Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

31 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Microarray analysis of Wild-type vs. Brpf1-deficient E8.75 mouse embryo

ABSTRACT: RNA was isolated from three pairs of wild-type and Brpf1-deficient E8.75 mouse embryos for microarray analysis. The cDNA samples were then labeled and mixed for hybridization with one array. The data from three arrays were obtained and used for bioinformatic analysis.

ORGANISM(S): Mus musculus

SUBMITTER: Xiang-Jiao Yang

PROVIDER: E-GEOD-63908 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Microarray analysis of Wild-type vs. Brpf1-deficient P4 mouse brain

Project description:RNA was isolated from three pairs of wild-type and Brpf1-deficient mouse brains (the dorsal cortex part) at postnatal day 4 for microarray analysis. The cDNA samples were then labeled and mixed for hybridization with one array. The data from three arrays were obtained and used for bioinformatic analysis.

2015-04-08 | E-GEOD-63909 | biostudies-arrayexpress

Inhibition of Met results in concomitant inhibition of Akt and STAT3 signaling pathways, while abrogation of negative feedback permits Erk reactivation

Project description:Amplification and activation of the Met receptor tyrosine kinase occurs up to 23% of gastric cancers, suggesting that Met is a therapeutic target in these cancers. However, the steady-state signaling events that occur during chronic Met activation, and mechanisms for resistance to Met small-molecule inhibitors, are poorly understood. Here we show that multiple gastric cancer cell lines harboring MET amplifications are dependent on Met signaling for proliferation and anchorage-independent growth. In these cells, short-term inhibition of Met leads to coordinated changes in gene expression; these include a rapid loss in expression of immediate-early genes, followed by decreased expression of genes involved in cell cycle and proliferation. Activation of Ras-Erk, PI3K-Akt and STAT3 pathways is attenuated by acute Met inhibition. STAT3 inhibition alone, but not individual inhibition of Mek or Akt, is sufficient to abrogate Met-dependent growth of these cells. However, following chronic Met inhibition, reactivation of Mek-dependent Erk phosphorylation occurs even in the presence of Met inhibitor corresponding with a downregulation of Erk negative regulators DUSP4/6. This provides a mechanism for the emergence of drug resistance. Our findings provide insights into innate resistance to a small-molecule Met inhibitor and highlight rational combination therapies that could be evaluated in clinical trials. Time series experiment, four cell lines, 2 treatments

2014-05-19 | E-GEOD-54532 | biostudies-arrayexpress

Profiling microRNAs in Eucalyptus grandis reveals no mutual relationship between alterations in miR156 and miR172 expression and adventitious root induction during development

Project description:Background: The change from juvenile to mature phase in woody plants is often accompanied by a gradual loss of rooting ability, as well as by reduced microRNA (miR) 156 and increased miR172 expression. Results: We characterized the population of miRNAs of Eucalyptus grandis and compared by Northern blot the gradual reduction in miR156 and increase in miR172 expression during development to the loss of rooting ability. Forty known and eight novel miRNAs were discovered and their predicted targets are listed. The expression pattern of nine miRNAs was determined during adventitious root formation in juvenile and mature cuttings. While the expression levels of miR156 and miR172 were inverse in juvenile and mature tissues, no mutual relationship was found between high miR156 expression and rooting ability, or high miR172 expression and loss of rooting ability. This is shown both in E. grandis and also in E. brachyphylla, in which explants that underwent rejuvenation in tissue culture conditions were also examined. Conclusions: It is suggested that in these Eucalyptus species, there is no correlation between the switch of miR156 with miR172 expression in the stems and the loss of rooting ability. Examination of microRNA in seedlings of Eucalyptus grandis

2014-10-01 | E-GEOD-58367 | biostudies-arrayexpress

Functional analysis of the TRIB1 associated locus (TRIBAL) linked to plasma triglycerides and coronary artery disease

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

2014-02-14 | E-GEOD-54957 | biostudies-arrayexpress

Comparison of microRNA Profiling Platforms (BeadChip)

Project description:Global miRNA expression profiling of human malignancies is gaining popularity in both basic and clinically driven research. But to date, the majority of such analyses have used microarrays and quantitative real-time PCR. With the introduction of digital count technologies, such as next-generation sequencing (NGS) and the NanoString nCounter System, we have at our disposal, many more options. To make effective use of these different platforms, the strengths and pitfalls of several miRNA profiling technologies were assessed, including a microarray platform, NGS technologies and the NanoString nCounter System. These results were compared to gold-standard quantitative real-time PCR. Comparison of non-small cell lung cancer cell lines grown in vitro (n = 5) and in vivo (n = 5) as xenograft models.

2013-10-22 | E-GEOD-51501 | biostudies-arrayexpress

TRIBAL overexpression in HepG2 cells

Project description:Objective - The TRIB1 locus has been linked to hepatic triglyceride metabolism in mice and to plasma triglycerides and coronary artery disease (CAD) in humans. The lipid associated SNPs identified by genome-wide association studies (GWAS) are located ~ 30 kb downstream from TRIB1 suggesting complex regulatory effects on genes or pathways relevant to hepatic triglyceride metabolism. The goal of this study was to investigate the functional relationship between common SNPs at the TRIB1 locus and plasma lipid traits. Methods & Results - Characterization of the risk locus reveals that it encompasses a gene, TRIB1 associated locus (TRIBAL) comprised of a well conserved promoter region and an alternatively spliced transcript. Bioinformatic analysis and re-sequencing identified a single nucleotide polymorphism (SNP), rs2001844, within the promoter region that associates with increased plasma triglycerides, reduced HDL-C and CAD risk. Furthermore, we show that rs2001844 is an expression trait locus (eQTL) for TRIB1 expression in blood and alters TRIBAL promoter activity in a reporter assay model. The TRIBAL transcript has features typical of long noncoding RNAs (lncRNA), including poor sequence conservation. Modulation of TRIBAL expression had limited impact on either TRIB1 or lipid regulatory genes mRNA levels in human hepatocyte models. In contrast, TRIB1 knockdown markedly increased TRIBAL expression in HepG2 cells and primary human hepatocytes. Conclusions - These studies demonstrate an interplay between a novel locus,TRIBAL, and TRIB1. TRIBAL is located in the GWAS identified risk locus, responds to altered expression of TRIB1, harbors a risk SNP that is an eQTL for TRIB1 expression and associates with plasma triglyceride concentrations. HepG2 hepatoma cells were stably infected with TRIBAL1 or no insert carrying lentiviruses

2014-02-14 | E-GEOD-54937 | biostudies-arrayexpress

Comparison of microRNA Profiling Platforms (NanoString)

2013-10-22 | E-GEOD-51504 | biostudies-arrayexpress

Comparison of microRNA Profiling Platforms

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

2013-10-22 | E-GEOD-51508 | biostudies-arrayexpress

Gene Expression of human bladder cancer cell line RT112 and Gemcitabine Resistant Bladder Cancer cell line RT112-Gr

Project description:In this research, Human OneArray Microarray analysis was performed to obtain broad spectrum information about the genes differentially expressed in human bladder cancer cell line RT112 and Gemcitabine Resistant Bladder Cancer cell line RT112-Gr.

2015-04-16 | E-MTAB-3495 | biostudies-arrayexpress

Transcription profiling of lung carcinoma and brain glioblastoma cells were analalyzed, with microarrays run both for control and treatment with dichloroacetate reveals a mitochondria-K+ channel axis is suppressed in cancer and its normalization promotes apoptosis inhibits cancer growth

Project description:The unique metabolic profile of most cancers (aerobic glycolysis) might confer apoptosis-resistance and be therapeutically targeted. Compared to normal cells, several human cancers have high mitochondrial membrane potential and low expression of the K+ channel Kv1.5, both contributing to apoptosis-resistance. Dichloroacetate (DCA), an inhibitor of the mitochondrial pyruvate dehydrogenase kinase (PDK), shifts metabolism from glycolysis to glucose oxidation, decreases mitochondrial membrane potential, increases mitochondrial-H2O2 and activates Kv channels in all cancer, but not normal cells; DCA upregulates Kv1.5 by an NFAT1-dependent mechanism. DCA induces apoptosis, decreases proliferation and tumor growth in vitro and in vivo, without apparent toxicity. Molecular inhibition of PDK2 by siRNA mimics DCA. The mitochondria-NFAT-Kv axis and PDK are important therapeutic targets in cancer; the orally available DCA is a novel selective anticancer agent. Experiment Overall Design: lung carcinoma and brain glioblastoma cells were analalyzed, with microarrays run both for control and treatment with DCA

2008-06-14 | E-GEOD-6014 | 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