Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MiR181a is a novel key player in the STAT3 mediated survival network of TCRab CD8+ T-LGL leukemia

ABSTRACT: miR181a is a novel key player in the STAT3 mediated survival network of TCRab CD8+ T-LGL leukemia

PROVIDER: PRJNA670710 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

miR181a is a novel key player in the STAT3 mediated survival network of TCRab CD8+ T-LGL leukemia [sRNA-Seq]

Project description:TCRαβ CD8 large granular lymphocyte (LGL) leukemia is a rare heterogeneous hematological disorder with a chronic disease course that mostly affects elderly. It is generally accepted that LGL cells arise as a consequence of chronic antigenic stimulation and inflammation and thrive because of dysregulation of mainly the STAT3 but also to some extent the ERK pathway, which are constitutively activated. In approximately 40% of patients this is due to STAT3 activating mutations, but for the other 60% it remains to be elucidated, why the STAT3 pathway is chronically activated. miRNAs are one of the most potent regulators in health and disease and are also linked with various leukemias. Therefore, we hypothesized that aberrant miRNA expression could contribute to dysregulation of the STAT3 pathway. miRNA sequencing in LGL leukemia cases and aged-matched healthy control TEMRA cells revealed overexpression of miRNA181a. Furthermore, gene set enrichment analysis (GSEA) of miRNA181a implicated its involvement in the STAT3 and ERK1/2 pathways. Phosphoflow analysis of STAT3, ERK1/2 in miR181a-transfected human CD8 T cells revealed that miR181a overexpression results in STAT3 and ERK1/2 phosphorylation. By using TL1, a human T-LGL cell line model, we have now established that miR181a is the common actor in T-LGL leukemia, driving STAT3 activation by SOCS3 inhibition in LGL leukemia patients. Additionally, miR181a induces ERK1/2 phosphorylation by inhibition of DUSP6. Taken together, our data show that miR181a is the missing link to explain why STAT3-unmutated patients show hyperactive STAT3.

2021-12-01 | GSE159878 | GEO

miR181a is a novel key player in the STAT3 mediated survival network of TCRab CD8+ T-LGL leukemia [RNA-Seq]

2021-12-01 | GSE159819 | GEO

miR181a is a novel key player in the STAT3 mediated survival network of TCRab CD8+ T-LGL leukemia [RNA-Seq]

Project description:miR181a is a novel key player in the STAT3 mediated survival network of TCRab CD8+ T-LGL leukemia [RNA-Seq]

| PRJNA670520 | ENA

miR181a is a novel key player in the STAT3 mediated survival network of TCRab CD8+ T-LGL leukemia [sRNA-Seq]

Project description:miR181a is a novel key player in the STAT3 mediated survival network of TCRab CD8+ T-LGL leukemia [sRNA-Seq]

| PRJNA670802 | ENA

miR181a is a novel key player in the STAT3 mediated survival network of TCRab CD8+ T-LGL leukemia

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-12-01 | GSE159879 | GEO

Lgl protein interactome - Lgl reduces endosomal vesicle acidification and Notch signaling by promoting the interaction between Vap33 and the V-ATPase complex

Project description:To identify Lgl binding proteins, we purified Lgl-containing protein complexes from cultured Drosophila S2 cells, using the single-step streptavidin purification from stable cell lines expressing SBP-tagged Lgl, followed by nanoLC-MS/MS analysis of the interactors. This study revealed the binding of Lgl to Vap33, which we further connected to the function of the vacuolar ATPase and regulation of Notch signaling.

2018-06-10 | PXD009568 | Pride

Involvement of hCMV in the ontogeny of CD4+ T-LGL

Project description:Recent studies suggest the potential involvement of common antigenic stimuli on the ontogeny of monoclonal TCRalphabeta+/CD4+/NKa+/CD8-/+dim T-large granular lymphocyte (LGL) lymphocytosis. Since healthy individuals show (oligo)clonal expansions of hCMV-specific TCRVbeta+/CD4+/cytotoxic/memory T-cells, we investigate the potential involvement of hCMV in the origin and/or expansion of monoclonal CD4+ T-LGL. A detailed characterization of those genes that underwent changes in T-LGL cells responding to hCMV was performed by microarray gene expression profile (GEP) analysis.

2008-09-01 | GSE12488 | GEO

Molecular profiling of LGL leukemia reveals role of sphingolipid signaling of cytotoxic lymphocytes

Project description:We used microarrays to expression profile peripheral blood mononuclear cells (PBMCs) from LGL leukemia patients and control subjects to identify survival pathways that render leukemic LGL resistant to activation induced cell death. Keywords: granular lymphocyte leukemia, PBMC

2008-05-01 | GSE10631 | GEO

MicroRNA microarray of Drosophila melanogaster extracted from cephalic complexes of lgl-hypomorph 3rd instar larvae

Project description:Single channel custom oligonucleotide array of 147 microRNAs to detect changes in expression of a lgl-hypomorph mutant versus wild-type 0, 3, and 5 day old 3rd instar lgl-hypomorph larvae were compared to 0 day 3rd instar wild-type larvae to test for differences in microRNA expression

2017-12-18 | GSE40293 | GEO

Andersson_et_al_2013

Project description:LGL leukemia is chronic clonal lymphoproliferative disorder, characterized by expansion of cytotoxic CD8+ T-cells or NK-cells. We compared gene expression of 2 LGL leukemia patients with STAT3 mutation (Patients 11 and 12) and 2 LGL leukemia patients without STAT3/STAT5b mutation (Patients 9 and 10) with CD8 and CD4 samples from healthy controls to assess different gene expression patterns between samples.

2013-11-14 | E-MTAB-2068 | 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