Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

HDAC1 and HDAC2 regulates TGF-b during Endothelial-to-Hematopoietic Transition [ChIP-Seq]

ABSTRACT: The first hematopoietic stem cells originate from hemogenic endothelium (HE), that trans-differentiate into the lumen to form hematopoietic clusters. The molecular mechanisms driving this transition are only poorly understood. Here, we present a complete and comprehensive study that shows the requirement for Transforming Growth Factor beta (Tgfbeta) signalling as the master regulator of triggering EHT from HE, including Runx1-/- HE. We employed RNA-Seq data on Hdac deficient HE, together with ChIP-Seq for HDAC1 and HDAC2 and on wild type HE that indicated its importance in EHT. We tested our findings extensively on HE derived from different sites/origin. In all instances we observed an increase in the frequency of EHT by decreasing Tgfbeta levels.

ORGANISM(S): Mus musculus

PROVIDER: GSE101681 | GEO | 2018/04/10

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

HDAC1 and HDAC2 regulates TGF-b during Endothelial-to-Hematopoietic Transition [RNA-Seq]

Project description:The first hematopoietic stem cells originate from hemogenic endothelium (HE), that trans-differentiate into the lumen to form hematopoietic clusters. The molecular mechanisms driving this transition are only poorly understood. Here, we present a complete and comprehensive study that shows the requirement for Transforming Growth Factor beta (Tgfbeta) signalling as the master regulator of triggering EHT from HE, including Runx1-/- HE. We employed RNA-Seq data on Hdac deficient HE, together with ChIP-Seq for HDAC1 and HDAC2 and on wild type HE that indicated its importance in EHT. We tested our findings extensively on HE derived from different sites/origin. In all instances we observed an increase in the frequency of EHT by decreasing Tgfbeta levels. Poly(A) RNA-sequencing on control and Hdac1 or Hdac2 deficient HE cells

2018-04-10 | GSE101682 | GEO

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

Expression data from primary MEF lacking either HDAC1, HDAC2 or both

Project description:Previously published data suggested some redundant functions between HDAC1 and HDAC2 in mouse. To test this hypothesis, we used microarrays to have a genome wide analysis at the transcription level of primary MEFs lacking HDAC1, HDAC2. MEF HDAC1 F/F were were transduced with two different retroviruses: one virus expresses the Tamoxifen-inducible cre recombinase Cre-ERT2 and the second virus expresses either a small hairpin micro-RNA against HDAC2 or a scrambled version. HDAC1F/F MEFs expressing either a scrambled micro-RNA or a micro-RNA against HDAC2 can be induced by addition of Tamoxifen to delete HDAC1, thereby generating four different genotypes: WT, HDAC1 KO, HDAC2 knockdown (Kd) and HDAC1/2 KO/Kd.

2010-07-30 | E-GEOD-20100 | biostudies-arrayexpress

Quantitative proteomic TandemMassTag analysis of intestinal epithelial cells (IEC) deleted for both Hdac1 and Hdac2

Project description:We have performed quantitative proteomic TandemMassTag to investigate proteomic changes after deletion of epigenetic eraser genes Hdac1 and Hdac2 in intestinal epithelial cells. 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 specific IEC function of HDAC1 and HDAC2, we have performed transcriptomic and quantitative proteomic approaches on IEC deficient in Hdac1 and 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.

2021-09-09 | PXD022558 | Pride

Expression data from enteroid deleted for HDAC1 or HDAC2

Project description: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.

2019-12-31 | GSE124146 | GEO

Roles of HDAC1 and HDAC2 in the developing mouse brain

Project description:In this study, we investigated the role of HDAC1 and HDAC2 in the developing mouse brain. We found that the removal of HDAC1 and HDAC2 caused severe malformation. To examine the molecular mechanisms underlying the cortical malformation, we examined the transcriptome in both WT and HDAC1/2 deficient brains. We found that many genes that are associated with transcription were misregulated in HDAC1 and HDAC2 mutant brains. This result provides a resource for studying gene expression controlled by HDAC1 and HDAC2.

2019-02-12 | GSE122834 | GEO

Functions of HDAC1 and HDAC2 in Schwann cells during postnatal

Project description:The aim of our study is to determine the functions of histone deacetylases (HDACs) 1 and 2 in Schwann cells during postnatal development of the peripheral nervous system (PNS). Schwann cells are the myelinating glial cells of the PNS. At birth, mouse sciatic nerves mature in 2 subsequent phases: 1/ big caliber axons get sorted into a 1 to 1 relationship with Schwann cells, 2/ Schwann cells build a myelin sheath around sorted axons. In mice where both HDAC1 & HDAC2 have been specifically knocked out in Schwann cells, both phases are impaired. HDACs are chromatin remodeling enzymes, they can thus alter gene expression directly. We want to identify which genes controlled by HDAC1 and HDAC2 in Schwann cells are necessary for the maturation of sciatic nerves. Because HDAC1 and HDAC2 can compensate for each other loss to some extend, we will first analyze changes of gene expression in HDAC1/HDAC2 double KO animals. We expect to gain critical insights into the molecular mechanisms controlling Schwann cell differentiation and myelination. This knowledge is of key importance for the success of regenerative medicine in peripheral neuropathies, nerve tumors, and transplantation paradigms in non-regenerative CNS lesions and in large PNS injuries. 3 double knockout mutants for HDAC1 and HDAC2 and 3 control littermates were analyzed. Tissues analyzed: sciatic nerves of 2 day-old mouse pups

2011-02-25 | E-GEOD-27451 | biostudies-arrayexpress

Collateral lethality between HDAC1 and HDAC2 exploits cancer-specific NuRD complex vulnerabilities

Project description:Histone deacetylases (HDACs) have been widely pursued as targets for anti-cancer therapeutics. However, many of these targets are universally essential for cell survival, which may limit the therapeutic window that can be achieved by drug candidates. By examining large collections of CRISPR/Cas9-based essentiality screens, we discovered a genetic interaction between HDAC1 and HDAC2 wherein each paralog is synthetically lethal with hemizygous deletion of the other. This collateral synthetic lethality is caused by recurrent chromosomal translocations that occur in diverse solid and hematological malignancies, including neuroblastoma and multiple myeloma. Using genetic deletion or dTAG-mediated degradation, we show that HDAC2 disruption suppresses the growth of HDAC1-deficient neuroblastoma in vitro and in vivo. Mechanistically, we find that targeted degradation of HDAC2 in these cells prompts the degradation of several members of the nucleosome remodeling and deacetylase (NuRD) complex, leading to diminished chromatin accessibility at HDAC2/NuRD-bound sites of the genome and impaired control of enhancer-associated transcription. Furthermore, we reveal that several of the degraded NuRD complex subunits are dependencies in neuroblastoma and multiple myeloma, providing motivation to develop paralog-selective HDAC1 or HDAC2 degraders. Altogether, we identify HDAC1/2 collateral synthetic lethality as a new therapeutic target and reveal a novel mechanism for exploiting NuRD-associated cancer dependencies.

2023-06-11 | PXD034444 | Pride

Expression data from intestine of HDAC1 and HDAC2 conditionally mutated mice

Project description:Acetylation and deacetylation of histones and other proteins depend on the opposing activities of histone acetyltransferases and histone deacetylases (HDACs), leading to either positive or negative gene expression changes. The use of HDAC inhibitors (HDACi) has uncovered a role for HDACs in the control of proliferation, apoptosis and inflammation. However, little is known of the roles of specific HDACs in intestinal epithelial cells (IEC). We investigated the consequences of ablating both Hdac1 and Hdac2 in murine IECs gene expression. HDAC1 and HDAC2 conditionally mutated mice were provided by Dr EN Olson (University of Texas Southwestern Medical Center, Dallas, TX) (Montgomery et al., 2007). Floxed HDAC1 and HDAC2 mice were crossed with villin-Cre transgenic mice to insure specific intestinal epithelial cell gene deletion (Madison et al., 2002). Total RNAs from the colon of three control and three HDAC1/2 IEC-specific knockout mice were isolated with the Rneasy kit (Qiagen, Mississauga, ON, Canada).

2013-06-08 | E-GEOD-47745 | biostudies-arrayexpress

Expression data from jejunum IEC deleted for both HDAC1 and HDAC2

Project description: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 IEC-deficient for Hdac1 and 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 normal IEC and HDAC1/2 deleted jejunum IEC.

2020-12-31 | GSE158522 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data