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Knockout of the B1 subunit of the GA-binding protein (GABP) [ChIP-seq]

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE224164 | GEO | 2025/06/11

REPOSITORIES: GEO

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Knockout of the B1 subunit of the GA-binding protein (GABP) [RNA-seq]

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 | GSE224165 | GEO

GABP determines the epigenetic status of mutant TERT promoter

Project description:Blocking telomerase is recognized as a key anti-cancer mechanism. Unlike in stem cells, levels of telomerase catalytic subunit TERT are limiting in reconstituting telomerase activity in somatic cells. However in some cancers, Tert is transcriptionally reactivated by mutations in its promoter. Given that Tert in stem cells is driven by WT Tert promoter, if we can selectively target Tert reactivation through mutant Tert promoters we can block telomerase activity specifically in cancer cells without toxicity in stem cells. Here we report the epigenetic regulation of Tert promoter comparing WT and mutant promoters. We showed that GABPA homodimerization through long-range interaction stabilizes Gabpa to drive Tert expression. Furthermore, BRD4 specifically activates the C250T mutant promoter via dual mechanism involving GABPA, thereby setting the stage for future therapeutics.

2017-02-27 | GSE77265 | GEO

Genome-wide mapping of the transcription factor GABP-alpha binding in human CD34+CD133+ hematopoietic progenitor cells.

Project description:We used ChIP-Seq to map GABP-alpha binding sites in human hematopoietic progenitor cells (HPCs). Coupled with functional assays using GABP-alpha deficient mouse model and bioinformatics analysis, we systematically determined a transcriptional module controlled by GABP in HPCs.

2010-12-10 | GSE24933 | GEO

Genome-wide mapping of the transcription factor GABP-alpha binding in human CD34+CD133+ hematopoietic progenitor cells.

2010-12-10 | E-GEOD-24933 | biostudies-arrayexpress

The transcription factor GABP selectively binds and activates the mutant TERT promoter in cancer

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

Knockout of the B1 subunit of the GA-binding protein (GABP)

Project description:Knockout of the B1 subunit of the GA-binding protein (GABP)

| PRJNA929996 | ENA

Knockout of the B1 subunit of the GA-binding protein (GABP) [ChIP-seq]

Project description:Knockout of the B1 subunit of the GA-binding protein (GABP) [ChIP-seq]

| PRJNA929997 | ENA

Knockout of the B1 subunit of the GA-binding protein (GABP) [RNA-seq]

Project description:Knockout of the B1 subunit of the GA-binding protein (GABP) [RNA-seq]

| PRJNA929998 | ENA

RNA-seq identified GLI1 as the target gene for GABP

Project description:We performed RNA-seq based transcriptomic analysis to evaluate differential protein expression in the kidneys of GABP overexpressing mice in db/m and GABP knockdown mice in db/db. The cluster analysis heat map shows the genetic changes . Compared with db/m mice, 734 differentially expressed genes, 525 upregulated genes and 209 upregulated genes . Compared with db/db mice, 82 genes were up-regulated and 82 genes were down-regulated in the kidneys of mice with GABP knockdown in db/db . Further, the classical pathway map in IPA database found that cell growth, proliferation, organ development and other pathways were activated after GABP overexpression. Cell growth, proliferation, organ development and other pathways were inhibited . It was further confirmed that GABP was associated with proliferation. Among differentially expressed genes, there were 9 differentially expressed genes up-regulated by GABP overexpression and down-regulated by GABP knockdown . Through the analysis of Ingenuity Pathway Analysis database, GABP and GLI1 were most closely related .

2024-10-05 | GSE244715 | GEO

High throughput sequencing of human HepG2 DNA immunoprecipitated with FOXA2, HNF4a and NRF2/GABP

Project description:In each cell type the expression of genes is regulated by the action of a large number of transcription factors, but so far we have only a rudimentary knowledge of the location of the gene regulatory elements where they bind. This can now be addressed with genome-wide ChIP experiments. In a previous ChIP-chip study of USF1 and USF2 we found evidence also of binding of GABP, FOXA2 and HNF4a within the enriched regions. Here we have applied ChIP-seq for these transcription factors and identified 3064 peaks of enrichment for GABP, 7266 for FOXA2 and 18783 for HNF4a. HNF4a and FOXA2 binding was found in at least half of the regions previously identified as bound by USF2 but not USF1, showing that they frequently bind the same regulatory elements. GABP peaks were found at transcription start sites whereas 94 % of FOXA2 and 90 % of HNF4a peaks were located at other positions. We developed a method based on the high resolution achieved by ChIP-seq to accurately define TFBS within peaks, and found the predicted sites to have an elevated conservation level compared to peak centers; however the majority of bindings were not evolutionary conserved. An unexpected interaction between HNF4a and GABP was seen at TSS, with as many as 1/3 of the HNF4a positive promoters being bound also by GABP, and co-immunoprecipitations show that these factors are in the same complex in the nucleus.

2009-06-09 | E-MTAB-115 | biostudies-arrayexpress

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