Che-1 is a RNA Polymerase II binding protein involved in the regulation of gene transcription. We have observed that Che-1 depletion induces apoptosis in several cancer cells expressing mutated forms of p53. We used microarrays to investigate classes of genes regulated by Che-1 in one of these cell lines.
Che-1 promotes tumor cell survival by sustaining mutant p53 transcription and inhibiting DNA damage response activation.
Specimen part, Cell line
View SamplesmRNA expression data were collected from patients with brain tumor to improve diagnostic of gliomas on molecular level.
Neuronal and glioma-derived stem cell factor induces angiogenesis within the brain.
No sample metadata fields
View SamplesChe-1 is a RNA Polymerase II binding protein involved in the regulation of gene transcription. Che-1 emerges as an important adaptor that connects transcriptional regulation, cell-cycle progression, checkpoint control, and apoptosis.
Che-1-induced inhibition of mTOR pathway enables stress-induced autophagy.
Cell line, Treatment
View SamplesTo determine early changes leading to human cell transformation (cancer) we exposed an immortalized human bronchial epithelial cell line, BEAS-2B, to one of four different metals that may cause cancer via inhalation in humans or rodents: 2.0 micro-Molar soluble sodium arsenite (NaAsO2), 0.50 micro-Molar potassium chromate (K2CrO4), 250 micro-Molar nickel (II) sulfate (NiSO4), 10 micro-Molar sodium meta-vanadate (NaVO3), or were left untreated (control). After a 30-60 day exposure, cells were rinsed of metals and seeded in soft agar. A small number of the cells formed colonies in the soft agar, demonstrating the potential for anchorage independent growth, a characteristic of cancer. These colonies that originated from a single cell were extracted from the agar and grown out in monolayer for 3-4 weeks. The RNA data provided here is taken from these cells. The significance it that the metal exposure was stopped many generations before the analysis, yet each sample demonstrates changes in gene expression based on the original metal exposure.
Gene expression changes in human lung cells exposed to arsenic, chromium, nickel or vanadium indicate the first steps in cancer.
Specimen part
View SamplesExpression data from Caenorhabditis elegans let-418(RNAi), mep-1(RNAi) and gfp(RNAi) L1 larvae.
Different Mi-2 complexes for various developmental functions in Caenorhabditis elegans.
Disease
View SamplesTC71 cells treated either with BEZ235 or DMSO
hnRNPM guides an alternative splicing program in response to inhibition of the PI3K/AKT/mTOR pathway in Ewing sarcoma cells.
No sample metadata fields
View SamplesThis study identified genomwide KCl inducible readthrough transcription. The project also includes a Cap-Seq experiment to identify transcriptional start sites, demonstrating that KCl does not activate downstream transcriptional start sites, but indeed does induce readthrough
Widespread Inducible Transcription Downstream of Human Genes.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Autophagy maintains the metabolism and function of young and old stem cells.
Specimen part
View SamplesAutophagy is critical for protecting HSCs from metabolic stress. Here, we used a genetic approach to inactivate autophagy in adult HSCs by deleting the Atg12 gene. We show that loss of autophagy causes accumulation of mitochondria and an oxidative phosphorylation (OXPHOS)-activated metabolic state, which drives accelerated myeloid differentiation likely through epigenetic deregulations rather than transcriptional changes, and impairs HSC self-renewal activity and regenerative potential.
Autophagy maintains the metabolism and function of young and old stem cells.
Specimen part
View SamplesOxidoreductase enzymes are critical to redox regulation of intracellular proteins within human cells. We used microarrays to identify which oxidreducatse genes are expressed in unstimulated human umbilical vein endothelial cells.
Naturally occurring free thiols within beta 2-glycoprotein I in vivo: nitrosylation, redox modification by endothelial cells, and regulation of oxidative stress-induced cell injury.
Specimen part
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