Proteinase 3
PRTN3proteinProteinase 3 released by activated neutrophils degrades fibrous-cap matrix proteins, promoting cap thinning and rupture.
Pathway placement
Cascade stepFibrous-cap degradation & rupture
Confidencehigh
RationaleNeutrophil serine protease; extracellular matrix degradation; cap destabilization.
Also acts inVascular inflammation
Druggability
DruggableYes
Known drugs / candidates0
Small-molecule tractableYes
Antibody tractableYes
EnsemblENSG00000196415
Type I vs non-Type I discrimination
ScoresLow-confidence (proxy)
R — rupture / Type-I55
C — non-Type-I64
A — assay feasibility68
E — evidence strength28
T1DI (composite)9
Specificity differential (R−C)-9
Non-Type-I axis panel
Does this marker also move in each non-Type-I setting? mag 0–3; higher means less Type-I-specific. n/a = no evidence retrieved, which is not the same as no change.
No non-Type-I axis 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)
- Novel Insights Into the Effects of Interleukin 6 Antagonism in Non-ST-Segment-Elevation Myocardial Infarction Employing the SOMAscan Proteomics Platform.Journal of the American Heart Association · 2020 · PMID 32515246 · doi