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ChIP-seq of E4F1 in mouse embryonic stem cells (mESCs)

ABSTRACT: E4F1 is a ubiquitously expressed zinc-finger protein of the Gli-Kruppel family that was first identified, more than 30 years ago, as a cellular target of the adenoviral oncoprotein E1A13S (Ad type V), required for transcriptional regulation of adenoviral genes. In order to decipher E4F1 cellular target genes, we performed chromatin immunoprecipitation of endogenous E4F1 in mouse embryonic stem cells. Both input and immunoprecipitated DNA were exhaustively sequenced and mapped on the mouse genome (mm9). Peak detection has been achieved by combining two peak calling algorithms. Intersection of the two E4F1 peak lists on each cell line were considered as E4F1 chromatin bound regions.

ORGANISM(S): Mus musculus

PROVIDER: GSE57221 | GEO | 2016/09/12

SECONDARY ACCESSION(S): PRJNA246034

REPOSITORIES: GEO

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ChIP-seq of E4F1 in primary mouse embryonic fibroblasts (MEFs) and in p53-/-, Ha-RasV12-transformed MEFs

Project description:E4F1 is a ubiquitously expressed zinc-finger protein of the Gli-Kruppel family that was first identified, more than 30 years ago, as a cellular target of the adenoviral oncoprotein E1A13S (Ad type V), required for transcriptional regulation of adenoviral genes. In order to decipher E4F1 cellular target genes, we performed chromatin immunoprecipitation of endogenous E4F1 in primary and in p53KO, Ha-RasV12-transformed MEFs. Both input and immunoprecipitated DNA were exhaustively sequenced and mapped on the mouse genome (mm9). Peak detection has been achieved by combining two peak calling algorithms. Intersection of the two E4F1 peak lists on each cell line were considered as E4F1 chromatin bound regions. Genome-wide mapping of E4F1 binding in mouse embryonic fibroblasts.

2015-04-01 | E-GEOD-57228 | biostudies-arrayexpress

ChIP-seq of E4F1 in primary mouse embryonic fibroblasts (MEFs) and in p53-/-, Ha-RasV12-transformed MEFs

2015-04-01 | GSE57228 | GEO

ChIP-seq of E4F1 in SUM159 triple negative breast cancer cell line

2022-03-01 | GSE128104 | GEO

Expression analysis of p53-/- and p53-/-, Ha-RasV12-transformed MEFs upon E4F1 gene inactivation

2015-04-01 | GSE57240 | GEO

Expression analysis of p53-/- and p53-/-, Ha-RasV12-transformed MEFs upon E4F1 gene inactivation

Project description:E4F1 is a ubiquitously expressed zinc-finger protein of the Gli-Kruppel family that was first identified, more than 30 years ago, as a cellular target of the adenoviral oncoprotein E1A13S (Ad type V), required for transcriptional regulation of adenoviral genes. In order to identify the p53-independent program controlled by E4F1, we performed microarray analyses in p53 KO and p53 KO; Ha-RasV12-transformed mouse embryonic fibroblasts (MEFs) in wild type and E4F1-inactivated cells. To address p53-independent E4F1 transcriptome, a 12 chip array study has been realized using total RNA recovered from wild-type (E4F1+/flox, CRE infected; odd Samples) MEFs and E4F1-depleted (E4F1-/flox, CRE infected; even Samples) MEFs in p53-/- (Samples 1 to 12) and p53-/-, Ha-RasV12 background (Samples 13 to 24). p53-/- MEFs were derived from 13.5-day mouse embryos. Transformed p53-/- MEFs were generated by infection with a recombinant retrovirus encoding for Ha-RasV12. Three independent biological replicates of wild-type and knock-out MEFs for E4F1 have been used on the two genetic backgrounds.

2015-04-01 | E-GEOD-57240 | biostudies-arrayexpress

RNA-seq of shE4F1 or shCTRL SUM159 triple negative breast cancer cell line treated or not with Gemcitabine

2022-03-01 | GSE128099 | GEO

E4F1 coordinates pyruvate metabolism and the activity of the elongator complex to ensure protein translation fidelity during neuronal development

Project description:The Leigh syndrome is a severe inborn neurodegenerative encephalopathy that is commonly associated with pyruvate metabolism defects. The transcription factor E4F1, a key regulator of the pyruvate dehydrogenase complex (PDC), was previously found to be mutated in Leigh syndrome patients but the molecular mechanisms leading to cell death in E4F1-deficient neurons remain unknown. Here, we show that E4F1 coordinates a transcriptional program involved in AcetylCoenzyme A (AcCoA) production by the PDC and its utilization by the Elongator complex to acetylate tRNAs and thereby enhance protein translation fidelity in the central nervous system. E4F1 directly regulates the expression of Dlat and Elp3, two genes encoding key subunits of the PDC and the Elongator complex. Consistently, genetic inactivation of E4f1 in neurons during mouse embryonic development decreased the activity of the PDC and of the Elongator complex, resulting in impaired tRNAs editing and the induction of an endoplasmic reticulum (ER) stress / unfolded protein response (UPR) that led to neuronal cell death and microcephaly. Impaired expression of ELP3 and activation of an ATF-driven UPR response was also observed in fibroblasts from Leigh syndrome patients harboring a homozygous E4F1K144Q mutation. Our findings identify a novel crosstalk between pyruvate metabolism and the regulation of protein translation that is perturbed in Leigh syndrome patients.

2022-12-20 | GSE158595 | GEO

Genome-Wide Gli3 Binding Sites in the E11.5 Mouse Limb Bud

Project description:Sonic hedgehog (Shh) signals via Gli transcription factors to direct digit number and identity in the vertebrate limb. We have characterized the Gli-dependent cis-regulatory network through a combination of whole genome ChIP-on-chip and transcriptional profiling of the developing mouse limb. These analyses identified approximately 5,000 high quality Gli3 binding sites, including all known Gli-dependent enhancers. Discrete binding regions exhibit a higher-order clustering, highlighting the complexity of cis-regulatory interactions. Further, Gli3 binds inertly to previously identified neural-specific Gli enhancers, demonstrating the accessibility of their cis-regulatory elements. Intersection of DNA binding data with gene expression profiles predicted 205 putative limb target genes. The supplementary bed file contains all 5,274 high quality binding Gli3 binding sites reported in the paper.

2008-09-15 | GSE11062 | GEO

The transcription factor E4F1 coordinates CHK1-dependent checkpoint and mitochondrial functions

Project description:The transcription factor E4F1 coordinates CHK1-dependent checkpoint and mitochondrial functions

| PRJNA246032 | ENA

E4F1 and ZNF148 are transcriptional activators of the A57C and wildtype TERT promoter

Project description:Point mutations within the TERT promoter are the most common recurrent somatic non-coding mutation identified across different cancer types, including glioblastoma, melanoma, hepatocellular carcinoma and bladder cancer. They are most abundant at C146T and C124T and more rare at A57C, with the latter originally described as a familial case but subsequently shown also to occur somatically. All three mutations create de novo ETS (E-twenty-six specific) binding sites and result in the reactivation of the TERT gene, allowing cancer cells to achieve replicative immortality. Here, we employed a systematic proteomics screen to identify transcription factors preferentially binding to the C146T, C124T and A57C mutations. While we confirmed binding of multiple ETS factors to the mutant C146T and C124T sequences, we identified E4F1 a an A57C-specific binder and ZNF148 as a TERT WT binder that is excluded from the TERT promoter by the C124T allele. Both proteins are activating transcription factors that bind specifically to the A57C and wildtype (at position 124) TERT promoter sequence in corresponding cell lines and upregulate TERT transcription and telomerase activity.

2023-11-04 | PXD037776 | Pride

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