Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Neutrophil Extracellular Traps Mediate Acute Liver Failure in Regulation of miR-223/neutrophil Elastase Signaling in Mice

ABSTRACT: Neutrophil Extracellular Traps Mediate Acute Liver Failure in Regulation of miR-223/neutrophil Elastase Signaling in Mice

PROVIDER: PRJNA830716 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR18885527.fastq.gz	Fastqsanger.gz
	SRR18885528.fastq.gz	Fastqsanger.gz
	SRR18885529.fastq.gz	Fastqsanger.gz
	SRR18885530.fastq.gz	Fastqsanger.gz
	SRR18885531.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

Neutrophil Extracellular Traps Mediate Acute Liver Failure in Regulation of miR-223/neutrophil Elastase Signaling in Mice

Project description:Marked enhancement of neutrophil infiltration of the liver is a hallmark of acute liver failure (ALF), a severe life-threatening disease with varying etiologies. However, the mechanisms underlying the regulation of neutrophil entry into the liver and their pathophysiological role during ALF development remain poorly characterized.

2025-04-02 | GSE201283 | GEO

Targeting Neutrophil Elastase in murine breast cancer tumors

Project description:To investigate the function of neutrophil elastase in breast cancer metastasis, as a function of time We then performed gene expression profiling analysis using data obtained from PyMT tumors (N=5 each) that are either WT or knockout for Neutrophil Elastase i.e. NEKO.

2023-10-21 | GSE217980 | GEO

Specific post-translational histone mod. of neutrophil extracellular traps as immunogens & potential SLE Ab targets.

Project description:This SuperSeries is composed of the following subset Series: GSE32542: Murine serum reactivity to common autoantigens in response to immunization with neutrophil extracellular traps GSE32543: Human and murine serum reactivity to specific histone posttranslational modifications in neutrophil extracellular traps Refer to individual Series

2012-01-26 | E-GEOD-32544 | biostudies-arrayexpress

Peptidylarginine deiminase 4 deficiency improves elastase-induced formation of neutrophil extracellular traps and emphysema in mouse lung

Project description:Neutrophil extracellular traps (NETs) are associated with the extracellular release of nuclear chromatin decorated with cytoplasmic proteins. Excessive release of NETs has been reported in chronic lung diseases, including chronic obstructive pulmonary disease (COPD). However, the role of NETs in the pathogenesis of COPD remains unclear. Peptidylarginine deaminase 4 (PAD4) contributes to NET formation. Therefore, in an elastase (ELS)-induced emphysema mouse model, we examined the role of PAD4 using the Padi4 gene knockout (KO) mice. First, we confirmed that ELS induced NET formation in the lungs. Although PAD4 deficiency did not affect the cellular profile of bronchoalveolar lavage fluid (BALF), PAD4 deficiency suppressed ELS-induced neutrophil migration and NET expression in the parenchyma of the lung. Additionally, PAD4 deficiency ameliorated emphysema and apoptosis in lung cells. Finally, we examined the effects of PAD4 on comprehensive gene expression signatures using RNA sequencing. Enrichment analysis of the transcriptomic data revealed that the expression of several genes associated with COPD pathogenesis was altered in the KO mice. Overall, the results suggest that PAD4 deficiency improves NET formation and emphysema in the lungs; this pathway can be a potential therapeutic target for the treatment of COPD.

2025-06-04 | GSE284684 | GEO

Neutrophil extracellular traps mediate articular cartilage damage and enhance the immunogenicity of cartilage components in rheumatoid arthritis

Project description:This study invesigates the effects of neutrophil extracellular traps (NETs) on articular cartilage degredation and resulting autoimmune responses in rheumatoid arthritis.

2020-08-10 | GSE150466 | GEO

Peptidylarginine deiminase 4 deficiency improves elastase-induced formation of neutrophil extracellular traps and emphysema in mouse lung

Project description:Peptidylarginine deiminase 4 deficiency improves elastase-induced formation of neutrophil extracellular traps and emphysema in mouse lung

| PRJNA1200037 | ENA

Proteomic analysis of neutrophil extracellular traps (healthy control, rheumatoid arthritis, systemic lupus erythematosus)_C4PR_LIV

Project description:Neutrophil Extracellular Traps (NETs) are chromatin-derived extracellular structures that are expelled from neutrophils in response to infectious or inflammatory stimuli. NET DNA structures are decorated with proteins including histones, myeloperoxidase and neutrophil elastase. NETs are implicated in the development of auto-immunity in diseases including rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) through the externalisation of intracellular neoepitopes e.g. dsDNA and nuclear proteins in SLE and citrullinated peptides in RA. The aim of this work was to use quantitative proteomics to identify and measure NET proteins produced by neutrophils from healthy individuals, and from patients with RA and SLE.

2019-02-18 | PXD011796 | Pride

Targeting Neutrophil Elastase in murine breast cancer tumors

Project description:Targeting Neutrophil Elastase in murine breast cancer tumors

| PRJNA901508 | ENA

Piezo1 induces neutrophil extracellular traps formation directing M1 macrophage differentiation

Project description:To research the neutrophil extracellular traps in the regulation of macrophages differentiation, we performed gene expression profiling analysis using data obtained from RNA-seq of mice and control with virus infection.

2024-07-10 | GSE220198 | GEO

The cytosolic DNA sensor cGAS recognizes Neutrophil Extracellular Traps

Project description:Neutrophil Extracellular Traps (NETs) are structures consisting of chromatin and antimicrobial molecules that are released by neutrophils during a form of regulated cell death called NETosis. NETs trap invading pathogens, promote coagulation and activate myeloid cells to produce Type I interferons (type I IFN), proinflammatory cytokines that regulate the immune system. The mechanism of NET recognition by myeloid cells is not yet clearly identified. Here we show that macrophages and other myeloid cells phagocytose NETs. Once in phagosomes, NETs translocate to the cytosol, where they activate the DNA sensor cyclic GMP-AMP synthase (cGAS) and induce type I IFN expression. cGAS recognizes the DNA backbone of NETs. Interestingly, the NET associated serine protease Neutrophil Elastase (NE) mediates the activation of the pathway. We confirmed that NETs activate cGAS in vivo. Thus, our findings identify cGAS as a major sensor of NETs, mediating the immune activation during infection and in auto-immune diseases.

2021-02-18 | PXD015579 | Pride

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