Transcription profiling by array of Fanconi Anemia patient (FANCA) EBV cell line transduced with control shRNA or a shRNA targeting p53 and treated with a Mitomycin C (MMC) pulse
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER:
PROVIDER: E-MTAB-1099 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:To evaluate the effect on gene expression by shRNA-58335, we evaluated gene expression by microarray analysis. Gene expression was measured in Huh-7 cells stably expressing shRNA-58335 or control shRNA after infection with adenovirus expressing p53 (Ad-p53) or LacZ (Ad-LacZ).
2015-01-01 | E-GEOD-56156 | biostudies-arrayexpress
Project description:Transcriptional profiling of primary human white preadipocytes after infection with lentiviral vector either containing shRNA directed against dipeptidypeptidase 4 (DPP4) or unspecific shRNA as negative control Treatment of cells with DPP4 shRNA or control shRNA was done in 4 biological replicates, the first sample of DPP4 KD was hybridized against the first sh-control sample, the second DPP4 smple against the second control sample and so on
2015-11-24 | E-GEOD-75328 | biostudies-arrayexpress
Project description:RNA from four independent cultures from each sh Kdm5c #1, sh Kdm5c #2 and non-targeting shRNA polyclonal cell lines were hybridized in dye-swap against a common reference of RNA from IB10 ES cells
2013-04-05 | E-MTAB-1177 | biostudies-arrayexpress
Project description:Although mutations in p53 are infrequent in human melanoma, its function is abnormal. In this study, whole genome bead arrays were used to examine the expression of p53 target genes in extracts from 6 melanoma cell lines, compared to extracts derived from diploid human melanocytes and fibroblasts, to provide a global assessment of aberrant p53 function. The expression of these genes was also examined in extracts derived from melanocytes and melanoma cell lines in which p53 expression had been inhibited using shRNA and compared to cells that had been transduced with a control shRNA. Total RNA extracted from 18 samples was analysed representing duplicates of 6 melanoma cell lines, 1 melanocyte cell line and 2 fibroblast cell lines. Melanoma cell lines were compared to normal cell lines. In addition, IgR3, Mel-RM and melanocyte cell lines were transduced with either control shRNA or p53 shRNA to evaluate the effect of p53 on its target genes. Cell lines transduced with control shRNA were compared to cell lines transduced with p53shRNA. Duplicates were analysed.
2011-12-01 | E-GEOD-29361 | biostudies-arrayexpress
Project description:The human TP53 gene is frequently mutated in tumors and cell lines. Unlike other tumor suppressors that are commonly inactivated by deletions or nonsense mutations, the majority of p53-mutations are missense point mutations that result in the expression of a full-length protein with an altered amino acid that has lost sequence specific DNA-binding. Expression of mutant p53 (mutp53) confers advantages to tumor cells and transcriptional regulation of several genes mediating the beneficial effects has been shown to play a role. However, molecular mechanisms of transcriptional regulation by mutp53 are still poorly understood. We used the glioblastoma-derived U-251 MG human cell line endogenously expressing mutp53 protein (R273H mutation) to analyze gene expression profiles on Agilent Whole Human Genome Microarray after transient and stable depletion of mutp53 expression. Gene expression data was correlated with a ChIP study on a custom tiling array to understand the contribution of endogenously expressed mutp53 to transcriptional regulation. This series of microarray experiments contains the gene expression profiles of glioblastoma-derived U-251 MG human cell lines engineered to constitutively express a p53-specific shRNA or scrambled control shRNA. To reverse the effect of mutp53 depletion, stable clones were modified by stable integration of a mutp53-R273H expression construct or empty pCDNA3 vector as a control. In addition, we performed gene expression analysis of U-251 MG cells transiently transfected with p53-specific siRNA or control siRNA (3 biological replicates each).
2012-12-10 | E-GEOD-35454 | biostudies-arrayexpress
Project description:We describe a synthetic interaction screen to identify genes preferentially required for proliferation of p53-deficient human cancer cells. An isogenic pair of p53+/+ and p53-/- human colorectal HCT116 cell lines was stably transduced with a short hairpin RNA (shRNA) library encoded by lentiviruses that integrate in the genomic DNA of the host. Comparison of the frequency of each type of integrated lentivirus in the 2 cell types at an early time point (40hrs) and after about 12 mitotic cycles (10days), reveals genes whose knockdown preferentially impaired growth of p53-/- or p53+/+ HCT116 cells. Keywords: Functional Genomics The region of the integrated lentiviruses is PCR amplified from genomic DNA of the two transduced cell populations at an early and a late time point.
2010-05-01 | E-GEOD-15967 | biostudies-arrayexpress
Project description:Transcriptional profiling of human BJ fibroblasts comparing control FF shRNA expressing cells vs. BRD7 shRNA expressing cells under two conditions, either untreated or treated with 8uM nutln-3a for 8 hours. This experiment was done using two independent shRNAs targeting BRD7. Nutlin-3a was used to stabilize p53 and induce its transcriptional activity. Two-condition experiment, FF shRNA cells vs. BRD7 shRNAs cells in two experimental conditions, either untreated or treated with nutlin-3a.
2010-07-01 | E-GEOD-22607 | biostudies-arrayexpress
Project description:NFBD1 (nuclear factor with BRCT domains 1), also known as MDC1 (mediator of DNA damage signaling 1), is a protein involved in the ATM signaling pathway in response to DNA damage. In addition to a role in signaling, NFBD1 possesses transactivation activity, suggesting that it may influence transcription. Furthermore, NFBD1 affects p53-mediated transcription in the presence of the DNA damaging agent adriamycin. Our goal was to determine if NFBD1 affects global gene expression with or without ionizing radiation-induced DNA damage. Moreover, we sought to separate p53-dependent from p53-independent events. Illumina microarray analysis was carried out on RNA extracted from cells treated with and without NFBD1 shRNA and/or p53 shRNA in the presence and absence of DNA damage. Surprisingly, we found that the expression of NFBD1-regulated genes was changed in both the presence and absence of DNA damage. Furthermore, most NFBD1-regulated genes were regulated independently of p53. The identification of NFBD1-regulated genes was confirmed with a second NFBD1-directed shRNA sequence. The role of NFBD1 in global gene expression both in the presence and absence of ionizing radiation was determined. p53-dependent and p53-dependent events regulated by NFBD1 depletion were studied. U2OS cells were treated with control, NFBD1 shRNA, and/or p53 shRNA-expressing retrovirus. Cells were then treated with ionizing radiation and total RNA was isolated for Illumina microarray analysis.
2011-06-16 | E-GEOD-23010 | biostudies-arrayexpress
Project description:The interaction between cancer and stroma plays a key role in tumor progression. Inactivation of p53 is often observed in stromal cells surrounding in cancer, suggesting that p53 in fibroblasts is involved in tumor progression. To elucidate the mechanism by which p53 loss in fibroblasts effect on proliferation and invasiveness of cancer cells, we performed comprehensive expression profiling analyses between p53 knockdown and control fibroblasts using GeneChip Human Genome U133 plus 2.0 arrays. Intact human fetal lung normal diploid fibroblasts TIG-7 cells and TIG-7 cells infected with lentiviruses for the expression of shRNA against p53 were used for RNA extraction and hybridization on Affymetrix microarrays.
2014-08-01 | E-GEOD-58753 | biostudies-arrayexpress
Project description:The functional organization of eukaryotic genomes correlates with specific patterns of histone methylations. Regulatory regions in genomes like enhancers and promoters differ in their extent of methylation of histone H3 at lysine-4 (H3K4), but it is largely unknown how the different methylation states are specified and controlled. Here, we show that the Kdm5c/Jarid1c/SMCX member of the Kdm5 family of H3K4 demethylases can be recruited to both enhancer and promoter elements in embryonic stem cells and neuronal progenitor cells via gene-specific transcription factors. Knockdown of Kdm5c deregulates transcription via local increases in H3K4me3. Our data show that restricting H3K4me3 modification at core promoters dampens transcription, but Kdm5c is required at enhancers for their full activity. Remarkably, an impaired enhancer function activates the intrinsic promoter activity of Kdm5c-bound distal elements. Our results demonstrate that the Kdm5c demethylase plays a crucial and dynamic role in the functional discrimination between enhancers and core promoters. RNA from four independent cultures from each sh Kdm5c #1, sh Kdm5c #2 and non-targeting shRNA polyclonal cell lines were hybridized in dye-swap against a common reference of RNA from IB10 ES cells.
2013-04-05 | E-GEOD-38862 | biostudies-arrayexpress