Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Tumor immune evasion arises through loss of TNF sensitivity [MC38]

ABSTRACT: Investigation of the transcriptional response to TNF and Interferon gamma or T cells

ORGANISM(S): Mus musculus

PROVIDER: GSE112252 | GEO | 2018/04/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Tumor immune evasion arises through loss of TNF sensitivity [Ado]

Project description:Investigation of the transcriptional response of wild type or Ado knockout MC38 cells to TNF

2018-04-01 | GSE112251 | GEO

Tumor immune evasion arises through loss of TNF sensitivity [MC38]

Project description:Tumor immune evasion arises through loss of TNF sensitivity [MC38]

| PRJNA445399 | ENA

Tumor immune evasion arises through loss of TNF sensitivity

Project description:Tumor immune evasion arises through loss of TNF sensitivity

| PRJNA445390 | ENA

Tumor immune evasion arises through loss of TNF sensitivity

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

2018-04-01 | GSE112253 | GEO

Tumor immune evasion arises through loss of TNF sensitivity [Ado]

Project description:Tumor immune evasion arises through loss of TNF sensitivity [Ado]

| PRJNA445398 | ENA

The effects of terbutaline or GW9508 on TNF-alpha and IFN gamma (TNF-alpha + IFN gamma) stimulation by HaCaT

Project description:G-protein coupled receptors (GPCRs) have diverse roles in physiological processes, including immunity. Gs-coupled GPCRs increase while Gi-coupled ones decrease intracellular cAMP. Previous studies suggest that, in epithelial cells, Gs-coupled GPCRs enhance whereas Gi-coupled GPCRs suppress pro-inflammatory immune responses. In order to examine the issue, we chose beta2 adrenergic receptor and GPR40 as representatives of Gs- and Gi- coupled GPCRs, respectively, and examined their effects on TNF-alpha and IFN-gamma-(TNF-alpha + IFN-gamma) induced gene expression by HaCaT. We used microarrays to detail the global changes of gene expression induced by a beta2 adrenergic receptor agonist terbutaline or GPR40 agonist GW9508 pre-treatment in TNF-alpha + IFN-gamma - stimulated HaCaT cells. HaCaT cells were pre-treated with terbutaline or GW9508, TNF-alpha + IFN-gamma were then added, and cultured for another 24 h. Cells were then used for RNA extraction and hybridization on Affymetrix microarrays. We sought to clarify changes in gene expression after 1) TNF-alpha + IFN-gamma, 2) TNF-alpha + IFN-gamma + terbutaline, and 3) TNF-alpha + IFN-gamma + GW9508 treatment. To this end, we set 4 groups of samples; 1) unstimulated group, 2) TNF-alpha + IFN-gamma-stimulated group, 3) TNF-alpha + IFN-gamma + terbutaline-stimulated group, and 4) TNF-alpha + IFN-gamma + GW9508-stimulated group. In each group, HaCaT cells were stimulated in triplicate wells (n=3).

2010-12-01 | E-GEOD-20297 | biostudies-arrayexpress

Interferon-gamma/TNF-treated human corneal epithelial cells

2011-09-06 | GSE31931 | GEO

Interferon-gamma/TNF-treated human corneal epithelial cells

Project description:Our experiment is to compare Glyco-gene expression by interferon-gamma/TNF-treated human corneal epithelial cells also treated either with cell communication glycoprotein 'lacritin' or negative control deletion construct 'C-25 lacritin'. In a newly developing story, lacritin but not C-25 protects human corneal epithelial cells from INFG/TNF-induced cell death. This expression array will help work out the mechanism of protection to complement phosphoblotting and shRNA approaches currently underway. Lacritin targets its coreceptor 'syndecan-1' in lacritin-dependent cell proliferation and secretion. Lacritin appears to be important in human 'dry eye' and in promoting corneal epithelial cell survival in the presence of inflammatory cytokines.

2011-09-05 | E-GEOD-31931 | biostudies-arrayexpress

CXCL10 promotes vascular permeability upon TNF-induced release from pericytes

Project description:Tumor necrosis factor alpha induces vascular permeability, playing an important role in inflammation. Also, TNF-induced vascular leakage is involved in the increased extravasation of nanoparticle formulated chemotherapeutics improving drug delivery and subsequently tumor response, and we found a positive correlation between the presence of pericytes in the tumor-associated vasculature and TNF-induced leakage. RNA sequencing and pathway analysis of TNF-stimulated versus non-stimulated pericytes and endothelial cells show significant upregulation of several pathways involving interferon regulating pathways with a high expression of CXCL10, also known as Interferon gamma-inducible protein 10 (IP-10) in TNF-stimulated pericytes. In addition, CXCL10 protein production was significantly increased in conditioned medium from TNF-exposed pericytes compared to the other conditions. In our animal studies, we observed that tumor types with high pericyte covered vessels show enhanced permeability when exposed to TNF, which can be blocked with a neutralizing CXCL10 antibody. Vice versa, tumors with vessels low in pericyte number do not respond to TNF, i.e., do not express elevated permeability. Importantly, this lack of pericyte coverage can be compensated by co-administration of CXCL10. Our finding reveals a mechanism where TNF induces CXCL10 release from pericytes, being at the basis of increased permeability and thus vascular leakage.

2022-07-01 | GSE203505 | GEO

KBM7 genetrap mutant cells stimulated with TNF-alpha and IFN-gamma

Project description:Transcriptional response of KBM7 cells to IFN-gamma or TNF-alpha was investigated in control or cells with genetrap insertions in JAK2 or TNFRS1A, respectively. The experiment shows that, as expected, cells lacking JAK2 or TNFRS1A expression display a severly blunted response to the tested cytokines. KBM7 genetrap mutant cells stimulated with TNF-alpha and IFN-gamma Sample WT_1 corresponds with the control sample for the IFN-gamma stimulation; Sample WT_2 corresponds with the control sample for the TNF-alpha stimulation. As the expected differences between the samples was large, only single replicates were performed for each condition

2013-08-09 | E-GEOD-48848 | 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