p53 is critically important in preventing oncogenesis but its role in non-cancer biology remains unclear. Macrophages exist as two subtypes (M1 and M2). Nutlin-3a (p53 activator) inhibits M2 gene expression and phenotype. p53 acts by suppressing transcription of c-Myc and thence regulates expression of a subset of M2 markers. This work has implications for our understanding of the mechanisms that regulate plasticity of macrophages in health and disease.
A unique role for p53 in the regulation of M2 macrophage polarization.
Specimen part, Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
No associated publication
Specimen part, Cell line
View SamplesPDX1 binds and regulates numerous genes involved in human pancreatic development but also binds hepatic genes
No associated publication
Cell line
View SamplesTotal 23 samples were derived from [1] HUVEC treated in the absence (0h) or presence of hypoxia (1, 2, 4, 8, 12, and 24 hrs) to determine hypoxia-regulated gene in endothelial cells, [2] control siRNA or HIF1 siRNA transfected HUVEC cells treated in the absence or presence of hypoxia, [3] control siRNA or KDM3A siRNA transfected HUVEC cells treated in the absence or presence of hypoxia, [4] ChIP-seq data for HIF1 binding sites and histone modifications under normoxia and hypoxia in endothelial cells.
Dynamic change of chromatin conformation in response to hypoxia enhances the expression of GLUT3 (SLC2A3) by cooperative interaction of hypoxia-inducible factor 1 and KDM3A.
Cell line, Treatment
View SamplesIn order to clarify the downstream target genes of SPAG4, we performed knockdown of SPAG4 using siRNA both under normoxia and hypoxia.
Sperm-associated antigen 4, a novel hypoxia-inducible factor 1 target, regulates cytokinesis, and its expression correlates with the prognosis of renal cell carcinoma.
Cell line
View SamplesAlthough various mechanisms have been inferred for combinatorial actions of multiple carcinogens, these mechanisms have not been well demonstrated in experimental carcinogenesis models. We evaluated mammary carcinogenesis initiated by combined exposure to various doses of radiation and chemical carcinogens. Female rats at 7 weeks of age were -irradiated (0.22 Gy) and/or exposed to 1-methyl-1-nitrosourea (20 or 40 mg/kg, single intraperitoneal injection) or 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (40 mg/kg/day by gavage for 10 days) and were observed until 50 weeks of age. The incidence of mammary carcinoma increased steadily as a function of radiation dose in the absence of chemicals; mathematical analysis supported an additive increase when radiation was combined with a chemical carcinogen, irrespective of the chemical species and its dose. Hras mutations were characteristic of carcinomas that developed after chemical carcinogen treatments and were overrepresented in carcinomas induced by the combination of radiation and MNU (but not PhIP), indicating an interaction of radiation and MNU at the level of initiation. The expression profiles of seven classifier genes, previously shown to distinguish two classes of rat mammary carcinomas, categorized almost all examined carcinomas that developed after individual or combined treatments with radiation (1 Gy) and chemicals as belonging to a single class; more comprehensive screening using microarrays and a separate test sample set failed to identify differences in gene expression profiles among these carcinomas. These results suggest that a complex, multilevel interaction underlies the combinatorial action of radiation and chemical carcinogens in the experimental model.
Molecular characterization of cancer reveals interactions between ionizing radiation and chemicals on rat mammary carcinogenesis.
Specimen part
View SamplesComparison of time-series gene expression pattern in hippocampus of hypoxia tolerant or sensitive rats. At 12 time-points ({0h, 1h, 3h, 12h, 24h, 48h} x 2) after ischemia operation, microdissected CA1 regions of the two groups were respectively subjected to oligonucleotide-based microarray analysis. MIAME information can be obtained at the web link.
No associated publication
No sample metadata fields
View SamplesThe functional activity of TRPM7 is essential for cell viability and growth, and its expression is up-regulated in certain pathological conditions. In order to assess the effects of TRPM7 activity on cellular gene expression, inducible HEK293 cell-lines harboring the wild-type mouse TRPM7 and a mutant lacking the kinase domain were established.
Alteration of the transcriptional profile of human embryonic kidney cells by transient overexpression of mouse TRPM7 channels.
Cell line
View SamplesPromyelocytic Leukemia Protein (PML) was first identified as a fusion product with the retinoic acid receptor alpha in Acute Promyelocytic Leukemia (APL). Although PML has previously been studied in cancer progression and various physiological processes, little is known about its functions in Embryonic Stem Cells (ESC). Here, we report that PML contributes to the maintenance of the ESC self-renewal by controlling the cell-cycle and sustaining the expression levels of crucial pluripotency factors. Transcriptomic analysis showed that the ablation of PML renders ESC prone to exit from the nave and acquire a primed-like pluripotent cell state. During differentiation PML influences cell fate decision by regulation of Tbx3. PML loss compromises the reprogramming ability of embryonic fibroblasts to induced Pluripotent Stem Cells (iPSC) by inhibiting the TGF pathway at the very early stages. Collectively, these results designate PML as a member of the regulatory network for ESC pluripotency and somatic cell reprogramming.
Promyelocytic Leukemia Protein Is an Essential Regulator of Stem Cell Pluripotency and Somatic Cell Reprogramming.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
H3K4/H3K9me3 Bivalent Chromatin Domains Targeted by Lineage-Specific DNA Methylation Pauses Adipocyte Differentiation.
Specimen part
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