E-GEOD-53321
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA231686
PROVIDER: E-GEOD-53321 | ExpressionAtlas | 2015-07-31
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-GEOD-53321-analysis-methods.tsv | Tabular | |||
| E-GEOD-53321-atlasExperimentSummary.Rdata | Rdata | |||
| E-GEOD-53321-configuration.xml | Xml | |||
| E-GEOD-53321-percentile-ranks.tsv | Tabular | |||
| E-GEOD-53321.condensed-sdrf.tsv | Tabular |
Items per page: 5 1 - 5 of 105 |
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Project description:Expression data from polarized macrophages: effect of p53
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Project description:We determined the effect of p53 activation on de novo protein synthesis using quantitative proteomics of newly synthesized proteins (pulsed stable isotope labeling with amino acids in cell culture, pSILAC) in combination with mRNA and non-coding RNA expression analyses by next generation sequencing (RNA-, miR-Seq) in the colorectal cancer (CRC) cell line SW480. Furthermore, genome-wide DNA binding of p53 was analyzed by chromatin-immunoprecipitation (ChIP-Seq). Thereby, we identified differentially regulated mRNAs (1258 up, 415 down), miRNAs (111 up, 95 down), lncRNAs (270 up, 123 down) and proteins (542 up, 569 down). Changes in mRNA and protein expression levels showed a positive correlation (r = 0.50, p < 0.0001). More transcriptionally induced genes displayed occupied p53 binding sites (4.3% mRNAs, 7.2% miRNAs, 6.3% lncRNAs, 5.9% proteins) than repressed genes (2.4% mRNAs, 3.2% miRNAs, 0.8% lncRNAs, 1.9% proteins), suggesting indirect mechanisms of repression. Around 50% of the downregulated proteins displayed seed-matching sequences of p53-induced miRNAs in the corresponding 3â??-UTRs. Moreover, proteins repressed by p53 significantly overlapped with those previously shown to be repressed by miR-34a. We confirmed upregulation of the novel direct p53 target genes LINC01021, MDFI, ST14 and miR-486 and showed that ectopic LINC01021 expression inhibited proliferation in SW480 cells. Furthermore, HMGB1, KLF12 and CIT mRNAs were confirmed as direct targets of the p53-induced miR-34a, miR-205 and miR-486-5p, respectively. In line with the loss of p53 function during tumor progression, elevated expression of HMGB1, KLF12 and CIT was detected in advanced stages of cancer. This study provides new insights and a comprehensive catalogue of p53-mediated regulations and p53 DNA binding in CRC cells.
2016-05-24 | MSV000079767 | MassIVE
Project description:p53 is critically important in preventing oncogenesis but its role in non-cancer biology remains unclear. Macrophages exist as two subtypes (M1 and M2). Nutlin-3a (p53 activator) inhibits M2 gene expression and phenotype. p53 acts by suppressing transcription of c-Myc and thence regulates expression of a subset of M2 markers. This work has implications for our understanding of the mechanisms that regulate plasticity of macrophages in health and disease. We used microarrays to study the global programme of gene expression in nutlin-3a and 10058F4 (C-myc inhibitor) treated polarised mouse macrophages 5 groups of cultured mouse macrophages: (i) M0 (untreated), (ii) M1, (iii) M2, (iv) M2+nutlin-3a, (v) M2+MYC inhibitor (10058F4). 3 biological replicates per treatment group.
2015-01-01 | E-GEOD-53321 | biostudies-arrayexpress
Project description:The specific roles of mutant p53’s dominant-negative (DN) or gain-of-function (GOF) properties in regulating acute response and long-term tumorigenesis is unclear. Using “knock-in” mouse strains expressing varying R246S mutant levels, we show that DN effect on transactivation is universally observed after acute p53 activation whereas the effect on cellular outcome is cell-type specific. Reducing mutant p53 levels abrogated the DN effect. Mutant p53’s DN effect protected against radiation-induced death, but did not accentuate tumorigenesis. Furthermore, the R246S mutant did not promote tumorigenesis compared to p53-/- mice in various models, even in the absence of MDM2, unlike the R172H mutant. Together, these data demonstrate that mutant p53’s DN property only affects acute responses, whereas GOF is not universal, being mutation-type specific. Transcriptomes of 4 samples of normal B cells and 12 Myc-induced B lymphoma cells harvested from mice of different p53 genotypes were profiled. Data was analysed by mixed model ANOVA using Partek.
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Project description:The specific roles of mutant p53’s dominant-negative (DN) or gain-of-function (GOF) properties in regulating acute response and long-term tumorigenesis is unclear. Using “knock-in” mouse strains expressing varying R246S mutant levels, we show that DN effect on transactivation is universally observed after acute p53 activation whereas the effect on cellular outcome is cell-type specific. Reducing mutant p53 levels abrogated the DN effect. Mutant p53’s DN effect protected against radiation-induced death, but did not accentuate tumorigenesis. Furthermore, the R246S mutant did not promote tumorigenesis compared to p53-/- mice in various models, even in the absence of MDM2, unlike the R172H mutant. Together, these data demonstrate that mutant p53’s DN property only affects acute responses, whereas GOF is not universal, being mutation-type specific. Transcriptomes of 10 normal thymi harvested from 4-5 weeks old mice of different p53 and mdm2 genotype were profiled. Data was analysed by mixed model ANOVA using Partek.
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Project description:p53 is critically important in preventing oncogenesis but its role in non-cancer biology remains unclear. Macrophages exist as two subtypes (M1 and M2). Nutlin-3a (p53 activator) inhibits M2 gene expression and phenotype. p53 acts by suppressing transcription of c-Myc and thence regulates expression of a subset of M2 markers. This work has implications for our understanding of the mechanisms that regulate plasticity of macrophages in health and disease. We used microarrays to study the global programme of gene expression in nutlin-3a and 10058F4 (C-myc inhibitor) treated polarised mouse macrophages
2015-01-01 | GSE53321 | GEO
Project description:Expression data from macrophages
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Project description:The specific roles of mutant p53’s dominant-negative (DN) or gain-of-function (GOF) properties in regulating acute response and long-term tumorigenesis is unclear. Using “knock-in” mouse strains expressing varying R246S mutant levels, we show that DN effect on transactivation is universally observed after acute p53 activation whereas the effect on cellular outcome is cell-type specific. Reducing mutant p53 levels abrogated the DN effect. Mutant p53’s DN effect protected against radiation-induced death, but did not accentuate tumorigenesis. Furthermore, the R246S mutant did not promote tumorigenesis compared to p53-/- mice in various models, even in the absence of MDM2, unlike the R172H mutant. Together, these data demonstrate that mutant p53’s DN property only affects acute responses, whereas GOF is not universal, being mutation-type specific. Transcriptomes of mouse embryonic fibroblasts harvested from embyros of different p53 genotypes were profiled. A total of 6 primary clones of MEFs were used and these cells were transformed with E1A/Ras. Data was analysed by mixed model ANOVA using Partek.
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Project description:The effects of diverse stresses on promoter selectivity and transcription regulation by the tumor suppressor p53 are poorly understood. We have taken a comprehensive approach to characterizing the human p53 network that includes p53 levels, binding, expression and chromatin changes under diverse stresses. Human osteosarcoma U2OS cells treated with anti-cancer drugs Doxorubicin or Nutlin-3 led to strikingly different p53 gene binding patterns based on ChIP-seq experiments. While two contiguous RRRCWWGYYY decamers is the consensus binding motif, p53 can bind a single decamer and function in vivo. Although the number of sites bound by p53 was 6-times greater for Nutlin-3 than Doxorubicin, expression changes induced by Nutlin-3 were much less dramatic compared to Doxorubicin. Unexpectedly, the solvent DMSO alone induced p53 binding to many sites common to Doxorubicin; however, this binding had no effect on target gene expression. Together, these data imply a two-stage mechanism for p53 transactivation where p53 binding only constitutes the first stage. Furthermore, both p53 binding and transactivation were associated with increased active histone modification H3K4me3. We discovered 149 putative new p53 target genes including several that are relevant to tumor suppression, revealing potential new targets for cancer therapy and expanding our understanding of the p53 regulatory network.
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