Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28340048.fastq.gz | Fastqsanger.gz | |||
| SRR28340049.fastq.gz | Fastqsanger.gz | |||
| SRR28340049_1.fastq.gz | Fastqsanger.gz | |||
| SRR28340049_2.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 4 of 4 |
Similar Datasets
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
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 report the first comprehensive analysis of p73 binding across the genome. Furthermore, we re-analyzed this p73 cistrome after perturbation with rapamycin, an inhibitor of mTOR and inducer of p73. Multiple determinants of p73 binding, activity, and function were evident, and were modulated by mTOR.
2011-01-05 | GSE15704 | GEO
Project description:The human osteosarcoma cell line SaOs2 was transduced with adenoviral vectors expressing TAp73α. Subsequent Co-IP/MS analysis characterised the p73 isoform-specific interactome. The raw data include identified cofactors and provide a basis for further research into p73-associated complexes.
2025-08-07 | PXD058816 | Pride
Project description:The human osteosarcoma cell line SaOs2 was transduced with adenoviral vectors expressing DNp73β. Subsequent Co-IP/MS analysis characterised the p73 isoform-specific interactome. The raw data include identified cofactors and provide a basis for further research into p73-associated complexes.
2025-08-07 | PXD058814 | Pride
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. Keywords: Transcription factor analysis
2008-08-06 | GSE11672 | 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.
2009-06-30 | GSE12224 | 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: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.
2010-11-23 | GSE25524 | 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:T helper (Th) cells play critical functions in response to infectious, allergic, and autoimmune diseases. Upon exposure to a given infectious agent or stimulus, different individuals vary in their Th cell responses, influencing the final disease outcome. To investigate the genetic factors that contribute to such differential immune responses, we performed a haplotype-based computational genetic analysis based on the phenotypic profiles of in vitro differentiated Th1 cells from 16 inbred mouse strains. And we identified genes including that encoding the p53 family protein, p73, with SNP patterns that correlated with the quantitative difference in IFNγ expression. Overexpression of p73 inhibited Th1 differentiation, as evaluated by reduced IFNγ expression, whereas shRNA knockdown or knockout of the p73 gene augmented IFNγ production. An inhibitory effect of p73 on Th1 differentiation was also observed in Stat1-/- cells, indicating that the effect was at least partially independent of STAT1. The DNA-binding activity of p73 is required for its inhibitory effect on IFNγ expression, as deletion of p73 DNA binding domain abolished IFNγ inhibition. A global gene expression analysis showed that 206 genes are differentially expressed more than two-fold in response to p73 overexpression, and 55 of these are direct target genes of p73 in Th1 cells, based on ChIP-seq analysis. p73 binding peaks were identified at a range of genes, including at the Il12rb2, Il24, and Il2ra loci, and p73 was implicated for regulating these genes based on reporter constructs containing WT or mutant p73 binding sites. Furthermore, p73 deficient mice had reduced disease severity in MOG induced EAE, with increased IFNg production from spinal cord infiltrating cells. Thus, p73 is a novel regulator of IFNγ expression, revealing a previously unanticipated role for p73 in Th1 cell differentiation.
2019-12-18 | GSE107368 | GEO