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Differential genome-wide profile of RBPJ, H3K4me1 and H3K4me3 as well as differential chromatin accessibility upon treatment with gamma-secretase inibithor (GSI) DAPT (ChIP-Seq).

ABSTRACT: The Notch signaling pathway regulates several processes including development and differentiation and its aberrant regulation leads to several diseases. Here, we investigated the differential chromatin accessibility, genome-wide distribution of the transcription factor RBPJ and the differential regulation of H3K4me1 and H3K4me3 upon pharmacological inhibition of the Notch pathway with gamma-secretase inibibitor (GSI) DAPT in mouse pre-T (Beko) cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE235981 | GEO | 2024/03/24

REPOSITORIES: GEO

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Differential genome-wide profile of RBPJ, H3K4me1 and H3K4me3 as well as differential chromatin accessibility upon treatment with gamma-secretase inibithor (GSI) DAPT (ATAC-Seq).

Project description:The Notch signaling pathway regulates several processes including development and differentiation and its aberrant regulation leads to several diseases. Here, we investigated the differential chromatin accessibility, genome-wide distribution of the transcription factor RBPJ and the differential regulation of H3K4me1 and H3K4me3 upon pharmacological inhibition of the Notch pathway with gamma-secretase inibibitor (GSI) DAPT in mouse pre-T (Beko) cells.

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Differential genome-wide profile of histone modifications upon treatment with gamma-secretase inibithor (GSI) DAPT [ChIP-seq]

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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.

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Differential gene expression of a gamma secretase inhibitor treated human oral squamous cell carcinoma cell line

Project description:Notch signalling regulates various cancer cell beahviors. Influence of notch signaling inhibitor, a gamma secretase inhibitor (DAPT) on human oral squamous cell carcinoma is not yet widely investigated. Here, the differential mRNA expression of DAPT treated HSC4 cell line was examined using RNA sequencing technique. Results demonstraetd that DAPT regulated various pathways in HSC4, including cell cycle and DNA replication pathways.

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CRISPR/Cas9 screen of T-ALL cells (DND-41) in the presence of DMSO, CB-103 or GSI (DAPT).

Project description:The efficacy of targeted therapies for treatment of cancer patients is often limited by development of drug resistance. Potential resistance mechanisms to pharmacological Notch1 inhibition mediated by GSI or CB-103 in T-ALL are currently unclear. Thus, we performed a genome-wide loss-of-function (LoF) CRISPR/Cas9 screen to identify genes responsible for resistance to Notch inhibition and novel combination therapies for efficient treatment of human T-ALL. We used a Notch-dependent human T-ALL cell line, DND-41, which responds moderately to both GSI and CB-103 treatment in vitro. DND-41 cells stably expressing Cas9 were infected with human GeCKO v2 CRIPSR libraries, containing 123,411 sgRNAs targeting 19,050 genes and treated with either vehicle, GSI or CB-103 for 21 days enabling both positive and negative selection of sgRNAs.

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Differential gene regulation in DAPT-treated Hydra reveals candidate direct Notch signalling targets

Project description:In Hydra, Notch inhibition causes defects in head patterning and prevents differentiation of proliferating nematocyte progenitor cells into mature nematocytes. To understand the molecular mechanisms by which the Notch pathway regulates these processes, we performed RNA-seq and identified genes that are differentially regulated in response to 48 h of treating the animals with the Notch inhibitor DAPT. To identify candidate direct regulators of Notch signalling, we profiled gene expression changes that occur during subsequent restoration of Notch activity and performed promoter analyses to identify RBPJ transcription factor-binding sites in the regulatory regions of Notch-responsive genes. Interrogating the available single-cell sequencing data set revealed the gene expression patterns of Notch-regulated Hydra genes. Through these analyses, a comprehensive picture of the molecular pathways regulated by Notch signalling in head patterning and in interstitial cell differentiation in Hydra emerged. As prime candidates for direct Notch target genes, in addition to Hydra (Hy)Hes, we suggest Sp5 and HyAlx. They rapidly recovered their expression levels after DAPT removal and possess Notch-responsive RBPJ transcription factorbinding sites in their regulatory regions

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Genome-wide analysis of gene expression changes in mouse keratinocytes induced by treatment with DAPT

Project description:Analysis of gene expression changes that occur in keratinocytes during reprogramming when they are treated with DAPT, a small molecule gamma-secretase inhibitor. The hypothesis tested in the present study was that Notch inhibition by DAPT treatment would promote reprogramming by inhibiting p21 activity while leaving p53 expression intact. Results provide important information of the gene expression changes in response to DAPT treatment, such as changes in the expression of p21, p21-responsive genes, p53, p53-responsive genes involved in apoptosis, and Notch-responsive genes.

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GSI, Human T-ALL

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2007-08-06 | GSE8416 | GEO

Genome-wide analysis of gene expression changes in mouse keratinocytes induced by treatment with DAPT

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