ChIP-seq for GABPα in T cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE101936 | GEO | 2017/07/28
SECONDARY ACCESSION(S): PRJNA395979
REPOSITORIES: GEO
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Project description:Ets family transcription factor GA-binding protein (GABP) regulates gene expression in CD4 and CD8 T cells. We used microarray to examine genes differentially expressed in GABP-sufficient (WT) and GABP-deficient (KO) CD4 and CD8 T cells
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Project description:A key model for understanding how large transcription complexes are targeted is the Drosophila dosage compensation system in which the Male-Specific Lethal (MSL) transcription complex specifically identifies and regulates the male X-chromosome. MSL complex is targeted to GA-containing sequences, but the most well-studied GA-binding transcription factor, GAGA Associated Factor (GAF), does not physically associate with MSL complex. Instead the Chromatin Linked Adapter for MSL Proteins (CLAMP) zinc-finger protein specifically targets MSL complex to GA-rich sequences on the X-chromosome. Here, we compare the binding relationships of CLAMP, GAF, and the MSL3 dosage compensation complex protein using ChIP-seq.
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Project description:Knockout of the B1 subunit of the GA-binding protein (GABP) [ChIP-seq]
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Project description:Knockout of the B1 subunit of the GA-binding protein (GABP)
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Project description:We knocked out different exons corresponding to different sections of GABP, a transcription factor known to bind to the telomerase reverse transcriptase (TERT) promoter with the G228 mutation. We investigated the effects of the knockouts in the regulation of TERT expression and other subunits of GABP. GABP genomic binding sites were determined through chromatin immunoprecipitation sequencing (ChIP-seq), and gene expression was determined through total RNA sequencing (RNA-seq). Combining data pertaining to GABP binding sites and gene expression provided insight into the molecular mechanisms of maintaining the length of telomeres in cancers.
2025-06-11 | GSE224164 | GEO
Project description:A central question in transcription factor biology is how a specific member of a transcription factor family occupies a promoter in vivo, when all family members bind the same consensus site in vitro. To uncover the mechanisms regulating DNA binding specificity within transcription factor families, we have used the techniques of chromatin immunoprecipitation coupled with genome-wide microarray analysis to query the occupancy of three members of the ETS transcription factor family in a human T-cell line. Unexpectedly, redundant occupancy was frequently detected while specific occupancy was less likely. An unbiased bioinformatics approach correlated redundant binding with consensus ETS binding sequences near transcription start sites, whereas specific binding sites diverged dramatically from the consensus, were coupled with a site for a cooperative binding partner, and were found further from transcription start sites. The specific and redundant DNA binding modes illustrate the regulation of transcription factor specificity in vivo and suggest two distinct roles for members of the ETS transcription factor family. Keywords: ChIP-chip
2007-07-27 | GSE7449 | GEO
Project description:The non-coding genome contributes substantially to the total cellular DNA mass and is thoutht to host regulatory cis-acting element, but may also code for some regulatory transcripts. Despite ist contribution to the genomic mass, it has barely recieved scientific attention. Much emphasis has been laid on the approximaetly 2% coding Region, although its transcription, in most cases is regulated at the level of the non-coding genome. In recent years, several studies have revealed disease-associated somatic mutations in regulatory regions of the non-coding genome. One most prominent example is the hotspot mutations in the core promoter region of the TERT gene. In several cancer entities, these alterations have been associated with dysregulation of telomerase activity and tumorigenesis. Novel binding sites are created for transcription factors of the ETS family and GABP for example has been shown to bind to these novel ETS sites. The entire spectrum of ETS family members that can bind is however still lacking. In ordert o fill this knowledge gap and understand the impact of such binding on tumor biology, we have used functional protein microarrays to identify ETS members that preferentially bind the mutant promoter and by means of transcription profiling, we have identified downstream targets of the binding events. We have used siRNA to knockdown FLI-1 and hTERT in cell lines from three cancer entities (NSCLC, PDAC and MCC) with the help oft he illumina beadchip arrays and we compared the transcriptional profiles of the cell lines under different knockdown conditions. We Identify CCND1 and E2F2 as direct targets of both TERT and FLI-1, and CMTM7 as an FLI1-only target. We show, for different cancer entities, that FLI-1 binds the TERT promoter and accelerates progression through the cell cycle by enhancing E2F2 and CCND1 expression
2019-06-10 | E-MTAB-7452 | biostudies-arrayexpress
Project description:A central question in transcription factor biology is how a specific member of a transcription factor family occupies a promoter in vivo, when all family members bind the same consensus site in vitro. To uncover the mechanisms regulating DNA binding specificity within transcription factor families, we have used the techniques of chromatin immunoprecipitation coupled with genome-wide microarray analysis to query the occupancy of three members of the ETS transcription factor family in a human T-cell line. Unexpectedly, redundant occupancy was frequently detected while specific occupancy was less likely. An unbiased bioinformatics approach correlated redundant binding with consensus ETS binding sequences near transcription start sites, whereas specific binding sites diverged dramatically from the consensus, were coupled with a site for a cooperative binding partner, and were found further from transcription start sites. The specific and redundant DNA binding modes illustrate the regulation of transcription factor specificity in vivo and suggest two distinct roles for members of the ETS transcription factor family. Keywords: ChIP-chip Chromatin IP from uninduced asynchronous Jurkat T cells, or HT29 colon cells using antibodies to three ETS transcription factors (ETS1, ELF1, and GABPa) or the transcription factors RUNX1 or E2F4. IP and whole input DNAs are amplified (WGA2 kit sigma) and labeled and compared by promoter microarrays (Agilent). Each experiment requires 2 microarrays to cover the genome. Proximal promoter arrays assay 1kb surrounding transcription start sites, extended promoter arrays assay 7kb surrounding transcription start sites. Each microarray is performed as two biological replicates with the exception of ETS1 in HT29 proximal promoter array which were done once, and ETS1 in Jurkat proximal promoter array which was done three times.
2007-07-27 | E-GEOD-7449 | biostudies-arrayexpress
Project description:Knockout of the B1 subunit of the GA-binding protein (GABP) [RNA-seq]
| PRJNA929998 | ENA
Project description:Reactivation of telomerase reverse transcriptase (TERT) expression enables cells to overcome replicative senescence and escape apoptosis, fundamental steps in the initiation of human cancer. Multiple cancer types, including up to 83% of glioblastomas (GBM), harbor highly recurrent TERT promoter mutations of unknown function but specific to two nucleotide positions. We identify the functional consequence of these mutations in GBM to be recruitment of the multimeric GABP transcription factor specifically to the mutant promoter. Allelic recruitment of GABP is consistently observed across four cancer types, highlighting a shared mechanism underlying TERT reactivation. Tandem flanking native ETS motifs critically cooperate with these mutations to activate TERT, likely by facilitating GABP heterotetramer binding. GABP thus directly links TERT promoter mutations to aberrant expression in multiple cancers.
| EGAS00001001242 | EGA