Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression profile of miR-17-92a-MSCV-IRES-Thy1.1 transduced P14 CD8+ T cells

ABSTRACT: During acute viral infections, effector CD8+ T cells differentiate into memory precursors or short-lived terminal effectors. miR-17-92a over-expression skews CD8+ effector cells to the terminal differentiation. We used microarray to identify the genes that are differentially expressed caused by miR-17-92a over-expression.

ORGANISM(S): Mus musculus

PROVIDER: GSE34217 | GEO | 2012/06/05

SECONDARY ACCESSION(S): PRJNA156545

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Expression profile of miR-17-92a-MSCV-IRES-Thy1.1 transduced P14 CD8+ T cells

Project description:During acute viral infections, effector CD8+ T cells differentiate into memory precursors or short-lived terminal effectors. miR-17-92a over-expression skews CD8+ effector cells to the terminal differentiation. We used microarray to identify the genes that are differentially expressed caused by miR-17-92a over-expression. CD8+ T cells from P14 TCR transgenic mice were infected with miR-17-92a-MSCV-IRES-Thy1.1 vector and transfer to C57BL6 recipients. Chimeras were infected with LCMV Armstrong. Thy1.1+ miR-17-92a-MSCV-IRES-Thy1.1 transduced P14 cells and Thy1.1- non-transduced P14 cells were sorted by FACS. RNA was extracted from samples, labeled, and hybridized to Affymetrix microarrays.

2012-06-04 | E-GEOD-34217 | biostudies-arrayexpress

Temporal expression of miR-17-92a regulates effector and memory CD8+ T cell differentiation

Project description:This SuperSeries is composed of the following subset Series: GSE34216: miRNA signatures of antigen specific CD8+ T cells at different stages of immune response to LCMV infection GSE34217: Expression profile of miR-17-92a-MSCV-IRES-Thy1.1 transduced P14 CD8+ T cells Refer to individual Series

2012-06-04 | E-GEOD-34218 | biostudies-arrayexpress

A Prospective Study of Colorectal Cancer Risk Population Screening Using Stool-based miR-92a Assay

Project description:Interventions: Screening Group:NA Primary outcome(s): miR-92a;hemoglobin Study Design: Diagnostic test for accuracy

| 81565 | ecrin-mdr-crc

The miR-92a–Cpeb3 axis safeguards neuronal function during neuroinflammation

Project description:Neuroinflammation causes neuronal injury in multiple sclerosis (MS) and other neurological diseases. MicroRNAs (miRNAs) are central modulators of cellular stress responses, but knowledge about miRNA–mRNA interactions that determine neuronal outcome during inflammation is limited. Here, we combined unbiased neuron-specific miRNA with mRNA sequencing to assemble the regulatory network that mediates robustness against neuroinflammation. As a critical miRNA-network hub we defined miR-92a. Genetic deletion of miR-92a exacerbated the disease course of mice undergoing experimental autoimmune encephalomyelitis (EAE), whereas miR-92a overexpression protected neurons against excitotoxicity. As a key miR-92a target transcript, we identified cytoplasmic polyadenylation element-binding protein 3 (Cpeb3) that was suppressed in inflamed neurons in mouse EAE and human MS. Accordingly, Cpeb3 deletion improved neuronal resistance to excitotoxicity and ameliorated EAE. Together, we discovered that the miR-92a–Cpeb3 axis confers neuronal robustness against inflammation and serves as potential target for neuroprotective therapies.

2023-11-06 | GSE220950 | GEO

Exosomal miR-92a-3p as a diagnostic biomarker for adenomyosis and its pathological mechanism

Project description:This study aimed to elucidate the role of microRNA miR-92a-3p in the pathogenesis of adenomyosis. We focused on understanding how miR-92a-3p in exosomes derived from ectopic lesions influences the behavior of endometrial cells, DRG neurons, and Human Umbilical Vein Endothelial Cells (HUVECs), and its potential as a non-invasive diagnostic biomarker. Our findings revealed that MiR-92a-3p is significantly upregulated in exosomes derived from ectopic lesions of adenomyosis. This upregulation was associated with enhanced migration and invasion capabilities in eutopic endometrial cells, DRG neurons, and HUVECs. Furthermore, the study demonstrated a significant correlation between the levels of MiR-92a-3p in urinary exosomes and the clinical symptoms of adenomyosis, suggesting its potential as a non-invasive biomarker for the disease. This study elucidates an exosomal signaling process via miR-92a-3p that drives pathological infiltration and angiogenesis to promote adenomyosis progression. Upregulated miR-92a-3p in biofluid exosomes shows promising non-invasive biomarker potential for diagnosis and monitoring of this disease. Our findings unveil novel targets and tools for improved clinical management.

2024-04-01 | GSE262302 | GEO

Project description:Temporal expression of miR-17-92a regulates effector and memory CD8+ T cell differentiation

| PRJNA149809 | ENA

mRNA microarray of HUVEC transfected with miR-92a-3p against non-specific control miRNA.

Project description:Colon cancer secretes miR-92a-3p via exosomes. To know the function of miR-92a-3p in extracellular space, we've set endothelial cells (ECs) as a recipient of the exosomes, and examined gene expressions in ECs.

2019-07-01 | E-MTAB-8093 | biostudies-arrayexpress

Microarray analyses and miR-92a target prediction in primary mediastinal large B-cell lymphoma (PMBL) samples

Project description:Micro RNAs (miRNAs) are a class of small, non-coding RNAs that post-transcriptionally control the translation and stability of mRNAs. In our study, we found a higher level of miR-92a in PMBL versus DLBCL. A bioinformatics approach combining in silico prediction and transcriptomic analyses on patient samples and transduced cell lines, enabled us to identify miR-92a target genes in PMBL.

2016-12-18 | E-MTAB-4165 | biostudies-arrayexpress

Pisolithus sp. 92A

Project description:Pisolithus sp. 92A Resequencing

| PRJNA444305 | ENA

Response to a LNA miR-92a inhibitor in immortalized human bronchial epithelial cells.

Project description:Lung cancer is the leading cause of cancer-related fatalities. Recent success developing genotypically-targeted therapies, with potency only in well-defined subpopulations of tumors, suggests a path to improving patient survival. We utilized a library of oligonucleotide inhibitors to microRNAs, a class of post-transcriptional gene regulators, to identify novel synthetic lethal interactions between miRNA inhibition and molecular mechanisms in NSCLC. Two inhibitors, those for miR-92a and miR-1226*, produced a toxicity distribution across a panel of 27 cell lines that correlated with loss of p53 protein expression. Notably, depletion of p53 was sufficient to confer sensitivity to otherwise resistant telomerase-immortalized bronchial epithelial cells. We found that both miR inhibitors cause sequence-specific down-regulation of the miR-17~92 polycistron, and this down-regulation was toxic only in the context of p53 loss. Mechanistic studies indicated the selective toxicity of miR-17~92 polycistron inactivation was the consequence of derepression of vitamin D signaling via suppression of CYP24A1; a rate limiting enzyme in the 1α,25-dihydroxyvitamin D3 metabolic pathway. Of note, high CYP24A1 expression significantly correlated with poor patient outcome in multiple lung cancer cohorts. Our results indicate that the screening approach utilized in this study can identify clinically relevant synthetic lethal interactions, and that vitamin D receptor agonists may show enhanced efficacy in p53-negative lung cancer patients. 2 cell lines, 2 conditions per cell line, 3 replicates per condition, RNA collected 48 hours post transfection

2014-12-10 | E-GEOD-64007 | 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