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Differential Notch target genes expression profile upon HDAC3 loss-of-function.

ABSTRACT: Differential Notch target genes expression profile upon HDAC3 loss-of-function.

PROVIDER: PRJNA416379 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6236480.fastq.gz	Fastqsanger.gz
	SRR6236481.fastq.gz	Fastqsanger.gz
	SRR6236482.fastq.gz	Fastqsanger.gz
	SRR6236473.fastq.gz	Fastqsanger.gz
	SRR6236483.fastq.gz	Fastqsanger.gz

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Differential Notch target genes expression profile upon HDAC3 loss-of-function.

Project description:The Notch signaling pathway regulates several differentiation and developmental processes in both pre- and post-natal life and its aberrant regulation leads to diseases, including cancer. Here, we investigated the role of histone deacetylase 3 (HDAC3) on the regulation of the Notch-dependent gene expression program in mouse pre-T (Beko) cells. We first defined Notch target genes as those genes that are downregulated upon inhibition of the Notch pathway using DAPT, a gamma-secretase inhibitor (GSI). Subsequently, we investigated the role of HDAC3 in the regulation of Notch target genes by shRNA- and pharmacologically (apicidin)-mediated loss-of-function of HDAC3.

2020-02-04 | GSE106361 | GEO

Differential Notch target genes expression profile upon GSI washout.

Project description:The Notch signaling pathway regulates several processes including development and differentiation and its aberrant regulation leads to several diseases. Here, we analyzed the gene expression profile upon washout of the Notch inhibitor DAPT in mouse pre-T (Beko) cells.

2024-03-24 | GSE235982 | GEO

Differential Notch target genes expression profile upon GSI washout.

Project description:Differential Notch target genes expression profile upon GSI washout.

| PRJNA988121 | ENA

Genome-wide profile of RBPJ and differential H3K27ac profile upon treatment with HDAC-inhibitor apicidin.

Project description:The Notch signaling pathway regulates several differentiation and developmental processes in both pre- and post-natal life and its aberrant regulation leads to diseases, including cancer. Here, we investigated the genome-wide distribution of the transcription factor RBPJ and the differential regulation of H3K27ac upon pharmacological inhibition of histone deacetylase 3 (HDAC3) with apicidin in mouse pre-T (Beko) cells.

2020-02-04 | GSE119797 | GEO

Identification of transcriptional changes due to loss of Hdac3 in liver at P17 and P28

Project description: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. Loss of Hdac3 triggered changes in gene expression consistent with inactivation of repression mediated by nuclear hormone receptors. Mechanistically, loss of Hdac3 increased the levels of Pparγ2, and treatment of these mice with a Pparγ antagonist partially reversed the lipid accumulation in the liver. In addition, gene expression analysis identified mTOR (mammalian target of rapamycin) signaling as being activated by deletion of Hdac3, and inhibition by rapamycin also affected the accumulation of neutral lipids in the Hdac3-null livers. Thus, Hdac3 has a key role in regulation of multiple signaling pathways in the liver, and deletion of Hdac3 disrupts normal metabolic homeostasis. Keywords: Genetic knockout of Hdac3 specifically in liver, and RNA analyzed from postnatal day 17 or 28 livers for transcriptional changes related to the given phenotypes

2008-05-22 | GSE10503 | GEO

Differential expression of genes upon E-cadherin loss of function

Project description:Differential expression of genes upon E-cadherin loss of function

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Genome wide analysis of differential gene expression of PFKFB3 under- or overexpression upon inhibition or activation of notch signaling in endothelial cells

Project description:Analysis of gene expression profiles upon PFKFB3 under- or overexpression during inhibition or activation of notch signaling. With this experiment we aimed to identify whether alterations in PFKFB3 could influence the expression pattern of angiogenic genes in conditions that favor a tip- or stalk cell gene signature. Total RNA was collected of human umbilical vein endothelial cells either under- or overexpressing PFKFB3 and/ or have inhibited or activated notch signaling respectively. Cells were harvested 48h after manipulation of PFKFB3 and notch levels.

2013-08-01 | E-GEOD-45750 | biostudies-arrayexpress

HDAC3 Inhibition Causes the Impairment in Development of Neocortical VIP Interneurons via dysregulation of Notch Signaling and Autism-like Behaviors

Project description:Autism spectrum disorders (ASDs) are a neurodevelopmental disorder characterized by impairments in social interactions and stereotyped behaviors. While ASD has a strong genetic background, environmental factors including toxins, pesticides, infection and drugs are also known to confer autism susceptibility, likely by inducing epigenetic changes. Exposure to Valproic acid (VPA), a drug for epilepsy and bipolar disorders, during pregnancy is highly associated with the risk of ASD children. In rodents, in utero VPA exposure can precipitate behavioral phenotypes related to ASD in the offspring. Since VPA is an inhibitor of histone deacethytransferase (HDAC) activity, it thought to cause ASD with epigenetic modification. However, the core mechanism by which prenatal VPA exposure causes onset of ASD is still not fully uncovered. Here we revealed that prenatal VPA exposure strongly influences development of vasoactive intestinal peptide (VIP) - positive neurons, a subtype of cortical GABAergic interneurons. The number of VIP+ interneurons was severely reduced in somatosensory area of VPA-exposed ASD animals. We then found that the reduction in VIP+ interneurons is caused by the inhibition of HDAC3 activity upon prenatal VPA exposure. Importantly, prenatal HDAC3 inhibition caused not only the selective reduction in VIP+ interneurons but also the ASD-like behaviors in mice. We then demonstrated that the HDAC3 inhibition aberrantly activates Notch signaling, which influences the cell fate determination of VIP+ interneuron progenitors in caudal ganglionic eminence. Thus, this study uncovers the mechanism by which specific HDAC inhibition during development influences a specific type of GABAergic interneurons in the ASD model. The findings provide a novel insight into the understanding of ASD pathophysiology.

2022-06-20 | GSE133932 | GEO

Regulation of gene expression in IECs by HDAC3

Project description:The development and severity of inflammatory bowel diseases (IBD) and other chronic inflammatory conditions can be influenced by host genetic and environmental factors, including signals derived from commensal bacteria. However, the mechanisms that integrate these diverse cues remain undefined. Here we demonstrate that intestinal epithelial cells (IECs) isolated from IBD patients exhibit decreased expression of the epigenome-modifying enzyme histone deacetylase 3 (HDAC3). Further, genome-wide analyses of murine IECs that lack HDAC3 (HDAC3?IEC) revealed that HDAC3 deficiency resulted in dysregulated gene expression coupled with alterations in histone acetylation. Critically, conventionally-housed HDAC3?IEC mice demonstrated loss of Paneth cells, impaired IEC function and alterations in the composition of intestinal commensal bacteria. In addition, HDAC3?IEC mice exhibited significantly increased susceptibility to intestinal damage and inflammation, indicating that epithelial expression of HDAC3 plays a central role in maintaining intestinal homeostasis. Strikingly, rederivation of HDAC3?IEC mice into germ-free conditions revealed that dysregulated IEC gene expression, Paneth cell homeostasis, and intestinal barrier function were largely restored in the absence of commensal bacteria. Collectively, these data indicate that the HDAC3 is a critical factor that integrates commensal bacteria-derived signals to calibrate epithelial cell responses required to establish normal host-commensal relationships and maintain intestinal homeostasis. In this study, we performed gene expression profiling to examine how the transcriptional profiles in primary live, EpCAM+ IECs from the large intestine differed between control HDAC3FF mice (3 biological replicates) and IEC-intrinsic knockout HDAC3?IEC mice (3 biological replicates).

2013-11-12 | E-GEOD-50188 | biostudies-arrayexpress

Nuclear Receptor Corepressors are Required for the Histone Deacetylase Activity of HDAC3 In Vivo (ChIP-Seq)

Project description: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. HDAC3 enriched genomic regions in WT and NS-DADm mice livers using Illumina GAIIx.

2013-01-01 | E-GEOD-42540 | biostudies-arrayexpress

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