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

E-GEOD-71451

Project description:Identification of MOL1-dependent genes II

2017-06-15 | E-GEOD-71451 | ExpressionAtlas

Arabidopsis thaliana

Project description:Identification of candidate Arabidillo target genes in Arabidopsis

| PRJNA99147 | ENA

miRNA array after p63 knock down in human squamous cell carcinoma

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

E-GEOD-63362

Project description:Identification of sexually dimorphically expressed genes in rat tissues

2015-11-23 | E-GEOD-63362 | ExpressionAtlas

E-GEOD-44146

Project description:Identification of TNF-induced genes that are IRAK1BP1 dependent

2015-07-10 | E-GEOD-44146 | ExpressionAtlas

E-MTAB-5762

Project description:Identification of driver genes in uterine leiomyosarcoma: RNA seq

2025-01-23 | E-MTAB-5762 | ExpressionAtlas