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Transcriptome of TNF-a-treated and untreated HeLa cells before and after TFIIB knockdown

ABSTRACT: Transcriptome of TNF-a-treated and untreated HeLa cells before and after TFIIB knockdown

PROVIDER: PRJNA414971 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6189790.fastq.gz	Fastqsanger.gz
	SRR6189781.fastq.gz	Fastqsanger.gz
	SRR6189791.fastq.gz	Fastqsanger.gz
	SRR6189782.fastq.gz	Fastqsanger.gz
	SRR6189792.fastq.gz	Fastqsanger.gz

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Transcriptome of TNF-a-treated and untreated HeLa cells before and after TFIIB knockdown

Project description:The goal of this study was to compare transcriptome of HeLa cells with or without TFIIB knockdown for gene expression changes in steady state or after TNF-a treatment. Although a broad effect on gene expression would be anticipated, TFIIB depletion led only to an altered expression of a limited number of genes.

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Gene knockdown suggests a new paradigm for transcription factor TFIIB functionality

Project description:Experimental and bioinformatic studies of transcription initiation by RNA polymerase II (RNAP2) have revealed a mechanism of RNAP2 transcription initiation less uniform across gene promoters than initially thought. However, the general transcription factor TFIIB is presumed to be universally required for RNAP2 transcription initiation. Based on bioinformatic analysis of data, TFIIB knockdown in primary and transformed cell lines, and in vitro transcription experiments, we report that TFIIB is dispensable for transcription of most human promoters, but is essential for HSV-1 gene transcription and replication. We report a novel cell cycle TFIIB regulation and involvement of the acetylated TFIIB variant in chromosomal condensation. Taken together, these results establish a new paradigm for TFIIB functionality as a determinant of the human transcriptome, which when downregulated has potent anti-viral effects.

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HeLa cells treated and untreated with Clinacanthus nutans DCM fraction

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Drosophila TFIIB ChIP-seq after CBP inhibition

Project description:TFIIB chromatin binding is drastically reduced genome-wide after 10 min of CBP (also known as nejire) inhibition.

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Epitranscriptomics m6A analyses reveal distinct m6A marks in tumor necrosis a (TNF-a)-treated HeLa cells

Project description:We have performed a epitranscriptomics study in which we first tretaed TNF-alpha in HeLa cells and DMSO was used as a negative control. Total RNA was isolated from TNF-alpha treated cells as well as control cells and apoptotic rate was determined by flow cytometry. Total RNAs were subjected to miCLIP to identify differentially m6A methylated RNAs. We then transcriptionally analyzed apoptotic genes which have differential m6A methylation in TNF-alpha tretament by qPCR. Afterthat, candidate genes were examined at the level of translation by polysome fractioantion assay.

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16MB binding of STAT1 and IRF1 transcription factors in IFNg treated and untreated HeLa cells using NimbleGen array

Project description:Analysis of STAT1 and IRF1 binding in IFNg treated and untreated HeLa cells for 6 hours was done using 50mer oligonucleotide probes at 30bp intervals tiling over non-repetitive 16MB gene locus (HG17).

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Comparative ChIP-chip analysis of general transcription factor TFIIB and negative cofactor NC2 in human B cells

Project description:A comparative ChIP-chip analysis of TFIIB and NC2 in human B cells reveals that basal core promoter architectures control the equilibrium between NC2 and preinitiation complexes. We conducted a comparative ChIP-chip and gene expression analysis of TFIIB in human B cells and analyze associated core promoter architectures. TFIIB occupancy relates well to gene expression, with the vast majority of promoters being GC-rich and lacking defined core promoter elements. TATA consensus and TATA-like motifs but not the previously in vitro defined TFIIB recognition elements (BREs) are enriched in approximately 5% of the genes. Further insight was obtained by performing a parallel ChIP-chip analysis of the TFIIB antagonist NC2. The latter identifies a highly related target gene set. Nonetheless, subpopulations show strong variations in TFIIB/NC2 ratios, with high NC2/TFIIB ratios correlating to promoters that show dispersed transcription start site patterns and lacking defined core elements. Conversely, high TFIIB/NC2 ratios select for conserved core promoter elements that include TATA and INR (initiator), the upstream TFIIB recognition element (BREu) and the downstream promoter element (DPE).

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