E-GEOD-20602
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA124773
PROVIDER: E-GEOD-20602 | ExpressionAtlas | 2025-01-24
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-GEOD-20602-analysis-methods.tsv | Tabular | |||
| E-GEOD-20602-atlasExperimentSummary.Rdata | Rdata | |||
| E-GEOD-20602-configuration.xml | Xml | |||
| E-GEOD-20602-percentile-ranks.tsv | Tabular | |||
| E-GEOD-20602-zoomifications-log.tsv | Tabular |
Items per page: 5 1 - 5 of 67 |
Similar Datasets
Project description:Human Nephrosclerosis Triggers a Hypoxia-Related Glomerulopathy
| PRJNA124773 | ENA
Project description:Transcription profiling by array of human mammary epithelial cells exposed to different environmental stresses: hypoxia, lactic acidosis, lactosis, acidosis and a combination of hypoxia and lactic acidosis
2025-01-24 | E-GEOD-9649 | ExpressionAtlas
Project description:DEAD-box RNA-binding proteins (RBPs) play a significant role in RNA metabolism to achieve cellular homeostasis, including miRNA biogenesis and transcription. Hypoxia induces stemness cell-like characteristics in cancer cells and promotes malignant progression. Despite the fact that hypoxia can induce the changes in protein and RNA modification, thereby regulating downstream gene expressions, how modifications at different molecular layers interplay with each other are poorly understood. Here we show that hypoxia induces HectH9-mediated K63-linked polyubiquitination of the DEAD-box protein DDX17 as well as reduces N6-methyladenosine (m6A) marks in pri-miRNAs. While m6A potentiates DDX17 binding to pri-miRNAs, decreased m6A modifications of pri-miRNAs and increased polyubiquitination of DDX17 under hypoxia lead to decreased DDX17 binding to pri-miRNAs binding. These events enhance the association of DDX17 with the ubiquitin receptor p300 and lead to a decrease in miRNA biogenesis, especially for miRNAs regulating stemness and stemness-related genes. In addition, polyubiquitinated DDX17 together with p300 upregulates H3K56Ac levels on the stemness and stemness-related genes, resulting in enhancement of tumor initiating ability. Post-transcriptionally, decreased miRNA production, including those targeting stemness genes or stemness-related genes, also facilitates tumor initiation. Together, hypoxia triggers DDX17 poly-ubiquitination, which orchestrates dual mechanisms to increase tumor initiating ability and promote tumor progression.
2018-03-09 | PXD006059 | JPOST Repository
Project description:Effect of hypoxia on the Represser Element-1 Silencing Transcription factor (REST) in Human
2025-01-23 | E-MTAB-2580 | ExpressionAtlas
Project description:Reduced oxygen availability (hypoxia) triggers adaptive cellular responses via hypoxia-inducible factor (HIF)-dependent transcriptional activation. Adaptation to hypoxia also involves transcription-independent processes like post-translational modifications, however these mechanisms are poorly characterized. Investigating the involvement of protein SUMOylation in response to hypoxia, we discovered that hypoxia strongly decreases the SUMOylation of Exosome subunit 10 (EXOSC10), the catalytic subunit of the RNA exosome, in a HIF-independent manner. EXOSC10 is a multifunctional exoribonuclease enriched in the nucleolus that mediates the processing and degradation of various RNA species. We demonstrate that the Ubiquitin-specific protease 36 (USP36) SUMOylates EXOSC10 and we reveal SUMO1/sentrin-specific peptidase 3 (SENP3) as the enzyme mediating deSUMOylation of EXOSC10. Under hypoxia, EXOSC10 dissociates from USP36 and translocates from the nucleolus to the nucleoplasm concomitant with its deSUMOylation. Loss of EXOSC10 SUMOylation does not detectably affect rRNA maturation but affects the mRNA transcriptome by modulating the expression levels of hypoxia-related genes. Our data suggest that dynamic modulation of EXOSC10 SUMOylation and localization under hypoxia regulates the RNA degradation machinery to facilitate cellular adaptation to low oxygen conditions.
2024-01-30 | GSE229894 | GEO
Project description:Effect of PCO1 overexpression [hypoxia]
2015-12-02 | E-GEOD-44343 | ExpressionAtlas
Project description:Hypoxia Triggers the Intravasation of Clustered Circulating Tumor Cells
| PRJNA522885 | ENA
Project description:Adaptation to low levels of O2 (hypoxia) is a universal biological feature across metazoans. Yet the underlying mechanisms how different species sense O2 deprivation remain to be deciphered. Here we functionally characterize a novel long non-coding RNA (lncRNA), LOC105369301, which we termed hypoxia-induced lncRNA for PLK1 stabilization or HILPS. HILPS exhibits appreciable basal expression exclusively in a broad range of human normal and cancer cells and is robustly induced by hypoxia inducible factor 1α (HIF1α). HILPS binds PLK1 and sequesters it from proteasome degradation. Stabilized PLK1 directly phosphorylates HIF1α and enhance its stability, constituting a positive feedforward circuit that reinforces oxygen sensing by HIF1α. HILPS inactivation triggers catastrophic adaptation defect during hypoxia in both normal and cancer cells. These findings introduce a mechanism that underlies the HIF1α identity deeply interconnected with PLK1 integrity, and identify the HILPS-PLK1-HIF1α pathway as a crucial oxygen-sensing axis in regulation of human physiological and pathogenic processes.
2023-10-18 | GSE230388 | GEO
Project description:This 58 arrays are the basis of our hypoxia story published in PLoS Medicine. The cell type, oxygen tension and time points are indicated. Abstract: BACKGROUND: Inadequate oxygen (hypoxia) triggers a multifaceted cellular response that has important roles in normal physiology and in many human diseases. A transcription factor, hypoxia-inducible factor (HIF), plays a central role in the hypoxia response; its activity is regulated by the oxygen-dependent degradation of the HIF-1alpha protein. Despite the ubiquity and importance of hypoxia responses, little is known about the variation in the global transcriptional response to hypoxia among different cell types or how this variation might relate to tissue- and cell-specific diseases. METHODS AND FINDINGS: We analyzed the temporal changes in global transcript levels in response to hypoxia in primary renal proximal tubule epithelial cells, breast epithelial cells, smooth muscle cells, and endothelial cells with DNA microarrays. The extent of the transcriptional response to hypoxia was greatest in the renal tubule cells. This heightened response was associated with a uniquely high level of HIF-1alpha RNA in renal cells, and it could be diminished by reducing HIF-1alpha expression via RNA interference. A gene-expression signature of the hypoxia response, derived from our studies of cultured mammary and renal tubular epithelial cells, showed coordinated variation in several human cancers, and was a strong predictor of clinical outcomes in breast and ovarian cancers. In an analysis of a large, published gene-expression dataset from breast cancers, we found that the prognostic information in the hypoxia signature was virtually independent of that provided by the previously reported wound signature and more predictive of outcomes than any of the clinical parameters in current use. CONCLUSIONS: The transcriptional response to hypoxia varies among human cells. Some of this variation is traceable to variation in expression of the HIF1A gene. A gene-expression signature of the cellular response to hypoxia is associated with a significantly poorer prognosis in breast and ovarian cancer. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Using regression correlation
2006-02-24 | E-GEOD-4185 | biostudies-arrayexpress