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Genomic location data for ectopic p73 in H1299 lung carcinoma cells

ABSTRACT: 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. Keywords: Transcription factor analysis

ORGANISM(S): Homo sapiens

PROVIDER: GSE11672 | GEO | 2008/08/06

SECONDARY ACCESSION(S): PRJNA109157

REPOSITORIES: GEO

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ChIP-Seq of human H1299 lung carcinoma cells - genomic location data for ectopic p73

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 transduced with TAp73beta or GFP expressing adenoviruses. Microarray analysis (on the GFP and TAp73beta samples) and ChIPSeq analysis (on the TAp73beta sample) were performed to identify candidate p73 target genes.

2009-08-30 | E-GEOD-11672 | biostudies-arrayexpress

Expression data from p73 over-expression in H1299 cells

2008-08-06 | GSE11626 | GEO

Transcription profiling by array of human p73 over-expressing H1299 cells

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

Identification of candidate p73 target genes

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. This SuperSeries is composed of the SubSeries listed below.

2008-08-06 | GSE11673 | GEO

Expression data from rapamycin treatment and/or p73 knock-down in Rh30 cells

2011-01-05 | GSE15703 | GEO

Transcription profiling of human H1299 cellls transformed with different p73/p53 constructs shows C-terminal diversity within the p53 family accounts for differences in DNA binding and transcriptional activity

Project description:The p53 family is known as a family of transcription factors with functions in tumor suppression and development. Whereas the central DNA binding domain is highly conserved among the three family members p53, p63 and p73, the C-terminal domains (CTDs) are diverse and subject to alternative splicing and post-translational modification. Here we demonstrate that the CTDs strongly influence DNA binding and transcriptional activity. While p53 and the p73 isoform p73ï§ have basic CTDs and form weak sequence-specific protein-DNA complexes, the major p73 isoforms ï¡, ï¢ and ï¤ have neutral CTDs and bind DNA strongly. A basic CTD has been previously shown to enable sliding along the DNA backbone and to facilitate the search for binding sites in the complex genome. Our experiments, however, reveal that a basic CTD also reduces protein-DNA complex stability, intranuclear mobility, promoter occupancy in vivo, transgene activation and induction of cell cycle arrest or apoptosis. A basic CTD in p53 and p73ï§ therefore provides both positive and negative regulatory functions presumably to enable rapid switching of protein activity in response to stress. In contrast, most p73 isoforms exhibit constitutive DNA binding activity consistent with a predominant role in developmental control. Experiment Overall Design: Infection of H1299 cell with different p73/p53 constructs by adenoviral system

2008-10-18 | E-GEOD-8660 | biostudies-arrayexpress

p53 and p73 ChIP-chip experiments in HCT116-3(6) cells

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

Expression data from rapamycin treatment and/or p73 knock-down in Rh30 cells

Project description:p73 is a p53 family transcription factor that plays critical roles during development and tumor suppression. We analyzed p73 activity using a combination of ChIP-on-Chip and gene expression profiling, both at baseline and after treatment with the mTOR inhibitor rapamycin. We generated an mTOR-p73 gene signature that predicts rhabdomyosarcoma tumor subtype and patient outcome, and is enriched for p73 target genes involved in mesenchymal stem cell differentiation and tumorigenesis. Rh30 rhabdomyosarcoma cells were infected with lentivirus (either control or expressing one of two RNAi constructs targeting p73) for 3 d, and treated with vehicle or 40 nM rapamycin for 24 h, and then total RNA was harvested. Experiments were performed in duplicate for a total of 8 samples. For p73 RNAi, a different targeting construct was used for each replicate.

2011-01-05 | E-GEOD-15703 | biostudies-arrayexpress

p53 and p73 ChIP-chip experiments in HCT116-3(6) cells

2009-06-30 | GSE12224 | GEO

Transcription profiling of mouseB-cell lymphomas with defined genetic alterations in p53 or p73

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

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