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ChIP-seq experiment analyzing binding of HDAC2 and HDAC3 to genomic loci in rat Neural Stem Cells

ABSTRACT: Binding of HDAC2 and HDAC3 was assayed using antibodies SC-7899x and SC-11417x examination of HDAC2 and HDAC3 binding in rat neural stem cells

ORGANISM(S): Rattus norvegicus

SUBMITTER: Ola Hermanson

PROVIDER: E-GEOD-57232 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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ChIP-seq experiment analyzing binding of HDAC2 and HDAC3 to genomic loci in rat Neural Stem Cells

Project description:Binding of HDAC2 and HDAC3 was assayed using antibodies SC-7899x and SC-11417x

2014-06-17 | GSE57232 | GEO

Mitotic H3K9 acetylation patterns are controlled by phase-specific activity of the histone deacetylases HDAC2, 3 and SIRT1

Project description:Histone acetylation play a fundamental role in many biological processes. H3K9ac is tightly linked to active transcription, and enriched in promoters, enhancers and insulators. During mitosis H3k9ac levels are reduced, and the mechanism of this reduction is not clear. Here, we used small molecules inhibitors of histone deacetylases and evaluated by immunofluorescence and western blots the involvement of each of the targeted enzymes in regulating H3K9ac during prophase, metaphase, anaphase, telophase and cytokinesis. We identified three histone deacetylases, HDAC2, HDAC3 and SIRT1, as modulators of H3K9ac mitotic levels. HDAC2 inhibition, increased global H3K9ac in prophase, whereas HDAC3 or SIRT1 inhibition, increased H3K9ac levels in metaphase. Next, we performed ChIP-seq in mitotic cells following specific inhibition of each of these histone deacetylases. While we observed a high concordance between the genomic areas impacted by HDAC2 and HDAC3, we detected a small set of loci that were unique to each condition, with HDAC3-specific targets being enriched for genes involved in mitosis regulation.

2022-08-14 | GSE168180 | GEO

Molecular and cellular consequences of genetic knockout of Hdac2 and Hdac3 in striatal medium spiny neurons of Huntington's disease knock-in mice

Project description:Somatic expansion of the Huntington’s disease (HD) CAG repeat drives the rate of a pathogenic process resulting in neuronal cell death. Although mechanisms of neuronal toxicity are not well delineated, transcriptional dysregulation is a likely contributor. Chromatin modifiers are implicated in both mechanisms of CAG instability and transcriptional dysregulation. Here, we tested whether histone deacetylase genes Hdac2 and Hdac3 modify molecular and cellular phenotypes in HttQ111 knock-in mice using conditional knockouts in striatal medium-spiny striatal neurons (MSNs) exhibiting extensive CAG expansion and exquisite disease vulnerability. MSN-specific Hdac2 or Hdac3 knockout attenuated CAG expansion, with the Hdac2 knockout impacting nuclear huntingtin pathology. Hdac2 knockout resulted in a substantial transcriptional response that included reversal of transcriptional dysregulation elicited by the HttQ111 allele. Our results identify novel modifiers of CAG expansion in MSNs, providing testable mechanistic hypotheses, and a potentially complex relationship between Htt and Hdac2 with implications for targeting transcriptional dysregulation in HD.

2020-06-01 | GSE148440 | GEO

Primary human erythroid progenitor cells HDAC1 and HDAC2 shRNA knockdown samples

Project description:Gene expression profiling was performed on primary human erythroid progenitor cells expressing a control shRNA (luciferase), two different HDAC1 shRNAs, and two different HDAC2 shRNAs. The worldwide burden of sickle cell disease is enormous, with over 200,000 infants born with the disease each year in Africa alone. Induction of fetal hemoglobin is a validated strategy to improve symptoms and complications of this disease. The development of targeted therapies has been limited by the absence of discrete druggable targets. We developed a novel bead-based strategy for the identification of inducers of fetal hemoglobin transcripts in primary human erythroid cells. A small-molecule screen of bioactive compounds identified remarkable class-associated activity among histone deacetylase (HDAC) inhibitors. Using a chemical genetic strategy combining focused libraries of biased chemical probes and reverse genetics by RNA interference, we have identified HDAC1 and HDAC2 as molecular targets mediating fetal hemoglobin induction. Our findings suggest the potential of isoform-selective inhibitors of HDAC1 and HDAC2 for the treatment of sickle cell disease. Gene expression profiling was performed on primary human erythroid progenitor cells expressing a control shRNA (luciferase, n=3), two different HDAC1 shRNAs (n=2 and n=3), and two different HDAC2 shRNAs (n=3 for each).

2010-07-29 | E-GEOD-22366 | biostudies-arrayexpress

HDAC1 and HDAC2 in fetal hemoglobin induction

Project description:This SuperSeries is composed of the following subset Series: GSE22366: Primary human erythroid progenitor cells HDAC1 and HDAC2 shRNA knockdown samples GSE22367: Primary human erythroid progenitor cells SAHA treatment samples GSE22368: Primary human erythroid progenitor cells NK57 treatment samples Refer to individual Series

2010-07-29 | E-GEOD-22369 | biostudies-arrayexpress

A HDAC4-HDAC2 complex composes an epigenetic sensor that links the DNA damage response to the senescent program by erasing H2BK120 acetylation [II]

Project description:Purpose: Identification of SEs in time course after HDAC4 depletion and correlation to the accumulation of DNA damage. Outcome: We discovered a novel epigenetic complex formed by HDAC4 and HDAC2 that is involved in the erasure of H2BK120 acetylation. The HDAC4/HDAC2 complex, through the dynamic deacetylation of H2BK120, modulates the efficiency of DNA repair by homologous recombination (HR) by controlling the recruitment of BRCA1 and CtIP to the site of lesions. Degradation of HDAC4 during senescence has a dual effect. First, it contributes to super-enhancers activation by limiting HDAC3 activity, and second, it causes the accumulation of damaged DNA.

2024-06-18 | GSE216861 | GEO

Effect of HDAC2 siRNA on HCC

Project description:Determine the effect and specificity of HDAC2 siRNA compared to SAHA inhibition of HDAC2 in hepatocellular carcinoma (HCC) Profile of treated cells compared to control Transcriptomic profiling

2014-10-02 | E-GEOD-52232 | biostudies-arrayexpress

Quantitative proteomic SILAC analysis of enteroids deleted for Hdac1 or Hdac2

Project description:We have exploited organoid SILAC approaches that we have previously developed (A SILAC-Based Method for Quantitative Proteomic Analysis of Intestinal Organoids.- Gonneaud A, Jones C, Turgeon N, Lévesque D, Asselin C, Boudreau F, Boisvert FM. -Sci Rep. 2016 Nov 30;6:38195. doi: 10.1038/srep38195) to investigate proteomic changes after deletion of epigenetic eraser genes Hdac1 and Hdac2 in enteroids. Both HDAC1 and HDAC2 are epigenetic erasers that drive specific and redundant gene expression patterns, in part by removing acetyl groups on histones. Deletion of these Hdac in intestinal epithelial cell (IEC) in vivo alters intestinal homeostasis, dependent on the Hdac deleted and the level of expression of both. To determine the intrinsic specific IEC function of HDAC1 and HDAC2, we have performed transcriptomic and quantitative proteomic approaches on enteroids deficient in Hdac1 or Hdac2. We have defined changes in both mRNA and protein expression patterns affecting IEC differentiation. We have identified IEC Hdac1- and Hdac2-dependent common as well as specific pathways and biological processes. These findings uncover unrecognized similarities and differences between Hdac1 and Hdac2 in IEC.

2019-11-14 | PXD011869 | Pride

Effect of HDAC2 siRNA on HCC

Project description:Determine the effect and specificity of HDAC2 siRNA compared to SAHA inhibition of HDAC2 in hepatocellular carcinoma (HCC)

2014-10-02 | GSE52232 | GEO

A HDAC4-HDAC2 complex composes an epigenetic sensor that links the DNA damage response to the senescent program by erasing H2BK120 acetylation [I]

Project description:Purpose: Recognize the specific H2BK120ac profile around HDAC4 binding sites in proliferating, pre-senescent, senescent and senescence escaped cells during the accumulation of dsDNA damage, compared to undamaged regions. Outcome: We discovered a novel epigenetic complex formed by HDAC4 and HDAC2 that is involved in monitoring H2BK120 acetylation. The HDAC4/HDAC2 complex, through the dynamic deacetylation of H2BK120, modulates the efficiency of DNA repair by homologous recombination (HR) by controlling the recruitment of BRCA1 and CtIP to the site of lesions. Degradation of HDAC4 during senescence has a dual effect. First, it contributes to super-enhancers activation by limiting HDAC3 activity, and second, it causes the accumulation of DNA damage.

2024-06-18 | GSE216677 | GEO

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