Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

14 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The effect of miR196a of overall gene expression in oral keratinocytes

ABSTRACT: We wished to assess the effect of miR196a on overall gene expression in reducing it in high expressing epithelial cells (D19 and B16) using antimiR196a and over expressing it in low-expressing cells (OKF4) using pre-miR196a. We transfected anti miR196a in to D19 and B16 oral keratinocytes which express high levels of miR196a in triplicate cultures, harvesting 24h after transfection. We transfected pre-miR196 in okf4 immorualised normal oral keratinocytes in duplicate culture. Successful transfection was ensured by qPCR. 16 Samples in total. 2 high expressing cells: control and anti-miR transfected, in triplicate. 1 low expressing cell: control and premiR transfected, in duplicate

ORGANISM(S): Homo sapiens

SUBMITTER: Keith Hunter

PROVIDER: E-GEOD-52810 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

The effect of miR196a of overall gene expression in oral keratinocytes

Project description:We wished to assess the effect of miR196a on overall gene expression in reducing it in high expressing epithelial cells (D19 and B16) using antimiR196a and over expressing it in low-expressing cells (OKF4) using pre-miR196a. We transfected anti miR196a in to D19 and B16 oral keratinocytes which express high levels of miR196a in triplicate cultures, harvesting 24h after transfection. We transfected pre-miR196 in okf4 immorualised normal oral keratinocytes in duplicate culture. Successful transfection was ensured by qPCR.

2013-11-28 | GSE52810 | GEO

Expression data comparing murine AE9a high and AE9a low expressing hematopoietic cells

Project description:Microarray analysis was performed to examine potential differences in target gene expression of AE9a expressing low cells compared to AE9a expressing high cells. Potential contributing factors to AE9a induced leukemia were investigated. Embryonic day 13.5 to 14.5 fetal liver cells were harvested from C57Bl6 females. Cells were cultured in StemSpan media with 50ng/ml rat recombinant SCF, 10ng/ml human IL-6, and 10ng/ml murine IL-3. After overnight stimulation, cells were collected and transduced with two rounds of retrovirus (MIG-AE9a). Post transduction, cells were collected, counted and transplanted into lethally irradiated BoyJ recipient mice. Cells were expanded two to three weeks in vivo, mice were sacrificed, and bone marrow (BM) harvested. c-Kit+ cells were sorted (BD FACS Aria) for 30% low and 30% high GFP-expressing populations. Six AE9a low and six AE9a high samples were compared. RNA was isolated via the Qiagen RNeasy RNA isolation kit and submitted to the CCHMC Microarray Core. Samples were hybridized to an Affymetrix Mouse Gene 1.0 ST chip. Data was normalized using Expression Console and was analyzed using Qlucore Omics Explorer software.

2016-07-19 | E-GEOD-84513 | biostudies-arrayexpress

Drosophila CNS mitochondrial DNA dysfunction microarray

Project description:Mitochondrial DNA (mtDNA) encodes essential components of the respiratory chain and loss of mtDNA leads to mitochondrial dysfunction and neurodegeneration. Mitochondrial transcription factor A (TFAM) is an essential component of mtDNA replication and a regulator of mitochondrial copy number in cells. Studies have shown that TFAM knockdown leads to mitochondrial dysfunction and respiratory chain deficiencies. Using gene expression analysis, we aimed to investigate the effects of mtDNA dysfunction in the CNS at the molecular level. We used microarray analysis to investigate gene expression in cases of mitochondrial dysfunction in the CNS. RNA was purified from the late third instar larval CNS from control larvae, or larvae over-expressing mitochondrial transcription factor A (TFAM) in post-mitotic neurons using the neuron specific driver nsyb-Gal4. Three replicates are included for each condition.

2013-12-20 | E-GEOD-53509 | biostudies-arrayexpress

Transciptome profile of neonatal small intestinal CD4 T cells

Project description:The intestine harbors more immune cells then the rest of the body together in order to maintain a state of tolerance towards the microbiota as well as food antigen on one side and recognition and immune response to invading pathogens on the other side. At birth the intestine transitions from a sterile organ to a highly exposed environment. At the same time the murine adaptive immune system starts to form and newly generated T and B cells home to the intestine. The present study aims to understand the function of CD4 T cells in the neonatal small intestine (SI). For that the transcriptional profiles of CD4 T cells isolated from the SI of 6- and 11-days-old neonates were compared to their counterparts in mLN and thymus as well as to adult CD4 T cells from the lamina propria (LP) and Peyers patches (PP). 4 true biological replicates in single color mode were analyzed in each group.

2015-05-22 | E-GEOD-60515 | biostudies-arrayexpress

mRNA profiling in aortic stenosis

Project description:We compared mRNA profiles of 10 participants with severe aortic stenosis undergoing aortic valve replacement to 10 samples donated post-mortem.

2017-04-27 | E-MTAB-3105 | biostudies-arrayexpress

Altered DNA methylation of glycolytic and lipogenic genes in liver from obese and type 2 diabetic patients [transcriptome analysis]

Project description:Type 2 diabetes is a complex disease associated with many underlying pathomechanisms. Epigenetic regulation of gene expression by DNA methylation has become increasingly recognized as an important component in the etiology of type 2 diabetes. We performed genome-wide methylome and transcriptome analysis in liver from severely obese patients with or without type 2 diabetes to discover aberrant pathways underlying the development of insulin resistance. We identified hypomethylation of five key genes involved in hepatic glycolysis, de novo lipogenesis and insulin resistance with concomitant increased mRNA expression and protein content. The CpG-site within the ATF-motif was hypomethylated in four of these genes in liver of non-diabetic and type 2 diabetic obese patients, suggesting epigenetic regulation of transcription by altered ATF-DNA binding. In conclusion, severely obese non-diabetic and type 2 diabetic patients have distinct alterations in the hepatic methylome and transcriptome and genes controlling glucose and lipid metabolism are hypomethylated at a regulatory site. Thus, obesity may epigenetically reprogram the liver towards increased lipid production and exacerbate the development of insulin resistance. To better understand the molecular mechanisms underlying the development of hepatic insulin resistance and type 2 diabetes at a molecular level, we performed a genome-wide methylome and transcriptome analysis of liver from non-obese metabolically healthy, obese non-diabetic and obese type 2 diabetic patients. Distinct DNA methylation and gene expression profiles were identified in liver from the obese and type 2 diabetic patients compared with the non-obese participants.

2016-03-08 | E-GEOD-64998 | biostudies-arrayexpress

Expression data from SDH-disabled GIST

Project description:Pediatric GIST commonly harbors a disabled succinate dehydrogenase complex (SDH), which yields tumors with highly conserved genomes but characteristic epigenomic signatures. Mysteriously, nearly half of such SDH-deficient GIST, including tumors from Carney Triad patients, lack identifiable mutations in SDH component genes and genes required for complex assembly (SDHA, SDHB, SDHC, SDHD, SDHAF, termed SDHx). Genomic sequencing coupled with DNA methylation and transcriptional profiling have exposed SDHC promoter-specific CpG island epimutation and concomitant gene silencing in the majority of SDHx-WT GIST. We performed whole genome expression profiling on 20 FFPE dSDH GIST tumors using Affymetrix U133P2 arrays which contain >54K gene target probesets. Included here were data from 7 SDHx-w.t. and 13 SDHx mutants that passed array QC.

2015-01-02 | E-GEOD-56670 | biostudies-arrayexpress

Nucleosome locations in human oral keratinocytes

Project description:Miccrococcal nuclease sequencing (MNase-seq) of chromatin from control and Snail2-expressing oral keratinocytes

2017-12-31 | GSE65191 | GEO

RNA-Seq of mouse E12.5 brain regions

Project description:Investigations into the roles for Pbx1 and its transcriptional network in dopaminergic neuron development and Parkinson's Disease Three samples each from dorsal midbrain, forebrain, hindbrain, Alar plate, and ventral midbrain

2016-07-22 | E-GEOD-82099 | biostudies-arrayexpress

Gene expression regulated by AGN193109 and 4-diehtylaminobenzaldehyde (DEAB) in mIMCD-3 cells

Project description:Retinoic acid (RA) is the bioactive derivative of vitamin A that regulates gene expression by activating RA receptors (RAR). By using a reporter mouse model, we recently showed that endogenous RA/RAR signaling was present in kidney collecting duct cells, and in mouse inner medullary collecting duct cell line (mIMCD-3). In order to unveil target genes of endogenous RA/RAR signaling in kidney collecting duct cells, whole genome microarray analysis was performed on mIMCD-3 cells treated with AGN193109, a pan-RAR antagonist, and 4-diethylaminobenzaldehyde (DEAB), an inhibitor of RA synthesizing enzyme. Specificity of gene expression regulation was confirmed by determining the reversibility of the regulation by simultaneous addtion of exogenous tRA. In the first set of experiment, mIMCD-3 cells were treated with either vehicle (0.1% ethanol and 0.1% DMSO) or 1 μM AGN193109 or 1 μM AGN193109+0.2 μM tRA. Three independent biological experiments were performed. In the second set of experiment, mIMCD-3 cells were treated with either vehicle (0.1% ethanol and 0.1% DMSO) or 25 μM DEAB or 25 μM DEAB+0. 01 μM tRA. Three independent biological experiments were performed. Treatment period for both sets of experiments were 24 hours.

2011-11-26 | E-GEOD-33955 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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