Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

36 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of NDRG3 over-expression and knockdown on cell response to hypoxia

ABSTRACT: This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

ORGANISM(S): Homo sapiens

SUBMITTER: Minho Kang

PROVIDER: E-GEOD-55214 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

A lactate-induced response to hypoxia.

Lee Dong Chul DC Sohn Hyun Ahm HA Park Zee-Yong ZY Oh Sangho S Kang Yun Kyung YK Lee Kyoung-Min KM Kang Minho M Jang Ye Jin YJ Yang Suk-Jin SJ Hong Young Ki YK Noh Hanmi H Kim Jung-Ae JA Kim Dong Joon DJ Bae Kwang-Hee KH Kim Dong Min DM Chung Sang J SJ Yoo Hyang Sook HS Yu Dae-Yeul DY Park Kyung Chan KC Yeom Young Il YI

Cell 20150416 3

Organisms must be able to respond to low oxygen in a number of homeostatic and pathological contexts. Regulation of hypoxic responses via the hypoxia-inducible factor (HIF) is well established, but evidence indicates that other, HIF-independent mechanisms are also involved. Here, we report a hypoxic response that depends on the accumulation of lactate, a metabolite whose production increases in hypoxic conditions. We find that the NDRG3 protein is degraded in a PHD2/VHL-dependent manner in normo ...[more]

PMID: 25892225

Similar Datasets

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 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

Gene expression profiling in LSD1 depleted Huh-1 cell line under hypoxic condition.

Project description:To investigate the role for LSD1 under hypoxia condition. we depleted LSD1 gene with siRNA in Huh-1 cell lines under 1% O2 hypoxia condtion, and than perforemed gene expression microarray analysis. Using Gene Set Enrichment Analysis (GSEA), determined to identify the biological pathway. Determined the gene expression profile of the LSD konckdown effect under hypoxia condition. Using Gene Set Enrichment Analysis (GSEA) decided to identify the biological pathways.

2016-08-10 | E-GEOD-85345 | biostudies-arrayexpress

Transcription profiling of human Burkittas lymphoma cell line, P493-6 to identify hypoxia responsive genes

Project description:Activation of glycolytic genes by HIF-1 is considered critical for metabolic adaptation to hypoxia. We found that HIF-1 also actively suppresses glucose metabolism through the tricarboxylic acid cycle (TCA) by directly trans-activating the gene encoding pyruvate dehydrogenase kinase 1 (PDK1). PDK1 inactivates the TCA cycle enzyme, pyruvate dehydrogenase (PDH), which converts pyruvate to acetyl-CoA. Forced PDK1 expression in hypoxic HIF-1Î±-null cells increases ATP levels, attenuates hypoxic ROS generation and rescues these cells from hypoxia-induced apoptosis. These studies reveal a novel hypoxia-induced metabolic switch that shunts glucose metabolites from the mitochondria to glycolysis to maintain ATP production and to prevent toxic ROS production. Experiment Overall Design: We sought to determine by microarray analysis of gene expression the genes responsive to hypoxia using the human B lymphocyte cell line, P493-6. Hypoxia-responsive genes were globally assessed in cells incubated in 0.1% O2 for 29 hours at which the highest HIF-1 levels were obtained

2008-06-12 | E-GEOD-4086 | biostudies-arrayexpress

Rhabdomyosarcoma cells (SJRH30) response to hypoxia: time course

Project description:Under hypoxic condition, solid tumor cells are known to involve gene expressions for adopting low O2 condition. We examined chronic hypoxia environment of human rhabdomyosarcoma cell (SJRH30), which is important for understanding characteristic of cancer in the body. We used microarrays to detail time development of gene expression by using new gene-set analysis called GSMTA and identified up/down-regulated gene sets during hypoxic stress. We measured gene expressions at four time-points during 24 hours (0h, 6h, 12h and 24h) under 1% hypoxic condition by Affymetrix GeneChip. GSMTA identified novel differentially-expressed gene set under hypoxic stress at each time point.

2012-12-31 | E-GEOD-22469 | biostudies-arrayexpress

A novel recurrent mutation in MITF predisposes to familial and sporadic melanoma

Project description:We identified a novel germline mutation of the microphthalmia-associated transcription factor (MITF - E318K). This mutation was found to be present in numerous melanoma families, as well as the general population, where its association with melanoma has a significant effect. We determined the effect of the E318K mutation on global MITF target gene transcription. We developed a tetracycline-inducible system for expression of wild type MITF or the E318K variant in melanoma cell lines with constitutively low or undetectable levels of endogenous MITF (HT144 and C32). We examined whole-genome expression profiles in these cells following induction of either wild-type or E318K MITF for 48 hours. Analysis suggests that the MITF E318K mutant exhibits differential transcriptional activity against some, though not all, target genes. Expression profiling by array

2011-12-01 | E-GEOD-31269 | biostudies-arrayexpress

Rhein, a novel Histone Deacetylase (HDAC) inhibitor with antifibrotic potency in human myocardial fibrosis

Project description:Although fibrosis depicts a reparative mechanism, maladaptation of the heart due to excessive production of extracellular matrix accelerates cardiac dysfunction. The anthraquinone Rhein was examined for its anti-fibrotic potency to mitigate cardiac fibroblast-to-myofibroblast transition (FMT). Primary human ventricular cardiac fibroblasts were subjected to hypoxia and characterized with proteomics, transcriptomics and cell functional techniques. Knowledge based analyses of the omics data revealed a modulation of fibrosis-associated pathways and cell cycle due to Rhein administration during hypoxia, whereas p53 and p21 were identified as upstream regulators involved in the manifestation of cardiac fibroblast phenotypes. Mechanistically, Rhein-mediated cellular effects were linked to the histone deacetylase (HDAC)-dependent acetylation status of p53 a posttranslational modification that acts protein stabilizing. Direct enzymatic testing revealed an inhibitory potency of Rhein for HDAC classes I/II. Functionally, Rhein inhibited collagen contraction in response to protein abundance of SMAD7, thus demonstrating its anti-fibrotic property in cardiac remodeling. In conclusion, this study identifies Rhein as a novel potent HDAC inhibitor and provides evidence that Rhein may contribute to the treatment of cardiac fibrosis as anti-fibrotic agent. As readily available drug with approved safety, repurposing of Rhein constitutes a promising potential therapeutic approach in the supplemental and protective intervention of cardiac fibrosis.

2020-03-23 | PXD016731 | Pride

Dynamics of intercellular and exosomal miRNAs in hypoxia-resistant cells

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-10-15 | E-GEOD-48983 | biostudies-arrayexpress

Simultaneous analysis of tumor and stromal gene expression profiles from xenograft models

Project description:Identifying the gene expression alterations that occur in both the tumor and stroma is essential to understanding tumor biology. We have developed a dual-species microarray analysis method that allows the dissection of both tumor and stromal gene expression profiles from xenograft models, based on limited interspecies cross-hybridization on Illumina gene expression beadchips. This methodology allows for simultaneous genome-wide analysis of gene expression profiles of both tumor cells and the associated stromal tissue. Data is provided regarding the crosshybridization of mouse liver RNA on human microarray, and MDA-MB-231 breast cancer cell line RNA on mouse microarray. Data is also provided for comparisons of MDA-MB-231 gene expression in vitro vs. in vivo, and mouse liver gene expression in control mice vs. stroma from MDA-MB-231 xenograft liver metastasis in tumor bearing mice A total of 18 samples were analyzed. Samples consist of 6 different types with each type in triplicate. Types are (1) MDA-MB-231 cell line grown in vitro and arrayed on mouse chips, (2) mouse liver from NOD/SCID mice arrayed on human chips, (3) MDA-MB-231 cell line grown in vitro arrayed on human chips, (4) MDA-MB-231 xenograft liver metastasis arrayed on human chips, (5) mouse liver from NOD/SCID mice arrayed on mouse chips, and (6) MDA-MB-231 xenograft liver metastasis arrayed on mouse chips. The overall design had three objectives: (1) to determine crosshybridizing probes based on sample types 1, 2, 3, and 5, (2) detect stromal and tumor expression using sample types 4 and 6, and (3) determine genes differentially expressed in tumor or metastasis compared to normal by comparing sample types 3 and 4 and comparing sample types 1 and 5.

2011-11-22 | E-GEOD-30993 | biostudies-arrayexpress

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