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ABSTRACT: Inhibition of Bromodomain and Extra Terminal (BET) domain activity modulates the IL-23R/IL17 axis and suppresses acute Graft-Versus-Host Disease

PROVIDER: PRJNA757357 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15595088_1.fastq.gz	Fastqsanger.gz
	SRR15595088_2.fastq.gz	Fastqsanger.gz
	SRR15595089_1.fastq.gz	Fastqsanger.gz
	SRR15595089_2.fastq.gz	Fastqsanger.gz
	SRR15595090_1.fastq.gz	Fastqsanger.gz

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Inhibition of Bromodomain and Extra Terminal (BET) domain activity modulates the IL-23R/IL17 axis and suppresses acute Graft-Versus-Host Disease

Project description:Inhibition of Bromodomain and Extra Terminal (BET) domain activity modulates the IL-23R/IL17 axis and suppresses acute Graft-Versus-Host Disease

| PRJNA762276 | ENA

Inhibition of Bromodomain and Extra Terminal (BET) domain activity modulates the IL-23R/IL17 axis and suppresses acute Graft-Versus-Host Disease [RNA-Seq]

Project description:Inhibition of Bromodomain and Extra Terminal (BET) domain activity modulates the IL-23R/IL17 axis and suppresses acute Graft-Versus-Host Disease [RNA-Seq]

| PRJNA762284 | ENA

Inhibition of Bromodomain and Extra Terminal (BET) domain activity modulates the IL-23R/IL17 axis and suppresses acute Graft-Versus-Host Disease [ChIP-seq]

Project description:Inhibition of Bromodomain and Extra Terminal (BET) domain activity modulates the IL-23R/IL17 axis and suppresses acute Graft-Versus-Host Disease [ChIP-seq]

| PRJNA762282 | ENA

BET bromodomain inhibition suppresses TH17-mediated pathology

Project description:IL-17-producing T helper (TH17) cells have been selected through evolution for their ability to control fungal and bacterial infections. It is also firmly established that their aberrant generation and activation results in autoimmune conditions. Using a characterized potent and selective small molecule inhibitor, we show that the bromodomain and extra-terminal domain (BET) family of chromatin adaptors plays fundamental and selective roles in human and murine TH17 differentiation from naM-CM-/ve CD4+ T cells, as well as in the activation of previously differentiated TH17 cells. We provide evidence that BET controls TH17 differentiation in a bromodomain-dependent manner through a mechanism that includes the direct regulation of multiple effector TH17-associated cytokines, including IL17, IL21 and GMCSF. We also demonstrate that BET family members Brd2 and Brd4 associate with the Il17 locus in TH17 cells, and that this association requires bromodomains. We recapitulate the critical role of BET bromodomains in TH17 differentiation in vivo and show that therapeutic dosing of the BET inhibitor is efficacious in mouse models of autoimmunity. Our results identify the BET family of proteins as a fundamental link between chromatin signaling and TH17 biology, and support the notion of BET inhibition as a point of therapeutic intervention in autoimmune conditions. 4 samples were analyzed: two conditions in duplicate. Naive T cells were placed in conditions leading to TH17 differentiation, with and without BET inhibitor. RNA was collected at 48 hours.

2013-09-20 | E-GEOD-37270 | biostudies-arrayexpress

BET bromodomain inhibition suppresses TH17-mediated pathology

Project description:IL-17-producing T helper (TH17) cells have been selected through evolution for their ability to control fungal and bacterial infections. It is also firmly established that their aberrant generation and activation results in autoimmune conditions. Using a characterized potent and selective small molecule inhibitor, we show that the bromodomain and extra-terminal domain (BET) family of chromatin adaptors plays fundamental and selective roles in human and murine TH17 differentiation from naïve CD4+ T cells, as well as in the activation of previously differentiated TH17 cells. We provide evidence that BET controls TH17 differentiation in a bromodomain-dependent manner through a mechanism that includes the direct regulation of multiple effector TH17-associated cytokines, including IL17, IL21 and GMCSF. We also demonstrate that BET family members Brd2 and Brd4 associate with the Il17 locus in TH17 cells, and that this association requires bromodomains. We recapitulate the critical role of BET bromodomains in TH17 differentiation in vivo and show that therapeutic dosing of the BET inhibitor is efficacious in mouse models of autoimmunity. Our results identify the BET family of proteins as a fundamental link between chromatin signaling and TH17 biology, and support the notion of BET inhibition as a point of therapeutic intervention in autoimmune conditions.

2013-09-20 | GSE37270 | GEO

ChIPSeq data from melanoma cancer cell line CHL-1 after Bromodomain and extra terminal (Bet) domain inhibitor treatment

Project description:Bromodomain and extra terminal domain (BET) inhibition reduces occupancy of BET-family proteins at promoter and enhancer sites finally leading to genome wide changes in gene transcription. We used ChIPSeq profiling to investigate genome wide changes in promoter and enhancer occupancy induced by BET inhibitors BAY 1238097 and OTX-015, respectively.

2017-09-30 | GSE95585 | GEO

Expression data from melanoma cancer cell line CHL-1 after Bromodomain and extra terminal domain inhibitor BAY 1238097 treatment

Project description:Bromodomain and extra terminal domain (BET) inhibtion reduces occupancy of BET-family at promoter and enhancer sites. This finally leads to genome wide changes in the transcription of specific genes. We used microarray profiling to investigate the changes made by BET inhibitor BAY 1238097, trying to identify the underlying changes of gene regulation that lead to sensitivity.

2017-10-31 | GSE92736 | GEO

Expression data from non-small cell lung cancer cell line DV90 after Bromodomain and extra terminal domain (BET) inhibitor JQ1 treatment

2016-03-31 | GSE75960 | GEO

Gene expression data for BET inhibitors

Project description:The BET (bromodomain and extra-terminal) family of acetyl-lysine reader proteins acts as transcriptional activators. BET inhibitors showed anti-cancer efficacies. We performed microarray analysis to characterize BET inhibitor-induced gene expression alterations.

2022-01-01 | GSE168780 | GEO

Expression data from non-small cell lung cancer cell line DV90 after Bromodomain and extra terminal domain (BET) inhibitor JQ1 treatment

Project description:Bromodomain and extra terminal domain (BET) inhibition reduces occupancy of BET-family proteins at promoter and enhancer sites resulting in changes in the transcription of specific genes. We used microarray profiling to investigate the transcriptional changes induced by BET inhibitor JQ1 treatment in DV90 cells to identify the underlying changes of gene regulation that lead to JQ1 sensitivity. DV90 cells (JQ1 sensitive non-small cell lung cancer cell line) were treated with 135 nM (IC50) or 785 nM (IC90) of JQ1 for 4h and 24h. DMSO treated controls served as reference and at least four replicates per condition were collected. RNA was extracted and hybridized to Affymetrix HuGene-2.1ST microarrays to identify treatment induced transcriptional changes.

2016-03-31 | E-GEOD-75960 | biostudies-arrayexpress

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