Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of NDRG3 expression on cell response to hypoxia

ABSTRACT: Analysis of Huh-7 hepatocarcinoma cell line depleted of NDRG3 or HIF-1α under hypoxic condition. HIF-1α and NDRG3 have distinct functions in hypoxia responses. Results provide insight into molecular basis of HIF-independent signaling in the development and progression of hypoxic tumors

ORGANISM(S): Homo sapiens

PROVIDER: GSE59729 | GEO | 2015/07/24

SECONDARY ACCESSION(S): PRJNA256092

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Effect of NDRG3 expression on cell response to hypoxia

Project description:Analysis of Huh-7 hepatocarcinoma cell line depleted of NDRG3 or HIF-1α under hypoxic condition. HIF-1α and NDRG3 have distinct functions in hypoxia responses. Results provide insight into molecular basis of HIF-independent signaling in the development and progression of hypoxic tumors Gene expression profiles of Huh-7 cells stably expressing NDRG3-shRNA or HIF-1α-shRNA under normoxia were compared to gene expression profiles of Huh-7 stable cells under hypoxia for 3, 6, 12 and 24 hours.

2015-07-24 | E-GEOD-59729 | biostudies-arrayexpress

Effect of NDRG3 or HIF-1α knockdown on cell response to hypoxia

2015-07-24 | E-GEOD-55212 | biostudies-arrayexpress

Effect of NDRG3 or HIF-1α knockdown on cell response to hypoxia

2015-07-24 | GSE55212 | GEO

Effect of NDRG3 overexpression on cell response to hypoxia

Project description:Analysis of HeLa cells overexpressing NDRG3 or exposed to hypoxic condition. Gene expression profiles of HeLa cells stably expressing NDRG3 were compared to gene expression profiles of HeLa stable cells expressing mock or hypoxia-mediated gene expression profiles.

2015-07-24 | E-GEOD-55211 | biostudies-arrayexpress

Effect of NDRG3 overexpression on cell response to hypoxia

Project description:Analysis of HeLa cells overexpressing NDRG3 or exposed to hypoxic condition.

2015-07-24 | GSE55211 | GEO

Stub1 acetylation by CBP/p300 attenuates chronic hypoxia-induced pulmonary hypertension by suppressing HIF-2α transcriptional activity

Project description:Chronic hypoxia induces pulmonary vascular remodeling and pulmonary hypertension (PH). While it is established that transcription factors, hypoxia-inducible factors (HIF-1α/HIF-2α) activate gene programs that drive hypoxia-induced PH, the mechanism of HIF-1/2 activation is less clear. Here, we report that carboxylterminus of Hsp70-interacting protein (CHIP or Stub1) modulates HIF-1α and HIF-2α transcription rather than reducing their stability. Knocking-down Stub1 reduced hypoxic activation of HIF-1α mRNA, protein, and activity while enhancing hypoxic induction of HIF-2α mRNA, protein, and target genes in pulmonary vascular cells. Mechanistically, CBP/p300-mediated acetylation of lysine (K287) inactivates the ubiquitin ligase activity of Stub1 and triggers its translocation from the cytoplasm into the nucleus. There, it recognizes the HIF promoter and hypoxia response elements (HREs) in target genes. Expression of Stub1-K287Q mutant (mimicking acetylation) enhanced hypoxia-induced HIF-1α expression, while acetyl-deficient Stub1-K287R mutant had the opposite effect on HIF-α but enhanced hypoxia-induced HIF-2α transcriptional activity. Endothelial-Stub1 transgenic mice tolerated chronic hypoxia better, had less pulmonary vascular remodeling, reduced pulmonary vascular resistance, and greater cardioprotection. Thus, Stub1 nuclear translocation enhances hypoxic induction of HIF-1α activity while suppressing deleterious effects of HIF-2α. These observations indicate that nuclear-Stub1 synergizes with HIF-1α to promote transcriptional responses and antagonizes HIF2α-driven PH in chronic hypoxia.

2023-04-01 | GSE221264 | GEO

Transcriptomic analysis of the HIF-1α impact on the gene expression profile of chicken fibroblasts under hypoxia

Project description:Hypoxia-inducible factor 1 (HIF-1) is a transcriptional regulator that mediates cellular adaptive responses to hypoxia. Hypoxia-inducible factor 1α (HIF-1α) is involved in the development of ascites syndrome (AS) in broiler chickens. Therefore, studying the effect of HIF-1α on the cellular transcriptome under hypoxic conditions will help to better understand the mechanism of HIF-1α in the development of AS in broilers. In this study, we analyzed the gene expression profile of the DF-1 cell line under hypoxic conditions by RNA-seq. Additionally, we constructed the HIF-1α knockdown DF-1 cell line by using the RNAi method and analyzed the gene expression profile under hypoxic conditions. The results showed that exposure to hypoxia for 48 hours had a significant impact on the expression of genes in the DF-1 cell line, which related to cell proliferation, stress response, and apoptosis. In addition, after HIF-1α knockdown more differential expression genes appeared than in wild-type cells, and the expression of most hypoxia-related genes was either down-regulated or remained unchanged. Pathway analysis results showed that differentially expressed genes were mainly enriched in pathways related to cell proliferation, apoptosis, and oxidative phosphorylation. Our study obtained transcriptomic data from chicken fibroblasts at different hypoxic times and identified the potential regulatory network associated with HIF-1α. This data provides valuable support for understanding the transcriptional regulatory mechanism of HIF-1α in the development of AS in broilers.

2023-11-15 | GSE244260 | GEO

Transcriptome analysis using Quant-RNAseq after NPM1 or HIF-1α silencing under normoxia or Hypoxia

Project description:Hypoxia inducible factor-1 (HIF-1) is a central transcriptional regulator of genes associated with adaptive responses to hypoxia. NPM1 is a histone chaperone found to associate with HIF-1α in a phosphorylation dependent manner and increase its activty. The aim of this study was to find if HIF-1α and NPM1 regualate gene expression under hypoxia. Transcriptome analysis using Quant-RNA-seq after HIF-1α or NPM1 silencing under hypoxia reveals a significant number of genes, the hypoxic expression of which depends on both proteins.

2021-12-15 | GSE158890 | GEO

Intermittent and sustained hypoxia exposures activate distinct transcriptional responses in human aortic endothelial cells

Project description:Endothelial cell (EC) dysfunction precedes the development of cardiovascular disease in OSA; however, the mechanisms by which ECs respond to these hypoxic events is poorly understood. To better understand EC responses to hypoxia, we examined the effects of both sustained hypoxia (SH) and intermittent hypoxia (IH) on the activation of HIF-1α in Endothelial Cells (ECs). While SH stabilized HIF-1α and led to its nuclear localization, IH didn’t activate HIF-1α and its downsteram gene expression. Using RNA-sequencing, we evaluated transcriptional responses of ECs to hypoxia. SH induced expression of HIF-1α and hypoxia response genes, while IH affected cell-cycle regulation genes.

2024-11-01 | GSE279434 | GEO

HIF1A ChIP-seq from primary human uterine smooth muscle cells (hMSMCs) in hypoxia

Project description:Uterine contraction, crucial for successful labor, has been proved to be enchanced by hypoxia, which underlying mechanisms are yet to be elucidated. We found blockade of HIF-1a caused contractility decrease in myometrium and myocytes in hypoxic models. ChIP-seq revealed that HIF-1α directly bound to gemone of 2 typical contraction-associated proteins, the promoter of GJA1 and intron of OXTR. Blockade of GJA1 led to significant decrease of myometrial contractions under hypoxic tissue model, whereas atosiban did not influence the contractility. The conducted research suggests that HIF-1α is required for the augmentation of myometrial contractility via regulating GJA1 under hypoxia.

2022-08-01 | GSE197160 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data