Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA132745 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Human embryonic kidney cell (HEK293) were treated with PAR2 peptide agonist 2f-LIGRLO-NH2 (1.5h, 3h, 6h and 12h) or trypsin (6h). Comparison of genes similarly regulated by both treatments allowed better characterization of PAR2 induced response as both agonists had been reported as non-specific for PAR2.
2010-11-19 | GSE24332 | GEO
Project description:Human embryonic kidney cell (HEK293) were treated with PAR2 peptide agonist 2f-LIGRLO-NH2 (1.5h, 3h, 6h and 12h) or trypsin (6h). Comparison of genes similarly regulated by both treatments allowed better characterization of PAR2 induced response as both agonists had been reported as non-specific for PAR2. Six conditioned experiments with 3 replicates each. Individual grown and harvested.
2010-11-19 | E-GEOD-24332 | biostudies-arrayexpress
Project description:A point mutation in GPCR-protease activated receptor-2 (F2RL1) renders PAR2 insensitive to FXa/Matriptase-dependent activation. We characterized the of impact of the PAR-2 G37I mutation on immune cell populations and gene expression in the gut.
2025-12-05 | GSE283949 | GEO
Project description:Coagulation protease signaling within the tumor-microenvironment (TME) causes cancer immune evasion and impairs immune checkpoint-inhibitor therapy. Tumor-associated macrophages produce factor X and drive immune-evasive protease activated receptor-2 (PAR2) signaling. Myeloid FXa-PAR2 signaling promotes the enrichment of resident-like macrophages displaying an immunosuppressive repair phenotype within the TME of mice with genetically induced spontaneous breast cancer development. Conversely, loss of FXa-PAR2 signaling favors the expansion of monocyte-derived macrophage subsets relevant for DNA-sensing, autophagy and cGAS-STING-IFNβ mediated stimulation of anti-tumor immunity. Thereby FXa suppresses the function of CD103+ dendritic cells relevant for priming, reactivation, and expansion of CD8+ T-cells, including antigen-experienced progenitor exhausted T-cells. Our findings thus emphasize the translational potential of FXa inhibition to synergize with immunotherapy.ompacted abstract
2025-07-09 | GSE214518 | GEO
Project description:MASLD and its more severe version, MASH, are attributable to metabolic dysfunction and are associated with cardiometabolic disease, atherothrombosis, and obesity. The exact pathophysiological mechanisms linking MASLD and CVD have yet to be elucidated but share common metabolic abnormalities that could interact synergistically to increase the risk of both heart disease and liver disease. Protease-activated receptor 2 (PAR2), a receptor activated by prothrombotic coagulation proteases that are dysregulated in inflammatory and fibrotic diseases, is emerging as a new drug target for MASH. Using patient samples, we discovered that expression of liver PAR2 is increased in the livers of obese patients with MASLD and MASH.To address the direct contribution of hepatocyte PAR2 to progression of MASLD and obesity, we fed hepatocyte-specific PAR2 knockout mice(PAR2dHep), whole-body PAR2-deficient mice(PAR2 KO), and control floxed WT mice(PAR2fl/fl) high-fat diet and conducted metabolic, biochemical and RNA-seq analyses. Hepatocyte-specific deletion of PAR2 caused a reduction in body weight and significantly lowered triglycerides and cholesterol levels in plasma and livers of mice fed high-fat diet. Analysis of bulk liver RNA seq data showed that global or hepatocyte-specific deletion of PAR2 resulted in significant improvements in fatty acid metabolic and reverse cholesterol transport pathways in liver.These data provide support that targeting hepatic PAR2 may potentially provide broad liver and cardiometabolic benefits to patients with MASLD and MASH.
2026-05-20 | GSE319296 | GEO
Project description:Protease-activated receptor 2 (PAR2) is a central regulator of intestinal barrier function, inflammation and pain. Upregulated intestinal proteolysis and PAR2-signaling are implicated in inflammatory bowel diseases (IBDs) and irritable bowel syndrome (IBS), conditions often associated with gut microbiome alterations. To identify potential bacterial regulators of PAR2 activity, we developed a functional assay for PAR2 processing and screened a library of diverse gut microbes. We found that multiple bacteria secrete proteases that cleave host PAR2. Using chemoproteomic profiling with a covalent irreversible inhibitor, we uncovered a previously uncharacterized Bacteroides fragilis serine protease 1 (Bfp1) and show that it cleaves and activates PAR2 in multicellular and murine models. PAR2 cleavage by Bfp1 disrupts the intestinal barrier, sensitizes nociceptors, and triggers colonic inflammation and abdominal pain. Collectively, our findings uncover Bfp1-mediated PAR2-processing as a new axis of host-commensal-interaction in the gut that has the potential to be targeted for therapeutic intervention in IBD or IBS.
2025-09-28 | PXD059166 | Pride
Project description:The mechanisms of allergen sensing and type 2 immune response initiation remain unclear. Using a house dust mite (HDM)-induced allergic airway model, we demonstrated that host detection of protease activity in HDM was crucial for initiating T helper type 2 (Th2) responses. This process was driven by the major allergen Der p 1, a cysteine protease, which was sensed by protease-activated receptor 2 (PAR2) on a novel population of perivascular lung macrophages expressing Ly6G and nuclear receptor Nur77. These macrophages required PAR2 and Nur77 for activation and accumulation and regulated conventional dendritic cell (mDC) migration to draining mediastinal lymph nodes (mLN) via cysteinyl leukotriene (CysLTs) production. CysLTs enhanced CCR7-driven migration of mDCs toward its ligand, CCL21, facilitating arrival to mLNs for T cell priming and expansion. Inhibiting CysLTs biosynthesis reduced mDC migration and dampened Th2 allergic responses, highlighting new therapeutic paths and mechanisms in type 2 immunity.
2025-12-10 | GSE305119 | GEO
Project description:The mechanisms of allergen sensing and type 2 immune response initiation remain unclear. Using a house dust mite (HDM)-induced allergic airway model, we demonstrated that host detection of protease activity in HDM was crucial for initiating T helper type 2 (Th2) responses. This process was driven by the major allergen Der p 1, a cysteine protease, which was sensed by protease-activated receptor 2 (PAR2) on a novel population of perivascular lung macrophages expressing Ly6G and nuclear receptor Nur77. These macrophages required PAR2 and Nur77 for activation and accumulation and regulated conventional dendritic cell (mDC) migration to draining mediastinal lymph nodes (mLN) via cysteinyl leukotriene (CysLTs) production. CysLTs enhanced CCR7-driven migration of mDCs toward its ligand, CCL21, facilitating arrival to mLNs for T cell priming and expansion. Inhibiting CysLTs biosynthesis reduced mDC migration and dampened Th2 allergic responses, highlighting new therapeutic paths and mechanisms in type 2 immunity.
2025-12-10 | GSE291081 | GEO
Project description:The mechanisms of allergen sensing and type 2 immune response initiation remain unclear. Using a house dust mite (HDM)-induced allergic airway model, we demonstrated that host detection of protease activity in HDM was crucial for initiating T helper type 2 (Th2) responses. This process was driven by the major allergen Der p 1, a cysteine protease, which was sensed by protease-activated receptor 2 (PAR2) on a novel population of perivascular lung macrophages expressing Ly6G and nuclear receptor Nur77. These macrophages required PAR2 and Nur77 for activation and accumulation and regulated conventional migratory dendritic cell (mDC) migration to draining mediastinal lymph nodes (mLN) via cysteinyl leukotriene (CysLTs) production. CysLTs enhanced CCR7-driven migration of mDCs toward its ligand, CCL21, facilitating arrival to mLNs for T cell priming and expansion. Inhibiting CysLTs biosynthesis reduced mDC migration and dampened Th2 allergic responses, highlighting new therapeutic paths and mechanisms in type 2 immunity.
2025-12-10 | GSE289548 | GEO
Project description:Epidermal transient receptor potential (TRP) channels are involved in complex interactions between the peripheral nervous system and the immune system in atopic dermatitis (AD). Recently, we identified that TRPV3 interacts with protease-activated receptor 2 (PAR2) to mediate non-histaminergic itch. However, the downstream molecular mechanisms following TRPV3 activation in keratinocytes remain unclear.This study aims to investigate whether TRPV3 channels regulate mast cells in the context of AD.
2026-01-01 | GSE297292 | GEO