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

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 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE57240 | GEO | 2015/04/01

SECONDARY ACCESSION(S): PRJNA246033

REPOSITORIES: GEO

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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

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 mouse embryonic stem cells (mESCs)

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

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Next-generation RNA sequencing of murine bladder cancer cells isolated from P53/PTEN KO tumors at different stages of the disease.

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Mus musculus

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

| PRJNA246033 | ENA

Expression profiling of KSR1-/- MEFs expressing KSR1 and/or H-RasV12

Project description:We engineered KSR1-/- mouse embryonic fibroblasts (MEFs) to express GFP alone, KSR1 or RasV12 and GFP, or KSR1, H-RasV12 and GFP, and performed gene expression profiling on all 4 cell lines.

2011-04-02 | GSE28228 | GEO

BRD7 is a candidate tumour suppressor gene required for p53 function

Project description:Oncogene-induced senescence (OIS) is a p53-dependent defence mechanism against uncontrolled proliferation. Consequently, many human tumours harbour p53 mutations while others show a dysfunctional p53 pathway, frequently by unknown mechanisms. We identified BRD7, a bromodomain-containing protein whose inhibition allows full neoplastic transformation in the presence of wild-type p53. Intriguingly, in human breast tumours harbouring wild-type, but not mutant p53, the BRD7 gene locus was frequently deleted and low BRD7 expression was found in a subgroup of tumours. Functionally, BRD7 is required for efficient p53-mediated transcription of a subset of target genes. BRD7 interacts with p53 and p300, and is recruited to target gene promoters, affecting histone acetylation, p53 acetylation, and promoter activity. Thus, BRD7 suppresses tumourigenicity by serving as a p53 cofactor required for efficient induction of p53-dependent OIS. We recorded mRNA expression profiles of BJ primary fibroblasts expressing the oncogene RasV12 and either control vector, one of two BRD7 knockdown vectors, or p53 knockdown vector. In addition, we profiled genome-wide protein DNA interactions for p53 and BRD7 using ChIP-Seq. p53- and BRD7-binding sites were recorded in RasV12-expressing BJ cells; as a control we used knockdown of the gene of interest (BRD7 or p53).

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