Bruton Tyrosine Kinase
BTKproteinBTK amplifies macrophage activation and lipid uptake into foam cells, accelerating plaque inflammation and destabilization.
Pathway placement
Cascade stepPlaque inflammation
Confidencehigh
RationaleMacrophage and B-cell kinase; drives foam-cell formation and inflammatory signaling in the atherosclerotic plaque.
Also acts inPlatelet activation
Druggability
DruggableYes
Known drugs / candidates24
Small-molecule tractableYes
Antibody tractableYes
EnsemblENSG00000010671
Type I vs Type II discrimination
ScoresLow-confidence (proxy)
R — rupture / Type-I65
C — confounder / Type-II81
A — assay feasibility72
E — evidence strength31
T1DI (composite)9
Specificity differential (R−C)-15.7
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)
- Key immune-related hub genes BTK, ITGAL and PTX3 mediate macrophage phenotypic shift and foam cell formation in the periodontitis-atherosclerosis axis.Molecular biology reports · 2025 · PMID 41231296 · doi