Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA340264 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR4069142.fastq.gz | Fastqsanger.gz | |||
| SRR4069143.fastq.gz | Fastqsanger.gz | |||
| SRR4069144.fastq.gz | Fastqsanger.gz | |||
| SRR4069145.fastq.gz | Fastqsanger.gz | |||
| SRR4069146.fastq.gz | Fastqsanger.gz |
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Project description:Several genome-wide transcriptome analyses that focused on p53-induced cellular responses in many cellular contexts have continued to expand the already vast p53-regulated transcriptional networks. To investigate post-transcriptional controls as an additional dimension of p53-directed gene expression responses we performed translatome analysis by polysomal profiling on MCF7 cells treated with Doxorubicin and Nutlin-3a. A comparison between the transcriptome and the translatome revealed a large number of uncoupled genes, whose transcription changes did not correlate with translation changes. Overall, we establish p53 as a master regulator of translational control and identify many p53 target genes affecting translation that can contribute to p53-dependent cellular responses. Keywords: p53, transcriptome, translatome, polysomal RNA, subpolysomal RNA, uncoupling, Doxorubicin, Nutlin-3a
2014-04-17 | GSE50650 | GEO
Project description:The goal of the study is to identify p53 target genes specific to macrophages using the p53 stabilizer, Nutlin-3. Macrophages were differentiated x-vivo from monocytes obtained from healthy volunteers either left untreated or treated for 2 hours with 100 ng/mL of lipopolysaccharide (LPS), 0.1%v/v of DMSO (vehicle control for Nutlin-3) or 10 micromolar Nutlin-3. Three replicates were included for each treatment group.
2014-05-21 | E-GEOD-43596 | biostudies-arrayexpress
Project description:Background: p53 plays a key role in determining the clinical features of B cell chronic lymphocytic leukemia (CLL). Disruption of p53 by point mutations, deletion at 17p13, or both, occurs in a fraction of cases at diagnosis and predicts poor survival and chemorefractoriness. In cells with functional p53, p53 activity is inhibited through interaction with MDM2. In fact, p53 can be activated upon exposure of cells to inhibitors of p53/MDM2 interaction, like Nutlins. Exposure of CLL cells to Nutlin-3 is effective in raising the levels of p53 protein with subsequent induction of cell cycle arrest and/or apoptosis, independently of the most relevant prognostic markers. Specific gene-sets and GEP were documented to be associated with response or resistance to Nutlin-3 exposure in p53(wt) or p53(del/mut) CLL. These findings may help to identify novel molecular targets for CLL therapy. Aim: to analyze the gene expression profile (GEP) induced by Nutlin-3 exposure in primary CLL cells from p53(wt) and p53(del/mut) cases. Methods: purified cells from 24 PB CLL samples, all characterized for IGHV mutational status, CD38 and ZAP-70 and p53 mutations (16 p53(wt) CLL, 8 p53(del/mut) CLL of which 6 with del17p13 and p53 mutations, 1 with del17p13 alone, and 1 with p53 mutations alone), were exposed to 10 uM Nutlin-3 for 24 hours. GEP was performed using a dual labelling strategy; the differential expression of the below reported genes were validated by quantitative real-time PCR. specific gene-sets and GEP were documented to be associated with response or resistance to Nutlin-3 exposure in p53(wt) or p53(del/mut) CLL. These findings may help to identify novel molecular targets for CLL therapy.
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2016-09-01 | E-GEOD-69148 | biostudies-arrayexpress
Project description:We investigated the genes that were most strongly activated by p53 in this immortalized human cell line following treatment with the MDM2 inhibitor nutlin-3a. To identify genes that were activated by p53, we comparatively analyzed parental cells and isogenic derivatives. Wild type, p53-knockout and cells harboring a heterozygous p53 A276P mutation were assessed.
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