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BET inhibitors suppress BZLF1 expression [MutuI DNA-seq]

ABSTRACT: BET inhibitors suppress BZLF1 expression [MutuI DNA-seq]

OTHER RELATED OMICS DATASETS IN: GSE84209GSE84212GSE84213GSE84210GSE84214GSE84211GSE98772GSE98773

PROVIDER: PRJNA328392 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR3822500.fastq.gz	Fastqsanger.gz
	SRR3822501.fastq.gz	Fastqsanger.gz
	SRR3822502.fastq.gz	Fastqsanger.gz
	SRR3822503.fastq.gz	Fastqsanger.gz
	SRR3822504.fastq.gz	Fastqsanger.gz

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Similar Datasets

BET inhibitors suppress BZLF1 expression [MutuI RNA-seq]

Project description:BET inhibitors suppress BZLF1 expression [MutuI RNA-seq]

| PRJNA328391 | ENA

BET inhibitors suppress BZLF1 expression [MutuI DNA-seq]

Project description:Lytic infection by the Epstein-Barr virus (EBV) poses numerous health risks, such as infectious mononucleosis and lymphoproliferative disorder. We demonstrate that JQ1 and other BET inhibitors block two different steps in the sequential cascade of the EBV life cycle: expression of the immediate-early gene BZLF1 and lytic genome replication. This represents a novel mode of action for antiviral drugs that may increase efficacy and decrease emergence of resistance. The sequenced total DNA data in this series show that JQ1 causes a decrease in EBV genome replication upon antibody induction.

2017-06-30 | GSE84210 | GEO

BET inhibitors suppress BZLF1 expression [MutuI RNA-seq]

Project description:Lytic infection by the Epstein-Barr virus (EBV) poses numerous health risks, such as infectious mononucleosis and lymphoproliferative disorder. We demonstrate that JQ1 and other BET inhibitors block two different steps in the sequential cascade of the EBV life cycle: expression of the immediate-early gene BZLF1 and lytic genome replication. This represents a novel mode of action for antiviral drugs that may increase efficacy and decrease emergence of resistance. The RNA-seq data below show that the first block by JQ1 occurs before transcription of any EBV lytic genes (see wigs of EBV transcriptomes). A subset of the same RNA-seq data (three replicates each of Mutu+vehicle was compared to Mutu+JQ1) was examined for changes in the human transcriptome, and those results are presented in the spreadsheet "Differential_Expression_GEO"

2017-06-30 | GSE84209 | GEO

BET inhibitors suppress lytic DNA replication [Akata-Zta DNA-seq]

Project description:Lytic infection by the Epstein-Barr virus (EBV) poses numerous health risks, such as infectious mononucleosis and lymphoproliferative disorder. We demonstrate that JQ1 and other BET inhibitors block two different steps in the sequential cascade of the EBV life cycle: expression of the immediate-early gene BZLF1 and lytic genome replication. This represents a novel mode of action for antiviral drugs that may increase efficacy and decrease emergence of resistance. The sequenced total DNA data below show that JQ1 and I-BET cause a decrease in EBV genome replication after induction.

2017-06-30 | GSE84212 | GEO

BET inhibitors suppress lytic DNA replication [Akata-Zta RNA-seq]

Project description:Lytic infection by the Epstein-Barr virus (EBV) poses numerous health risks, such as infectious mononucleosis and lymphoproliferative disorder. We demonstrate that JQ1 and other BET inhibitors block two different steps in the sequential cascade of the EBV life cycle: expression of the immediate-early gene BZLF1 and lytic genome replication. This represents a novel mode of action for antiviral drugs that may increase efficacy and decrease emergence of resistance. The RNA-seq data below show that the second block causes a decrease in expression of late but not early lytic genes.

2017-06-30 | GSE84211 | GEO

BET inhibitors suppress lytic DNA replication [Akata-Zta DNA-seq]

Project description:BET inhibitors suppress lytic DNA replication [Akata-Zta DNA-seq]

| PRJNA328410 | ENA

BET inhibitors suppress lytic DNA replication [Akata-Zta RNA-seq]

Project description:BET inhibitors suppress lytic DNA replication [Akata-Zta RNA-seq]

| PRJNA328406 | ENA

RAPID RESISTANCE TO BET INHIBITORS IS MEDIATED BY FGFR1 IN GLIOBLASTOMA

Project description:Bromodomain and extra-terminal domain (BET) proteins are therapeutic targets in several cancers including the most common malignant adult brain tumor glioblastoma (GBM). Multiple small molecule inhibitors of BET proteins have been utilized in preclinical and clinical studies. Unfortunately, BET inhibitors have not shown efficacy in clinical trials enrolling GBM patients. One possible reason for this may stem from resistance mechanisms that arise after prolonged treatment within a clinical setting. However, the mechanisms and timeframe of resistance to BET inhibitors in GBM is not known. To identify the temporal order of resistance mechanisms in GBM we performed quantitative proteomics using multiplex-inhibitor bead mass spectrometry and demonstrated that resistance to BET inhibitors in GBM treatment occurs rapidly within hours and involves the fibroblast growth factor receptor 1 (FGFR1) protein. Small molecule inhibition of BET proteins and FGFR1 simultaneously induces synergy in reducing GBM tumor growth in vitro and in vivo. Further, FGFR1 knockdown synergizes with BET inhibitor mediated reduction of GBM cell proliferation. Collectively, our studies suggest that co-targeting BET and FGFR1 may dampen resistance mechanisms to yield a clinical response in GBM.

2024-06-16 | PXD043214 | Pride

Selective inhibition of CD4+ T-cell cytokine production and autoimmunity by BET protein and c-Myc inhibitors

Project description:Bromodomain-containing proteins bind acetylated lysine residues on histone tails and are involved in the recruitment of additional factors that mediate histone modifications and enable transcription. A compound, I-BET-762, that inhibits binding of an acetylated histone peptide to BRD4 and other proteins of the BET (bromodomain and extra-terminal domain) family, was previously shown to suppress the production of pro-inflammatory proteins by macrophages and block acute inflammation in mice. Here we investigate the effect of I-BET-762 on T cell function. We show that treatment of naïve CD4+ T cells with I-BET-762 during early differentiation modulates subsequent cytokine production, and inhibits the ability of Th1-skewed cells to induce autoimmune pathogenesis in a model of experimental autoimmune encephalomyelitis (EAE) in vivo. The suppressive effects of I-BET-762 on T-cell mediated inflammation were not due to inhibition of expression of the pro-inflammatory cytokines, IFN-. or IL-17, but correlated with the ability to suppress GM-CSF production from CNS-infiltrating T cells, resulting in decreased recruitment of macrophages and granulocytes. The effects of I-BET-762 were distinct from those of the fumarate ester, dimethyl fumarate (DMF), a candidate drug for treatment of multiple sclerosis (MS). Our data suggest that I-BET and DMF could have complementary roles in the treatment of MS, and provide a strong rationale for inhibitors of BET-family proteins in the treatment of autoimmune diseases, based on their dual ability to suppress granulocyte and macrophage recruitment by T cells as well as production of pro-inflammatory proteins by macrophages. RNA from resting or activated CD4+ T cells grown in the presence of a control substance (DMSO or Control-768) or two different concentrations of I-BET-762, was hybridized to the chip. There are 3 biological replicates for a total of 2 (cell states) x 4 (conditions) x 3 (replicates) = 24 samples.

2012-08-03 | E-GEOD-39886 | biostudies-arrayexpress

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

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