Gene expression profile of normoxic versus hypoxic HeLa cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE33521 | GEO | 2011/11/08
SECONDARY ACCESSION(S): PRJNA148803
REPOSITORIES: GEO
Similar Datasets
Project description:To identify new primary HIF target genes we cultured HeLa cells under short period (6 hours) of mild hypoxia (1% oxygen) Hypoxia-induced gene expression in HeLa cells was measured after 6h exposure to 1% oxygen and compare to normoxic
2011-11-08 | E-GEOD-33521 | biostudies-arrayexpress
Project description:The purpose of experiment is to compare the mRNA expression differences between HeLa cells conditioned with normoxia 21% oxygen and hypoxia 1% oxygen at 6h and 20h.
2016-03-11 | GSE79069 | GEO
Project description:We used HeLa cells that overexpress GFP-tagged SRSF6 (4-fold) were grown in normal conditions (Normoxia, 21% oxygen) or hypoxic conditions (Hypoxia, 0.2% oxygen). compared the binding pattern of SRSF6 between normoxia, 4h hypoxia and 24h hypoxia.
2023-01-03 | GSE198308 | GEO
Project description:The purpose of experiment is to compare the mRNA expression differences between HeLa cells conditioned with normoxia 21% oxygen and hypoxia 1% oxygen at 6h and 20h. Total RNA was obtained from HeLa cells for 4 different conditions, 3 biological replicate experiments were performed, resulting in a total of 12 samples.
2016-03-11 | E-GEOD-79069 | biostudies-arrayexpress
Project description:We used HeLa cells that express GFP-tagged SRSF6 at physiological levels and subjected them to 4 h or 24 h hypoxia (0.2% oxygen). Cells grown in normal conditions were used as control (Normoxia, 21% oxygen). We performed iCLIP using anti-GFP antibodies and compared the binding pattern of SRSF6 between normoxia, 4h hypoxia and 24h hypoxia.
2023-01-03 | GSE198309 | GEO
Project description:DNA binding profiling of endogenous HIF1A on proximal promoters in human HeLa cells exposed to 1% oxygen (hypoxia), using normoxic cells (21% oxygen) as reference.<br><br>Biological background: The Hypoxia Inducible Factor Family of transcription factors is proposed as the main orchestrator of the cellular response to hypoxia. HIFs are heterodimers of a HIF alpha and a HIF beta subunit. HIF alpha protein stability is regulated by oxygen-dependent proteasomal degradation, and hence HIFs are strongly stabilized in hypoxia.<br><br>Purpose of the study: a number of HIF1 ChIP-chip studies have been reported, employing various cell types, array platforms and HIF antibodies, and the overlap of HIF binding locations in these studies is relatively small. The aim of this study was to characterize HIF1 binding in an additional cell line (HeLa), and employing a different HIFalpha antibody.<br><br>Experimental design: We conducted a total of six hybridizations employing four biological replicates. For two biological replicates, we performed dye-swap technical replicate experiments.<br><br>Results summary: We identified 55 HIF binding locations in HeLa cells (FDR<2%). While this number is relatively low compared to previous studies, presumably due to limiting antibody sensitivity, the overlap with data from other cell lines is comparable to our HeLa data.
2012-05-20 | E-MEXP-3499 | biostudies-arrayexpress
Project description:Oxygen is vital for the development and survival of mammals. In response to hypoxia, the brain initiates numerous adaptive responses at the organ level as well as at the molecular and cellular levels, including the alteration of gene expression. Astrocytes play critical roles in the proper functioning of the brain; thus the manner in which astrocytes respond to hypoxia is likely important in determining the outcome of brain hypoxia. Here, we used microarray gene expression profiling and data-analysis algorithms to identify and analyze hypoxia-responsive genes in primary human astrocytes. We also compared gene expression patterns in astrocytes with those in human HeLa cells and pulmonary artery endothelial cells (ECs). Remarkably, in astrocytes, five times as many genes were induced as suppressed, whereas in HeLa and pulmonary ECs, as many as or more genes were suppressed than induced. More genes encoding hypoxia-inducible functions, such as glycolytic enzymes and angiogenic growth factors, were strongly induced in astrocytes compared with HeLa cells. Furthermore, gene ontology and computational algorithms revealed that many target genes of the EGF and insulin signaling pathways and the transcriptional regulators Myc, Jun, and p53 were selectively altered by hypoxia in astrocytes. Indeed, Western blot analysis confirmed that two major signal transducers mediating insulin and EGF action, Akt and MEK1/2, were activated by hypoxia in astrocytes. These results provide a global view of the signaling and regulatory network mediating oxygen regulation in human astrocytes.. This SuperSeries is composed of the following subset Series:; GSE3045: Astrocytic response to hypoxia; GSE3051: HeLa response to hypoxia Experiment
2007-10-26 | E-GEOD-4483 | biostudies-arrayexpress
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. 12 samples; 4 genotypes [CBP+/flox (flox1), p300 +/flox (flox2), CBP CH1/flox;p300 CH1/CH1 (triCH1flox1),CBP CH1/CH1;p300 CH1/flox (triCH1flox2)] , 2 treatments (normoxia and hypoxia).
2007-12-15 | E-GEOD-3196 | biostudies-arrayexpress
Project description:Differential expression of the oxygen sensitive hypoxia-inducible transcription factor (HIF) subunits HIF-1a and HIF-2a occurs in many tumor types, but the underlying regulatory mechanisms remain poorly understood. Here we investigate the role of mTOR complex in the regulation of HIF expression in cells cultured under hypoxic conditions. Neuroblastoma SK-N-BE(2)c cells were treated with DMSO or the mTORC complex inhibitor PP242 and cultured at hypoxia for 24, 48 or 72 hours.
2016-07-03 | E-GEOD-69833 | biostudies-arrayexpress
Project description:Oxygen is vital for the development and survival of mammals. In response to hypoxia, the brain initiates numerous adaptive responses at the organ level as well as at the molecular and cellular level, including the alteration of gene expression. Astrocytes play critical roles in the proper functioning of the brain, thus the manner in which astrocytes respond to hypoxia is likely important in determining the outcome of brain hypoxia. We used microarray gene expression profiling and data analysis algorithms to identify and analyze hypoxia-responsive genes in primary human astrocytes. We also compared the gene expression patterns in astrocytes with those in human HeLa cells and pulmonary artery endothelial cells (ECs). Remarkably, in astrocytes, 5 times as many genes were up-regulated as down-regulated, whereas in HeLa and pulmonary ECs, as many or more genes were down-regulated as up-regulated. More genes encoding hypoxia-inducible functions, such as glycolytic enzymes and angiogenic growth factors, were strongly induced in astrocytes compared to HeLa cells. The extent of induction was also greater than in HeLa cells. Further, gene ontology and computational algorithms revealed that many target genes of the EGF and insulin signaling pathways and the transcriptional regulators Myc, Jun and p53 were selectively altered by hypoxia in astrocytes and HeLa cells to a varying degree. These results provide a global view of the signaling and regulatory network mediating oxygen regulation in astrocytes, in comparison with that in HeLa cells. Keywords: response to hypoxia
2006-03-16 | GSE3051 | GEO