Project description:We report a pharmacologically inducible vasculoprotective mechanism in pulmonary arterial endothelial cells (PAEC) in response to DNA damage by p53 and a novel PPARgamma/p53 transcription factor complex.
Project description:We report a pharmacologically inducible vasculoprotective mechanism in pulmonary arterial endothelial cells (PAEC) in response to DNA damage by p53 and a novel PPARgamma/p53 transcription factor complex.
Project description:To identify a novel lncRNA regulated by mutp53. Wtp53 and 5 different hotspots mutation of p53 were transiently transfected into HEK-293T cells and compared with plasmid vector (pcDNA6A-Flag).
Project description:We report that p53 knockdown changed AR-DNA binding across the genome. We found fewer AR-binding sites in the absence of p53. Examination of AR-DNA binding after p53 knockdown in LNCaP cells
Project description:Tumor suppressor p53 regulates various role in the cell including cell cycle arrest, DNA repair and apoptosis. Current research achieved to investigate p53 target genes in human osteosarcoma cell line-SaOS2 cell. Examination of p53 binding protein by transfecting flag-tagged wild type p53 into SaOS2 cells.
Project description:Tumor suppressor p53 regulates various role in the cell including cell cycle arrest, DNA repair and apoptosis. Current research achieved to investigate p53 target genes in human osteosarcoma cell line-SaOS2 cell.
Project description:The tumor suppressor p53 regulates the differentiation of embryonic stem (ES) cells upon DNA damage. However, our understanding of this critical tumor suppressive role of p53 in ES cells is limited, mainly because of the lack of molecular mechanism. Here, we report a widespread cross-regulation of p53-mediated DNA damage signaling and the pluripotent gene network in ES cells using chromatin-immunoprecipitation assay-based sequencing (ChIP-seq) and gene expression microarray. Upon DNA damage, p53 directly regulates the transcription of 3644 genes (p<0.005) in mouse ES cells. Genome-wide analysis revealed a dramatic difference between the regulation of p53-activated and -repressed genes. p53 mainly regulates the promoter regions of activated genes, whereas the main regulatory regions for repressed genes reside in distal regions. Among p53-repressed genes, many are pluripotent transcription factors of ES cells, such as Oct4, Nanog, Sox2, Esrrb, c-Myc, n-Myc and Sall4. Strikingly, these transcriptional factors also directly regulate the transcription of the Trp53 gene, highlighting a previously under-estimated transcriptional regulation of p53 in ES cells. Therefore, p53 signaling and ES pluripotent transcriptional networks form an intertwined circuitry. Together, our results provide mechanistic insights into the crosstalk of p53-mediated DNA damage and ES cell "stemness" transcriptional gene networks and shed light on the tumor suppressive function of p53 in ES cells. The goal of this experiment is to identify the gene expression changes after adriamycin treatment in a p53-dependent manner. Total six samples: triplicates for untreated mES cells and triplicates for mES cells treated with adriamycin.
Project description:We mapped the genomic binding sites of the tumor suppressor protein p53 in the human colorectal cancer cell line HCT116 and report here that the binding patterns of endogenous wild type p53 differed significantly between the genomes of the cancer cell line HCT116 and the normal human IMR90 fibroblasts (GSE31558) under the same experimental conditions (6 hr treatment with 5-fluorouracil). p53 binding differences affect promoter regions, CpG islands and major families of human repeat elements such as LTR, LINE and SINE. While p53 genomic binding sites residing in repeats have been reported before, we show here that the fraction of the p53 genomic binding sites residing in different repeat families differs between the normal and cancer human cell lines. We confirm that the p53 genomic binding sites in HCT116 cells are excluded from CpG islands, an observation we made previously based on analysis of data reported by others. While the p53 ability to elicit stress-specific and cell-type-specific responses is well documented, how this specificity is established, at the level of binding to the genome and/or during post-binding events, represents an open question. Our data indicate that p53 binding to the human genome is cell line-specific and highly selective. The differences in the p53 genome-wide binding patterns between the cancer cell line HCT116 and the normal cell line IMR90, namely exclusion from CpG islands and enrichment at repeats in HCT116, likely reflect cancer-associated epigenetic changes in the chromatin. Identification of genomic p53 binding sites in HCT116 cells by ChIP-seq.
