Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Investigation of molecular events underlying the miR192-mediated modulation of inflammatory response

ABSTRACT: Investigation of molecular events underlying the miR192-mediated modulation of inflammatory response

PROVIDER: PRJNA577060 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Investigation of molecular events underlying the miR192-mediated modulation of inflammatory response

Project description:To understand the molecular mechanism underlying the miR192-mediated modulation of inflammatory response, we have employed whole genome microarray expression profiling of bone-marrow derived macrophages transfected with miR192. In order to distingish the effect of miR192 on inflammatory response from the effecct of IL-6, RNA was isolated from miR192-transfected and R848-stimulated macrophages in the presence or absence of anti-IL-6 Ab during the culture.

2019-11-18 | GSE138758 | GEO

Investigation of the mechansim underlying the inflammatory phenotype in Group A ependymoma

Project description:Inflammatory response has been identified as a molecular signature of high-risk Group A ependymoma (EPN). To better understand the biology of this phenotype and aid therapeutic development, transcriptomic data from Group A and B EPN patient tumor samples, and additional malignant and normal brain data, were analyzed to identify the mechanism underlying EPN group A inflammation. Gene expression profiles of Group A and B EPN were contrasted to identify inflammatory transcriptional profiles (GSEA analysis). Candidate inflammatory mechanism genes were examined across a broader cohort of pediatric and adult brain tumor types and normal brain. Gene expression profiles were generated from surgical tumor and normal brain samples (n=149) using Affymetrix HG-U133plus2 chips (Platform GPL570).

2015-02-27 | E-GEOD-66354 | biostudies-arrayexpress

Investigation of the mechansim underlying the inflammatory phenotype in Group A ependymoma

2015-02-27 | GSE66354 | GEO

Salt induces hepatic inflammatory response through epigenetic modulation of SIRT3

Project description:Salt induces hepatic inflammatory response through epigenetic modulation of SIRT3

| PRJNA761356 | ENA

Modulation of tumor drug sensitivity and inflammatory signaling through CMTM4

Project description:Modulation of tumor drug sensitivity and inflammatory signaling through CMTM4

| PRJNA1179308 | ENA

Investigation of signaling requirements underlying cardiac induction of human pluripotent stem cells

Project description:Investigation of signaling requirements underlying cardiac induction of human pluripotent stem cells

| PRJNA279185 | ENA

The Role of Leishmania GP63 in Modulation of Innate Inflammatory Response to Leishmania major Infection

Project description:Leishmaniasis is a disease caused by the protozoan parasite Leishmania known to affect millions of individuals worldwide. In recent years, we have established the critical role played by Leishmania zinc-metalloprotease GP63 in the modulation of host macrophage signaling and functions, favouring its survival and progression within its host. Leishmania major lacking GP63 was reported to cause limited infection in mice, however it is still unclear how GP63 may influence the innate inflammatory response and parasite survival in an in vivo context. Therefore, we were interested in analyzing the early innate inflammatory events upon Leishmania inoculation within mice and establish whether Leishmania GP63 influences this initial inflammatory response. Experimentally, L. major WT, L. major GP63 KO or L. major GP63 rescue were intraperitoneally inoculated in mice and inflammatory cells recruited were characterized microscopically and by flow cytometry (number and cell type), and their infection determined. Pro-inflammatory markers such as cytokines, chemokines and extracellular vesicles (EVs, e.g. exosomes) were monitored and proteomic analysis was performed on exosome contents. Data obtained from this study suggest that Leishmania GP63 does not significantly influence the pathogen-induced inflammatory cell recruitment, but rather their activation status and effector function. Concordantly, internalization of promastigotes during early infection could be influenced by GP63 as less L. major KO amastigotes were found within host cells and appear to maintain in host cells over time. Collectively this study provides a clear analysis of innate inflammatory events occurring during L. major infection and further establish the prominent role of the virulence factor GP63 to provide favorable conditions for host cell infection.

2022-01-01 | GSE189385 | GEO

Recombinant RANKL causes modulation of inflammatory signaling pathways in C2C12 myotubes

Project description:Recombinant RANKL causes modulation of inflammatory signaling pathways in C2C12 myotubes

| PRJNA629356 | ENA

The cell-based control and underlying mechanism for inflammatory bone loss

Project description:Inflammatory bone loss (IBL) is primarily caused by elevated osteoclast (OC) activity during chronic inflammation. However, the specific OC precursors (OCPs) responding to the inflammatory signals and the underlying mechanisms leading to IBL are poorly understood. We identified two OCP subsets: Ly6ChiCD11bhi inflammatory OCPs (iOCPs) specifically responsible for IBL, and homeostatic Ly6ChiCD11blo (hOCPs), not involved in IBL. Functional and proteomic characterization revealed that while the iOCPs are rare and display low osteoclastogenecity under normal conditions, they expand during chronic inflammation and generate OCs with enhanced activity. In contrast, the hOCPs are abundant and highly osteoclastogenic under normal conditions but are unresponsive to the inflammatory environment and generate OCs with low activity. We identified TNF-α and the S100A8/A9 proteins as key regulators, specifically controlling the iOCP response during chronic inflammation. Our findings offer iOCPs as new therapeutic targets and potential biomarkers to combat IBL in a wide range of inflammatory conditions.

2022-04-08 | PXD031791 | Pride

Investigation of molecular events underlying the IL-6-mediated Th1 inhibition in tumor-bearing mice

Project description:To understand the molecular mechanism underlying the IL-6-mediated attenuation of Th1 differentiation in tumor-bearing animals, we have employed whole genome microarray expression profiling of CD4+ T cells isolated from tumor-bearing mice. In order to distingish the effect of IL-6/sIL-6R signaling augmented in tumor-bearing mice from the effecct of other tumor-derived signals, we isolated CD4+ T cells that were primed in tumor free-mice and in the mice inoculated with ovalbumin (OVA)-expressing MCA205 fibrosamcoma, in conjunction of anti-IL-6R Ab injection. We found that Th2-like gene signature such as Il4, IL10, Ccr4, and c-maf was up-regulated in CD4+ T cells primed in tumor-bearing mice. However,the expression of other Th2 master regulator Gata3 gene, or Tfh-related genes (Bcl6, Cxcr5, and Batf) was not substantially augmented in tumor-bearing mice as compared with those in tumor-free mice. These expressions were abrogated by IL-6R blockade, suggesting that the expression of these Th2-like gene set and the other IL-6 signal-dependent genes like Klf1, Bcl11a, and Klf4 are candidate regulators responsible for IL-6 signaling-mediated Th1 inhibition in tumor-bearing animals.

2017-01-04 | GSE93105 | 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