E2F4 and its cofactor transfection vs empty vector transfection
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Vishy Iyer
PROVIDER: E-GEOD-21439 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:The transcription factor E2F4 is a member of the E2F family of regulators which has critical roles in cell cycle control and differentiation. We investigated the genome-wide binding profile of E2F4 using a newly developed peak calling program based on a kernel density estimation and identified approximately 16 thousands E2F4 binding sites at a 1% FDR threshold, which potentially modulate 7,346 downstream target genes. Gene Ontology (GO) functional analysis of E2F4 target genes revealed several novel functions of E2F4 including I-kappaB kinase/NF-kappaB cascade, protein transport and targeting, protein folding, and sterol biosynthetic process. In addition to mRNA target genes, E2F4 also binds and regulates some miRNA targets such as let-7a, mir-17 and mir-22. Interestingly, we found that about 20% of E2F4 sites are in intergenic regions, which suggests that E2F4 may function at enhancer sites. De novo motif discovery revealed 5 novel, significantly enriched motifs within E2F4 sites. Only 5% of binding sites contain a canonical motif, indicating that E2F4 can use diverse motifs to bind DNA and regulate transcription. Overexpression of E2F4 and its cofactors such as RBL2 and DP-1, followed by microarray analysis, revealed that E2F4 functions as an activator and a repressor. Taken together, our genome-wide E2F4 ChIP sequencing data provided evidences of versatile physiological roles of E2F4 and insights into its functions. This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2010-11-01 | E-GEOD-21489 | biostudies-arrayexpress
Project description:Transcriptional profiling of E2F4 target genes upon overexpression of E2F4 and it cofactors
2010-11-01 | GSE21439 | GEO
Project description:The transcription factor E2F4 is a member of the E2F family of regulators which has critical roles in cell cycle control and differentiation. In order to fully understand the physiological roles of E2F4 and the regulatory networks it mediates, and to reveal its relationships with other members of the E2F family, it is essential to comprehensively identify E2F4 target sites throughout the genome. Here, we investigated genome-wide E2F4 targets in human lymphoblastoid cells using the recently developed unbiased target discovery technique of ChIP sequencing. We sequecned E2F4 ChIP and corresponding Input
2010-11-01 | E-GEOD-21488 | biostudies-arrayexpress
Project description:The transcription factor E2F4 is a member of the E2F family of regulators which has critical roles in cell cycle control and differentiation. We investigated the genome-wide binding profile of E2F4 using a newly developed peak calling program based on a kernel density estimation and identified approximately 16 thousands E2F4 binding sites at a 1% FDR threshold, which potentially modulate 7,346 downstream target genes. Gene Ontology (GO) functional analysis of E2F4 target genes revealed several novel functions of E2F4 including I-kappaB kinase/NF-kappaB cascade, protein transport and targeting, protein folding, and sterol biosynthetic process. In addition to mRNA target genes, E2F4 also binds and regulates some miRNA targets such as let-7a, mir-17 and mir-22. Interestingly, we found that about 20% of E2F4 sites are in intergenic regions, which suggests that E2F4 may function at enhancer sites. De novo motif discovery revealed 5 novel, significantly enriched motifs within E2F4 sites. Only 5% of binding sites contain a canonical motif, indicating that E2F4 can use diverse motifs to bind DNA and regulate transcription. Overexpression of E2F4 and its cofactors such as RBL2 and DP-1, followed by microarray analysis, revealed that E2F4 functions as an activator and a repressor. Taken together, our genome-wide E2F4 ChIP sequencing data provided evidences of versatile physiological roles of E2F4 and insights into its functions. This SuperSeries is composed of the SubSeries listed below.
2010-11-01 | GSE21489 | GEO
Project description:2091 mock vs. 2091 E2F4 IP - Human 13K promoter microarray 2091 cells were serum starved for 72hours and fixed with formaldehyde. Keywords: repeat sample
2005-01-01 | GSE1861 | GEO
Project description:This experiment is a part of global location analysis of the human DREAM complex including subunits: E2F4, RBL2/p130, LIN9 and LIN54. Specifically, the regions in Human Promoter Array 1.0R (GPL5082) bound by: E2F4 in G0-arrested T98G cells E2F4 in S-phase synchronized T98G cells LIN54 in G0-arrested T98G cells LIN54 in S-phase synchronized T98G cells LIN9 in G0-arrested T98G cells LIN9 in S-phase synchronized T98G cells p130 in G0-arrested T98G cells p130 in S-phase synchronized T98G cells were compared with input chromatin. MAT (Model-based Analysis for Tiling Arrays) .bar and .bed output files provided as supplementary files. Keywords: CHiP-chip genomic DNA
2007-04-17 | GSE7516 | GEO
Project description:We performed ChIP-Seq for hallmark TFs (Ets1, Runx1), histone modification marks (H3K4me1, H3K4me2, H3K4me3, H3K27me3, H3K36me3), total RNA Pol II, short RNA-Seq as well as nucleosome mapping mainly in murine Rag2 -/- thymocytes. We also performed ChIP-Seq for E47 as well as nucleosome mapping, gene expression microarray analysis in CD4+ CD8+ DP thymocytes. Overall, we find a key role for the transcription factor Ets1, contributing towards alpha beta T cell lineage commitment via differential transactivation of stage-specific genes orchestrated by dynamic, co-association -mediated chromatin remodeling, as well as transcription dependent generation of a specialized chromatin structure at the TCR beta locus. Genome-wide analysis via ChIP-Seq for Ets1, Runx1, total RNA Pol II binding, H3K4me1, H3K4me2, H3K4me3, H3K27me3, H3K36me3, short RNA-Seq, Mnase-Seq in murine Rag2 -/- thymocytes, ChIP-Seq for E47, Mnase-Seq and gene expression microarray analysis in DP thymocytes This Series represents ShortRNA-Seq data.
2014-04-01 | E-GEOD-56358 | biostudies-arrayexpress
Project description:A core pathophysiology underlying many respiratory diseases is multiciliated cell dysfunction leading to inadequate mucociliary clearance. Due to the prevalence and high variability of etiologies of MCC dysfunction in respiratory diseases, it is critical to understand the mechanisms controlling multiciliogenesis that may be targeted to restore functional mucociliary clearance. Multicilin, in complex with E2F4, is necessary and sufficient to drive multiciliogenesis in airway epithelium, however this does not apply to all cell types nor occur evenly across all cells in the same cell population. In this study we investigated we further investigate how co-factors regulate the ability of Multicilin to drive multiciliogenesis. Combining data in mouse embryonic fibroblasts and human bronchial epithelial cells we identify RBL2 as an inhibitor of the transcriptional activity of Multicilin. Both knockdown of RBL2 and phosphorylation of RBL2 driven by exposure to an air-liquid interface in the presence of Multicilin activated multiciliogenesis demonstrating a dynamic interaction regulating the differentiation of human airway epithelial cells. Identification of this mechanism has important implications for facilitating MCC differentiation in diseases where mucociliary clearance is impeded.
2024-01-31 | GSE235682 | GEO
Project description:Dicer initiates RNA interference by generating small RNAs involved in various silencing pathways. Dicer participates in centromeric silencing, but its role in the epigenetic regulation of other chromatin domains has not been explored. Here we show that Dicer1 deficiency in Mus musculus leads to decreased DNA methylation, concomitant with increased telomere recombination and telomere elongation. These DNA-methylation defects correlate with decreased expression of Dnmt1, Dnmt3a and Dnmt3b DNA methyltransferases (Dnmts), and methylation levels can be recovered by their overexpression. We identify the retinoblastoma-like 2 protein (Rbl2) as responsible for decreased Dnmt expression in Dicer1-null cells, suggesting the existence of Dicer-dependent small RNAs that target Rbl2. We identify the miR-290 cluster as being downregulated in Dicer1-deficient cells and show that it silences Rbl2, thereby controlling Dnmt expression. These results identify a pathway by which miR-290 directly regulates Rbl2-dependent Dnmt expression, indirectly affecting telomere-length homeostasis. Keywords: Cell type comparison
2008-04-22 | GSE11229 | GEO