Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptional profile comparing Hep3B transfected with miR-19b inhibitor with Hep3B transfected with control

ABSTRACT: miR-19b was up-regulated with hepatocellular carcinoma. We compared the transcriptional profile of Hep 3B transfected with miR-19b inhibitor with Hep3B transfected with control to identify genes affected by miR-19b knockdown.

ORGANISM(S): Homo sapiens

PROVIDER: GSE69519 | GEO | 2015/07/22

SECONDARY ACCESSION(S): PRJNA285784

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Transcriptional profile comparing Hep3B transfected with miR-19b inhibitor with Hep3B transfected with control

Project description:miR-19b was up-regulated with hepatocellular carcinoma. We compared the transcriptional profile of Hep 3B transfected with miR-19b inhibitor with Hep3B transfected with control to identify genes affected by miR-19b knockdown. Hep 3B_miR-19b transfected vs Hep 3B_control transfected

2015-07-22 | E-GEOD-69519 | biostudies-arrayexpress

A global transcriptome analysis of human epidermal keratinocytes upon overexpression of microRNA-19a or microRNA-19b or microRNA-20a

Project description:Several members from microRNA 17-92 cluster, i.e. miR-19a, miR-19b and miR-20a, were found up-regulated in human epidermal keratinocytes at wound-edges compared to the intact skin; however their biological role in keratinocytes during wound repair has not been studied. To study the genes regulated by miR-19a, miR-19b and miR-20a, we transfected miRNA specific mimics, i.e. pre-miR-19a, pre-miR-19b or pre-miR-20a into human primary epidermal keratinocytes to overexpress them. We performed a global transcriptome analysis of keratinocytes upon overexpression of miR-19a or miR-19b or miR-20a using Affymetrix arrays.

2017-02-15 | GSE93110 | GEO

Transcription profiling of human Hep3B cells transfected with L1CAM

Project description:To compare the transcription profiling between empty vector transfected Hep3B and L1CAM transfected Hep3B

2011-08-01 | E-MEXP-1357 | biostudies-arrayexpress

Homo sapiens

Project description:Transcriptional profile comparing Hep3B transfected with miR-19b inhibitor with Hep3B transfected with control

| PRJNA285784 | ENA

MicroRNA-19b exacerbates systemic sclerosis through promoting Th9 cells

Project description:Systemic sclerosis (SSc) is a chronic autoimmune disease characterized with fibrosis of skin and multiple vital organs, but the immunological pathogenesis of SSc remains largely unknown. We show here that microRNA-19b (miR-19b) promotes IL-9-producing CD4+ T cells (Th9) that exacerbate SSc. Specifically, TGF-b plus IL-4 induced expression of TNF receptor associated factor 6 (TRAF6) through phosphorylated Smad3 linker region site Serine 213 (p-Smad3L-Ser213) and activated it through K63 ubiquitination by suppressing the leucine-rich-repeat-containing protein 3 (NLRC3). TRAF6 consequently formed complex with and activated TGF-b activated kinase 1 (TAK1). TAK1 promoted nuclear factor kappa B (NFκB) p65 activation, which then specifically upregulated miR-19b. miR-19b activated Il9 gene expression and promoted Th9 differentiation by directly targeting and suppressing atypical E2F family member E2f8 gene, a repressor for Il9 gene transcription. Importantly, Th9 cells played a critical role in the development and pathogenesis of experimental SSc by promoting the fibrosis in mice induced with Bleomycin. miR-19b and IL-9 were increased in CD4+ T cells in experimental SSc in mice and also in patients with SSc. Strikingly, inhibition of miR-19b resulted in fewer Th9 cells and attenuated fibrotic manifestations and ameliorated the disease in SSc mice. Our study identifies miR-19b as a key factor of Th9 cells that are involved in the pathogenesis of SSc. Our findings should have clinical implications for patients with SSc.

2024-08-21 | GSE269954 | GEO

miR-19b-3p Overexpression in Human Skeletal Muscle Cells

Project description:The object of this data set was to indentify genes altered by miR-19b-3p in differentiated human skeletal muscle myotubes.

2020-01-01 | GSE126187 | GEO

Expression data comparing Hep3B Caveolin-1 (Cav1) knockdown cells with Hep3B non-target control cells

Project description:To identify genes regulated by Cav1 Affymetrix Human Genome U133 Plus 2.0 GeneChip Hep3B cells with or without knockdown of Cav1

2016-03-01 | E-GEOD-75994 | biostudies-arrayexpress

miR-17-92 sustains lymphoma growth by fine-tuning MYC

Project description:The synergism between c-MYC and miR-17-19b, a truncated version of the miR-17-92 cluster, is well documented during tumor initiation. However, little is known about miR-17-19b function in established cancers. Here we investigate the role of miR-17-19b in c-MYC-driven lymphomas by integrating SILAC-based quantitative proteomics, transcriptomics and 3’ UTR analysis upon miR-17-19b overexpression. We identify over one hundred novel miR-17-19b targets, of which 40% are co-regulated by c-MYC. Down-regulation of a new miR-17/20 target Chek2 increases the recruitment of HuR to c-MYC transcripts, resulting in the inhibition of c-MYC translation and thus interfering with in vivo tumor growth. Hence, in established lymphomas, miR-17-19b fine-tunes c-MYC activity through a tight control of its function and expression, ultimately ensuring cancer cell homeostasis. Our data highlight the plasticity of miRNA function, reflecting changes in the mRNA landscape and 3’ UTR shortening at different stages of tumorigenesis.

2015-11-06 | PXD002810 | Pride

Expression data of Hep3b cells transfected with si-WIPI2 and si-NC

Project description:Expression data of Hep3b cells transfected with si-WIPI2 and si-NC

| PRJNA587165 | ENA

Differential gene expression in Hep3B and Hep3B SOX4-/- cells

Project description:Overexpression of SOX4 in various kinds of cancers specimen was associated with poor prognosis of patients; however, the role of SOX4 in angiogenesis or tumor microenvironment modulation remains unclear. Therefore the endogenous SOX4 was knockout and the differential gene expression between Hep3B and Hep3B SOX4-/- cells were examined via genechip. We found that the differentially expressed genes, EzH2, a SOX4-associated partner, and CXCL12, were repressed in Hep3B SOX4-/- cells compared with parental Hep3B; these results were further assessed via qRT-PCR in Hep3B SOX4-/- versus Hep3B cells.

2020-12-01 | GSE141909 | GEO

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