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Synthetic transcription elongation factors

ABSTRACT: Synthetic transcription elongation factors

PROVIDER: PRJNA388392 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5627040.fastq.gz	Fastqsanger.gz
	SRR5627050.fastq.gz	Fastqsanger.gz
	SRR5627060.fastq.gz	Fastqsanger.gz
	SRR5627070.fastq.gz	Fastqsanger.gz
	SRR5627080.fastq.gz	Fastqsanger.gz

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ChIP-RX of GM15850 cells treated with synthetic transcription elongation factors

Project description:Switching a paused RNA polymerase II into productive elongation is tightly-regulated, especially at genes involved in human development and disease. To exert control on this rate-limiting step, we designed sequence-specific synthetic transcription elongation factors (Syn-TEFs). These molecules are composed of programmable DNA-binding ligands flexibly tethered to a small molecule that binds a component of the transcription elongation machinery. The resultant bifunctional molecules convert constituent modules from broad-spectrum inhibitors of transcription into a gene-specific stimulator of transcriptional elongation. Here, we present Syn-TEF1, a molecule that actively facilitates transcription across repressive GAA repeats that silence frataxin expression in Friedreich’s ataxia, a debilitating and ultimately lethal neurodegenerative disease with no effective therapy.

2017-12-06 | GSE99402 | GEO

RNA-seq of GM15850 and GM15851 cells treated with synthetic transcription elongation factors.

2017-12-06 | GSE99400 | GEO

Chd1 co-occupancy with early transcription elongation factors

Project description:We report the genome-wide Chd1 co-occupancy with early transcription elongation factors

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Chd1 co-occupancy with early transcription elongation factors

Project description:We report the genome-wide Chd1 co-occupancy with early transcription elongation factors ChIP-seq for Chd1 and elongating RNA polymerase II

2014-10-23 | E-GEOD-56061 | biostudies-arrayexpress

Transcription elongation factors are in vivo-specific cancer dependencies in glioma

Project description:Transcription elongation factors are in vivo-specific cancer dependencies in glioma

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Dynamics of transcription elongation are finely-tuned by dozens of regulatory factors

Project description:Understanding the complex network and dynamics that regulate transcription elongation requires quantitative analysis of RNA polymerase II (Pol II) behavior in a wide variety of regulatory environments. We performed native elongating transcript sequencing (NET-seq) in 42 strains of S. cerevisiae, each missing a known elongation regulator including RNA processing factors, transcription elongation factors, histone variants, chromatin modifiers, and chromatin remodelers and chaperones. For each strain, we determined differentially expressed genes, measured levels of antisense transcription, examined sites of high polymerase density, and identified single-nucleotide loci of Pol II pausing. For each elongation phenotype, we found that wild-type Pol II activity sits in the middle of the dynamic range, indicating that elongation is balanced by the opposing effects of many factors. We find that Pol II elongation at sites of RNA processing is co-transcriptionally controlled by key regulators. Furthermore, Pol II pauses frequently across gene bodies at locations that vary across deletion strains. Meta-analysis of all datasets finds that commonly differentially-expressed genes across the deletion strains exhibit more extreme antisense transcription and polymerase pausing, revealing a link between elongation activity and gene regulation. Thus, regulation of transcription elongation impacts co-transcriptional processing and overall gene expression through precisely balancing Pol II activity by a diverse array of factors.

2021-08-11 | GSE159603 | GEO

Dynamics of transcription elongation are finely-tuned by dozens of regulatory factors

Project description:Dynamics of transcription elongation are finely-tuned by dozens of regulatory factors

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Epigenetic Profile in Transcription elongation factors are in vivo-specific cancer dependencies in glioma

Project description:Glioblastoma ranks as one of the most lethal human cancers, with no effective therapies. To discover novel therapeutic targets, here we performed parallel in vivo and in vitro RNA interference screens of epigenetic regulators and show that transcription elongation factors are essential for human glioblastoma cell survival in vivo, but not in vitro. Context-specific dependency in vivo is driven by microenvironment-induced global changes in the cancer epigenome. JMJD6, a top in vivo-specific hit, binds at enhancers and correlates with increased transcription of known pause-controlled genes. JMJD6 knockdown in patient-derived glioblastoma cells enhances survival of mice bearing orthotopic tumors. Moreover, elevated levels of JMJD6 alone, as well as transcription elongation factors collectively, informs tumor grade and predicts poor prognosis for patients. Our work provides a rationale for targeting transcription elongation as a therapeutic strategy in glioblastoma and, more broadly, the power of in vivo phenotypic screening to identify therapeutically relevant targets in cancer.

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Synthetic transcription elongation factors

Project description:This SuperSeries is composed of the SubSeries listed below.

2017-12-06 | GSE99403 | GEO

Synthetic transcription elongation factors license transcription across repressive chromatin.

Project description:The release of paused RNA polymerase II into productive elongation is highly regulated, especially at genes that affect human development and disease. To exert control over this rate-limiting step, we designed sequence-specific synthetic transcription elongation factors (Syn-TEFs). These molecules are composed of programmable DNA-binding ligands flexibly tethered to a small molecule that engages the transcription elongation machinery. By limiting activity to targeted loci, Syn-TEFs convert constituent modules from broad-spectrum inhibitors of transcription into gene-specific stimulators. Here we present Syn-TEF1, a molecule that actively enables transcription across repressive GAA repeats that silence frataxin expression in Friedreich's ataxia, a terminal neurodegenerative disease with no effective therapy. The modular design of Syn-TEF1 defines a general framework for developing a class of molecules that license transcription elongation at targeted genomic loci.

| S-EPMC6037176 | biostudies-literature

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