Effects of GABP knockdown on the transcriptome of macaque fibroblast cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA833936 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR19026000.fastq.gz | Fastqsanger.gz | |||
| SRR19026001.fastq.gz | Fastqsanger.gz | |||
| SRR19026002.fastq.gz | Fastqsanger.gz | |||
| SRR19026003.fastq.gz | Fastqsanger.gz | |||
| SRR19026004.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 8 |
Similar Datasets
Project description:We identified a total of 2,058 GABP-regulated genes (1,067 up-regulated and 991 down-regulated genes in the GABP knockdown cells) with the threshold of Padj < 0.05 and Fold change > 1.5.
2025-02-01 | GSE201987 | GEO
Project description:Effects of NCL Knockdown on Fibroblast-Like Synoviocytes
| PRJNA1115139 | ENA
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
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: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
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
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. Examination of the role of GABP in hematopoietic stem cells
2010-12-10 | E-GEOD-24933 | biostudies-arrayexpress
Project description:Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by systemic inflammation, synovial hyperplasia, and the destruction of bone and cartilage. Despite the use of various immunosuppressive disease-modifying antirheumatic drugs (DMARDs), a considerable proportion of RA patients remain symptomatic. As RA progresses, fibroblast-like synoviocytes (FLSs) undergo a phenotypic transition to an aggressive state, making them attractive non-immune cellular targets for RA treatment. However, there are currently no clinically available therapies that selectively ablate RA-FLSs due to the lack of specific molecular targets. Our research focuses on the knockdown of the nucleolin (NCL) gene in RA-FLSs. NCL is expressed in the cell of RA-FLSs and plays a crucial role in their aggressive transition. By specifically knocking down NCL, we observed significant inhibition of the harmful phenotypes exhibited by RA-FLSs.
2024-12-31 | GSE268214 | GEO
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. ArrayExpress Release Date: 2009-06-10 Publication Title: Molecular interactions between HNF4a, FOXA2 and GABP identified at regulatory DNA elements through ChIP-sequencing Publication Author List: Ola Wallerman, Mehdi Motallebipour, Stefan Enroth, Kalicharan Patra, MadhuSudan Reddy Bysani, Jan Komorowski, Claes Wadelius Person Roles: submitter Person Last Name: Wallerman Person First Name: Ola Person Mid Initials: Person Email: ola.wallerman@genpat.uu.se Person Phone: Person Address: IGP, Rudbecklab Person Affiliation: Uppsala University
2011-02-05 | GSE25694 | GEO
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