Protease-activated receptor 2
F2RL1proteinPAR-2 activation by trypsin amplifies vascular inflammation and monocyte/macrophage infiltration destabilizing the atherosclerotic plaque.
Pathway placement
Cascade stepPlaque inflammation
Confidencehigh
RationaleG-protein-coupled receptor activated by trypsin; drives leukocyte recruitment and pro-inflammatory signaling.
Also acts inCap degradation / rupture
Druggability
DruggableYes
Known drugs / candidates0
Small-molecule tractableYes
Antibody tractableYes
EnsemblENSG00000164251
Type I vs Type II discrimination
ScoresLow-confidence (proxy)
R — rupture / Type-I60
C — confounder / Type-II54
A — assay feasibility68
E — evidence strength24
T1DI (composite)9
Specificity differential (R−C)+5.3
Confounder panel (Type-II drivers)
No confounder evidence retrieved.
Tier: light (literature co-occurrence proxy — lower confidence). See the discrimination table for all markers.
Assay & specimen
Class-level default (no specific cleared assay)— generic method inferred from analyte class; confirm against a specific product insert before use.
Specimen
Serum or plasma
Collection tube
Serum separator (gold/red-top, SST) · K2/K3-EDTA (lavender-top)
Method / principle
Sandwich immunoassay (ELISA) — research-grade unless a cleared assay exists
Reagent / substrate
Matched anti-target antibody pair (capture + labeled detection)
Platform
ELISA microplate or multiplex (Luminex/MSD)
Turnaround · availability
Send-out / research · Research-grade (no universal clinical assay)
Literature evidence(1)
- Expression of ectopic trypsin in atherosclerotic plaques and the effects of aprotinin on plaque stability.Archives of biochemistry and biophysics · 2020 · PMID 32603715 · doi