inhibitors have been considered as new agent by effects such as cell cycle arrest, apoptosis, anti-angiogenic effects and autophagy and utilized in clinical applications for chemotherapy. we previously reported that HDAC 1, 4, 6 and 8 were higly expressed in MDA-MB-231 than MCF-7 cells and HDAC1, 6 and 8 excepting HDAC4 were associated with invasion that is very important factor in cancer progression. However, HDAC4 did not affect in invasion. To investigate interaction between chemoresistance and HDAC4 expression, we establish stable cells overexpressing HDAC4 in MCF-7 cells. Cells overexpressed HDAC4 were increased cytotoxicity about 5-FU and identified 356 differentially expressed genes using Ilumina array. Based on array result, we selected SMAD4 as a candidate gene related with chemoresistance because SMAD4 was previously reported evaluation of chemoresistance to 5-FU. We purpose that HDAC4 regulated with SMAD4 expression through acetylation in SMAD4 promoter region. HDAC4 directly bound a part of SMAD4 promoter. Total RNA obtained from cells overexpressed HDAC4 cDNA in MCF-7 compared to control cells.
2013-11-01 | E-GEOD-42242 | biostudies-arrayexpress
Project description:Histone Deacetylase 4 (HDAC4) is known to contribute to cardiac remodeling processes. We wanted to identify and compare different genome wide targets of HDAC4 to well described interaction partners and its functional consequences. Therefore, we used a model of adult cardiomyocytes isolated from HDAC4 knockout mice and Wildtyp (WT) controls. We looked for HDAC4s contribution to changes of activating histone modifications (H3K4me3, H3K9ac, H3K27ac) and repressive pendants (H3K9me2 and H3K27me3).
2021-09-15 | E-MTAB-7319 | biostudies-arrayexpress
Project description:Reversible protein acetylation provides a central mechanism for controlling gene expression and cellular signaling events. It is governed by the antagonistic commitment of two enzymes families: the histone acetyltransferases (HATs) and the histone deacetylases (HDACs). HDAC4, like its class IIa counterparts, is a potent transcriptional repressor through interactions with tissue-specific transcription factors via its N-terminal domain. Whilst the lysine deacetylase activity of the class IIa HDACs is much less potent than that of the class I enzymes, HDAC4 has been reported to influence protein deacetylation through its interaction with HDAC3. To investigate the influence of HDAC4 on protein acetylation, we employed the unbiased AcetylScan proteomic screen. We identified many proteins known to be modified by acetylation, but found that the absence of HDAC4 had no effect on the acetylation profile of the murine neonate brain. This is consistent with the biochemical data suggesting that HDAC4 may not function as a lysine deacetylase, but these in vivo data do not support the previous report showing that the enzymatic activity of HDAC3 might be modified by its interaction with HDAC4. To complement this work, we used Affymetrix arrays to investigate the effect of HDAC4 knock-out on the transcriptional profile of the postnatal murine brain. There was no effect on global transcription, consistent with the absence of a differential histone acetylation profile. Validation of the array data by Taq-man qPCR indicated that only protamine 1 and Igfbp6 mRNA levels were increased by more than one-fold and only CamK4 was decreased. The lack of a major effect on the transcriptional profile is consistent with the cytoplasmic location of HDAC4 in the P3 murine brain. mRNA expression analysis was performed by microarray in 3-day-old HDAC4 KO pups and WT littermates. Ten samples were analysed for each genotype. Microarray quality control was performed using the software package provided on RACE (http://race.unil.ch).
2014-07-30 | E-GEOD-49383 | biostudies-arrayexpress
Project description:HDACs play crucial role in epigenetic modulation through deacetylation of histone and non-histone substrates in critical process of normal development and cancer. Moreover, HDAC inhibitors have been considered as new agent by effects such as cell cycle arrest, apoptosis, anti-angiogenic effects and autophagy and utilized in clinical applications for chemotherapy. we previously reported that HDAC 1, 4, 6 and 8 were higly expressed in MDA-MB-231 than MCF-7 cells and HDAC1, 6 and 8 excepting HDAC4 were associated with invasion that is very important factor in cancer progression. However, HDAC4 did not affect in invasion. To investigate interaction between chemoresistance and HDAC4 expression, we establish stable cells overexpressing HDAC4 in MCF-7 cells. Cells overexpressed HDAC4 were increased cytotoxicity about 5-FU and identified 356 differentially expressed genes using Ilumina array. Based on array result, we selected SMAD4 as a candidate gene related with chemoresistance because SMAD4 was previously reported evaluation of chemoresistance to 5-FU. We purpose that HDAC4 regulated with SMAD4 expression through acetylation in SMAD4 promoter region. HDAC4 directly bound a part of SMAD4 promoter.
2013-11-01 | GSE42242 | GEO