Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression changes between naïve and IL-1β + TGF-β2 dual cytokine licensed equine mesenchymal stem cells

ABSTRACT: Gene expression changes between naïve and IL-1β + TGF-β2 dual cytokine licensed equine mesenchymal stem cells

PROVIDER: PRJNA1078316 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR28014000_1.fastq.gz	Fastqsanger.gz
	SRR28014000_2.fastq.gz	Fastqsanger.gz
	SRR28014001_1.fastq.gz	Fastqsanger.gz
	SRR28014001_2.fastq.gz	Fastqsanger.gz
	SRR28014002_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 24

Similar Datasets

Gene expression changes between naïve and IL-1β + TGF-β2 dual cytokine licensed equine mesenchymal stem cells

Project description:The study objectives were to 1) determine mesenchymal stem cell (MSC) surface expression of major histocompatibility complex (MHC) class I and transcriptome-wide gene expression changes following IL-1β + TGF-β2 dual licensing and 2) evaluate if IL-1β + TGF-β2 dual licensed MSCs had greater ability to positively modulate tenocyte function compared to naïve MSCs.

2024-02-25 | GSE256139 | GEO

Expression in equine cartilage stimulated with IL-1β in vitro

Project description:The objective was to study the time-course effects of interleukin-1β (IL-1β) on equine articular cartilage, with the aim to identify genes of relevance for cartilage pathology in osteoarthritis. Changes in gene expression related to inflammation, extracellular matrix, and phenotypic alterations was studied.

2018-05-02 | GSE100083 | GEO

β2 ADRENERGIC SIGNALING STIMULATES EARLY IL-1β SECRETION IN MACROPHAGES BY INDUCING MAPK-DEPENDENT Il1b TRANSCRIPTION [ATAC-Seq]

Project description:Activating β2 adrenergic receptor (β2AR) on macrophages inhibits the expression of several proinflammatory cytokines, a phenomenon primarily associated with NF-κB inhibition. IL-1β is a hallmark inflammatory cytokine, and NF-κB plays a role in the transcriptional activation of Il1b in the priming phase of the NLRP3 inflammasome. Here, we report that contrarily to expectations, β2AR signaling stimulated transcription of the Il1b gene, either alone or in combination with TLR ligands. Moreover, in vivo experiments demonstrated that mice with increased sympathetic tonus (Adra2ac-/-) produced higher levels of IL-1β in a β2AR-dependent manner during alum-induced peritonitis. Assay for Transposase-Accessible Chromatin using Sequencing (ATAC-Seq) experiments, genome-wide analyses of clustered genomic regions and the utilization of pharmacological inhibitors revealed that β2AR-induced Il1b expression occurs in PKA-, MAP Kinases- and AP-1-dependent manner. Our findings describe that β2AR signaling can regulate macrophage effector function in a complex way that may involve gene-specific mechanisms increasing the expression of pro-inflammatory cytokines such as IL-1β.

2025-12-19 | GSE278578 | GEO

β2 ADRENERGIC SIGNALING STIMULATES EARLY IL-1β SECRETION IN MACROPHAGES BY INDUCING MAPK-DEPENDENT Il1b TRANSCRIPTION [RNA-Seq]

2025-12-19 | GSE278577 | GEO

β2 ADRENERGIC SIGNALING STIMULATES EARLY IL-1β SECRETION IN MACROPHAGES BY INDUCING MAPK-DEPENDENT Il1b TRANSCRIPTION [RNA-Seq]

Project description:β2 ADRENERGIC SIGNALING STIMULATES EARLY IL-1β SECRETION IN MACROPHAGES BY INDUCING MAPK-DEPENDENT Il1b TRANSCRIPTION [RNA-Seq]

| PRJNA1167809 | ENA

β2 ADRENERGIC SIGNALING STIMULATES EARLY IL-1β SECRETION IN MACROPHAGES BY INDUCING MAPK-DEPENDENT Il1b TRANSCRIPTION [ATAC-Seq]

Project description:β2 ADRENERGIC SIGNALING STIMULATES EARLY IL-1β SECRETION IN MACROPHAGES BY INDUCING MAPK-DEPENDENT Il1b TRANSCRIPTION [ATAC-Seq]

| PRJNA1167808 | ENA

Inflammasome-independent IL-1β activation via staphopain A protease of Staphylococcus aureus

Project description:Interleukin-1β (IL-1β) is a pivotal mediator of innate immunity, essential for orchestrating the acute inflammatory response. While the canonical activation of IL-1β involves cleavage of its inactive precursor (pro-IL-1β) by the inflammatory cysteine protease caspase-1, certain bacterial proteases, such as those secreted by group A Streptococcus and Pseudomonas aeruginosa, can also activate pro-IL-1β. In this study, we demonstrate that infection of human N/TERT-1 immortalized keratinocytes by Staphylococcus aureus induces IL-1β processing independently of the classical inflammasome pathways. Biochemical analysis reveals that a secreted factor from S. aureus cleaves pro-IL-1β at a site proximal to the canonical caspase-1 cleavage site, rendering the cytokine bioactive. Specifically, we identify the secreted cysteine protease staphopain A as responsible for this cleavage. Our findings highlight a novel mechanism of inflammasome-independent IL-1β activation through microbial proteases, expanding the understanding of pathogen-host interactions in immune responses, specifically in the skin.

2025-10-27 | PXD057289 | Pride

Equine Laminitis vs Control.

Project description:Equine lameller tissues were collected to compare normal vs laminitis generated differences in transcriptom level. Keywords: Laminitis, Equine, Diseased foot

2008-03-22 | GSE7360 | GEO

Antagonizing IL-1β to treat GBM

Project description:Monocytes and monocyte-derived macrophages (MDM) from blood circulation infiltrate and promote glioblastoma growth by, at least partially, expressing pro-inflammatory cytokine IL-1β . Using SC-RNA seq, we analyze how IL1a and IL1b differentially contibute to tumor growth.

2023-10-13 | GSE200348 | GEO

In vitro effects of equine autologous conditioned serum and autologous equine serum on inflamed chondrocyte pellets

Project description:The aim of the study was to investigate the effects of autologous equine serum (AES) incubated for 24 h and autologous conditioned serum (ACS) on inflamed equine chondrocyte pellets in vitro.

2023-04-19 | GSE152253 | 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