Homo sapiens
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PROVIDER: PRJNA113705 | ENA |
REPOSITORIES: ENA
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Project description:p53 and p73 ChIP-chip experiments in HCT116-3(6) cells
| PRJNA113679 | ENA
Project description:Gene expression profiling of immortalized human mesenchymal stem cells with hTERT/E6/E7 transfected MSCs. hTERT may change gene expression in MSCs. Goal was to determine the gene expressions of immortalized MSCs.
2010-09-25 | GSE24338 | GEO
Project description:The p53-family of transcription factors share a highly homologous DNA binding domain and have overlapping and distinct biological functions. Using chromatin immunoprecipitation in combination with NimbleGen promoter arrays and a Model-based Algorithm for Promoter arrays (MAP), we performed a direct comparison of the promoter occupancy profiles of p53 and p73 before and after treatment with hydroxyurea (HU). We have found that p53 and p73 bind to common promoters before HU treatment. After HU treatment, we found that p53-bound promoters are likely to also bind p73, but p73 binds to additional promoters that that do not bind p53. Among them, we showed that p73 but not p53 is recruited to the promoter of MLH3, which encodes a mismatch repair protein. The differential effects of HU on the promoter occupancy profiles of p53 and p73 suggest that these related transcription factors have divergent functions in DNA damage response. The main goal of this study is to examine the effect of HU on the promoter occupancy profiles of p53 and p73. One biological sample from HCT116-(6) cells treated with or without Hydroxyurea was subjected to ChIP-chip analysis using a model based algorithm for promoter arrays (MAP).
2009-06-30 | E-GEOD-12224 | biostudies-arrayexpress
Project description:The main goal of this study is to integrate gene expression analysis with ChIP-chip study. To examine the relationship between promoter occupancy and gene expression, we transiently depleted p53 and p73 via small interfering RNA (siRNA) in HCT116-3(6) cells and then performed microarray analysis of 32,000 genes before or after HU treatment using the Phalanx expression array platform. We found that only 6%-14% of p53 and p73 bound promoters at FDRMAP <0.05 exhibited significant changes in mRNA expression when p53 and p73 were simultaneously knocked-down by siRNA. The minimal correlation between binding and regulation of expression is consistent with previous observations of the lack of transcriptional effects at many transcription factor binding sites.
2009-06-30 | GSE12242 | GEO
Project description:Transcriptional profiling of human mesenchymal stem cells comparing normoxic MSCs cells with hypoxic MSCs cells. Hypoxia may inhibit senescence of MSCs during expansion. Goal was to determine the effects of hypoxia on global MSCs gene expression.
2011-02-19 | GSE20463 | GEO
Project description:Gene methylation profiling of immortalized human mesenchymal stem cells comparing HPV E6/E7-transfected MSCs cells with human telomerase reverse transcriptase (hTERT)- and HPV E6/E7-transfected MSCs. hTERT may increase gene methylation in MSCs. Goal was to determine the effects of different transfected genes on global gene methylation in MSCs.
2011-08-25 | GSE23936 | GEO
Project description:Induction of apoptosis by the tumor suppressor p53 is known to protect from Myc-driven lymphomagenesis. The p53 family member p73 is also a pro-apoptotic protein, which is activated in response to oncogenes like Myc. We therefore investigated whether p73 provides a similar protection from Myc-driven lymphomas as p53. To generate B-cell lymphomas with defined genetic alterations in p53 or p73, we crossed the Eµ-Myc transgenic to mice heterozygous for germ-line deletions in p53 (p53+/) or p73 (p73+/-). Lymphomas which have spontaneously developed in Eµ-Myc transgenic animals with the genotypes p53+/+, p53+/-, p73+/+, p73+/- or p73-/- were isolated when the animals were moribund and further processed for gene expression profiling with 22.5K cDNA microarrays.
2008-12-05 | E-MEXP-1620 | biostudies-arrayexpress
Project description:The integral role of p53 in tumor suppression has promted many laboratories to perform extensive analyses of signaling pathways downstream of the p53 family of sequence-specific DNA binding transcription factors (p53 and its homologs p63 and p73). Despite the ability of p73 to regulate many p53 family target genes, little is known about the specific pathways that modulate p73 during development, tumorigenesis and tumor therapy. In this study we present a gene signature-based approach for connecting signaling pathways to transcription factors, as exemplified by p73. We generated a p73 gene signature by integrating whole-genome chromatin immunoprecipitation and expression profiling.
2008-08-06 | GSE11626 | GEO
Project description:The integral role of p53 in tumor suppression has promted many laboratories to perform extensive analyses of signaling pathways downstream of the p53 family of sequence-specific DNA binding transcription factors (p53 and its homologs p63 and p73). Despite the ability of p73 to regulate many p53 family target genes, little is known about the specific pathways that modulate p73 during development, tumorigenesis and tumor therapy. In this study we present a gene signature-based approach for connecting signaling pathways to transcription factors, as exemplified by p73. We generated a p73 gene signature by integrating whole-genome chromatin immunoprecipitation and expression profiling. Experiment Overall Design: H1299 lung carcinoma cells were infected with p73 expressing or control adenovirus for 5 h and then harvested.
2008-10-20 | E-GEOD-11626 | biostudies-arrayexpress
Project description:A central challenge in human cancer therapy is the identification of pathways that control tumor cell survival and chemosensitivity in the absence of functional p53. The p53-related transcription factors p63 and p73 exhibit distinct, p53-independent roles in development and cancer: p73 promotes genome stability and mediates chemosensitivity, while p63 largely lacks these p53-like functions and instead promotes proliferation and cell survival. Here, we identify a new and physiologically important mechanism of p63/p73 cross-talk which governs the balance between pro-survival and pro-apoptotic programs in both human and murine squamous cell carcinoma. Through comprehensive profiling of p63-regulated microRNAs (miRs), we identified a subset which target p73 for inhibition, including miR-193a-5p, a direct endogenous transcriptional target repressed by p63 and activated by pro-apoptotic p73 isoforms in both normal cells and tumor cells in vivo. Consequently, chemotherapy treatment causes p63/p73-dependent induction of this miR, thereby limiting chemosensitivity due to miR-mediated feedback control of p73. We demonstrate that interrupting this feedback by inhibiting miR-193a suppresses tumor cell viability and induces dramatic chemosensitivity both in vitro and in vivo. Thus, we have identified a direct, miR-dependent regulatory circuit mediating inducible chemoresistance, whose inhibition provides a new therapeutic opportunity in p53-deficient tumors. Knockdown of endogenous p63 by p63-directed or control lentiviral shRNA in JHU-029 human SCC cells at 48h, in duplicate experiments. Array analysis showing the fold-change and direction of change for all miRs regulated > 1.5-fold in p63-ablated versus control samples
2010-11-23 | E-GEOD-25524 | biostudies-arrayexpress