Expression data from TAp73+/+ and TAp73-/- MEFs
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE62236 | GEO | 2014/10/11
SECONDARY ACCESSION(S): PRJNA263562
REPOSITORIES: GEO
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Project description:The aim of the experiment was to analyse the gene expression differences between MEFs containing TAp73 or without TAp73, at basal levels in normal culture conditions, and upon treatment with hypoxia (by incubation in 1% oxygen) for 4 or 8 hrs. The analysis indicate that absence of TAp73 leads to changes in multiple cellular and biological processes. TAp73-/- and Tap73+/+ MEFs that were untreated, or treated with hypoxia (in 1% oxygen) for 4 and 8 hours were used for gene expression analysis
2014-10-11 | E-GEOD-62236 | biostudies-arrayexpress
Project description:Although being essential to respiratory and reproductive tracts multiciliogenesis, TAp73 is dispensable for multiciliogenesis in the ventricles. TAp73 KO is accompanied by dramatic changes in ciliogenic microRNAs miR34bc and miR449 family members, suggestin TAp73 functions partially thorugh posttranscriptional nodes in brain ciliogenesis.
2019-05-21 | GSE108385 | GEO
Project description:Hepatocyte dedifferentiation is a major source of hepatocellular carcinoma (HCC), but its mechanisms are unknown. We explored the p73 expression in HCC tumors and studied the effects of transcriptionally active p73 (TAp73) in HCC cells. Expression profiles of p73 and patient clinical data were collected from the Genomic Data Commons (GDC) data portal and the TSVdb database, respectively. Global gene expression profiles were determined by pan-genomic 54K microarrays. The Gene Set Enrichment Analysis was used to identify TAp73-regulated gene sets. The effects of TAp73 were analyzed in monolayer cell culture, 3D-tumoroid and xenograft models in zebrafish using western blot, flow cytometry, fluorescence imaging, real-time polymerase chain reaction (RT-PCR), immunohistochemistry and morphological examination. TAp73 was significantly upregulated in HCC, and its high expression indicated poor patient survival. The induced expression of TAp73 caused landscape expression changes including genes involved in growth signaling, cell cycle, stress response, immunity, metabolism and development. HCC cells overexpressing TAp73 had lost hepatocyte lineage biomarkers including ALB, CYP3A4, AFP, HNF4α. In contrast, TAp73 upregulated genes promoting cholangiocyte lineage such as YAP, JAG1 and ZO-1, accompanied with an increase in metastatic ability. Our findings strongly suggest that TAp73 is a major promoter of malignant dedifferentiation of HCC cells Hepatocellular carcinoma (HCC) is a highly complex and heterogeneous type of cancer. Hepatocyte dedifferentiation is one of the important steps in the development of HCC. However, its molecular mechanisms are not well known. In this study, we report that TAp73 which is the major transcriptionally active form of p73 is overexpressed in HCC. Mechanically, TAp73 suppresses the expression of the hepatocyte markers including CYP3A4, AFP, ALB, HNF4a, while increasing the expression of several cholangiocyte markers in HCC cell lines. In conclusion, this report reveals a pro-oncogenic role for TAp73 in liver cancer.
2021-03-10 | GSE162860 | GEO
Project description:Cancer stem cells (CSCs) are resistant to conventional chemotherapy and are hence responsible for cancer relapse. Pluripotency is a characteristic of CSCs which allows them to rapidly proliferate while maintaining the ability to differentiate into various lineages. We found that TAp73, but not its homologue p53, is required for the pluripotency of CSCs. TAp73 knockdown (KD) decreased SOD1 levels, increased ROS production and disturbed metabolism which induced differentiation and abrogated pluripotency in CSCs. TAp73 related decrease in pluripotency is linked to increased autophagy and senescence in CSCs. Furthermore, TAp73 KD also decreased the levels of pluripotency factor Sox-2 within heterogeneous cancer cell lines. Interestingly, TAp73-deficient CSCs strongly lose tumorigenic potential in mice and tumors that did form had significantly lower levels of SOD1 and pluripotency marker Oct4. Our findings reveal a unique role of TAp73 in CSCs development that is important to consider while devising future therapeutic strategies against cancer.
2019-03-05 | PXD005407 | Pride
Project description:The CH1 protein interaction domain of the transcriptional coactivators p300 and CBP is thought to interact with HIF-1alpha and this interaction is thought to be critical to the expression of HIF-1alpha target genes in response to hypoxia. To test the requirement of the CH1 domain for gene expression in response to hypoxia, rimary mouse embryonic fibroblasts (MEFs) were generated from C57Bl/6x129/Sv F2 e14.5 embryos that contain a deletion in the CH1 domain of three of four alleles of CBP and p300. The remaining allele of p300 or CBP was a conditional knock out allele. Control MEFs with only a single conditional knockout allele of p300 or CBP were also generated. At passage 3 MEFs were infected with Cre Adenovirus and grown until they had expanded at least 100 fold. Subconfluent MEFs were treated with 21% oxygen (normoxia) or 0.1% oxygen (hypoxia) with 5% carbon dioxide at 37 C in a humid chamber for 6hrs. At the start of treatment, medium was removed and replaced with medium (DMEM+10% FBS+pen-strep+ l-glu) that had been preequilibrated overnight in normoxia or hypoxia as appropriate. Immediately after treatment, cells were lysed in Trizol for RNA extraction. Keywords: genetic modification, dose response
2005-10-24 | GSE3196 | GEO
Project description:The goal of this study is to use H3K4me3 signal to mark the promoter regions of the p73 gene. The p73 gene expresses TAp73 and DNp73 isoforms, which use two different promoters. H3K4me3 is generally associated with the promoter of a gene and, therefore, can be used to mark the promoters for TAp73 and DNp73.
2021-04-16 | GSE169716 | GEO
Project description:Comparison of luminal and basal breast cancer cells under acute normoxia and hypoxia. Cells were plated in 96-well plates and incubated 24 hrs under normoxia or hypoxia after which the wells were washed once with cold PBS and lysed using TempO-Seq lysis buffer for 15 min at room temperature. Samples were stored at −80 °C before shipping to BioClavis for whole genome TempO-Seq analysis. For normoxia (NX) 21% oxygen was used and for hypoxia (HX) 1%oxygen was used. Each condition has 3 biological replicates.
2023-06-01 | E-MTAB-12234 | biostudies-arrayexpress
Project description:A core evolutionary function of the p53 family is to protect the genomic integrity of gametes. However, the role of p73 in the male germline is unknown. Here we uncover that TAp73 unexpectedly functions as adhesion and maturation factor of the seminiferous epithelium orchestrating spermiogenesis. TAp73KO and p73KO mice, but not M-NM-^TNp73KO mice, display a M-bM-^@M-^Xnear-empty seminiferous tubuleM-bM-^@M-^Y phenotype due to massive premature loss of immature germ cells. Its cellular basis are defective cell-cell adhesions of developing germ cells to Sertoli nurse cells, with secondary degeneration of Sertoli cells including the blood-testis-barrier, thereby disrupting the adhesive integrity and maturation of the germ epithelium. At the molecular level, TAp73, produced in germ cells, controls a coordinated transcriptional program of adhesion- and migration-related proteins including peptidase inhibitors, proteases, receptors and integrins required for germ-Sertoli cell adhesion and dynamic junctional restructuring. Thus, the testis emerges as unique organ with strict division of labor among all family members: p63 and p53 safeguard germline fidelity, while TAp73 ensures fertility by enabling sperm maturation. 3 mice each for control wildtype and TAp73 knockout mice
2014-03-07 | E-GEOD-52124 | biostudies-arrayexpress
Project description:We investigated the downstream mechanisms by which TAp73β regulate apoptosis.
2005-12-01 | E-MEXP-349 | biostudies-arrayexpress