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FES Proto-Oncogene, Tyrosine Kinase
Pathway / Plaque inflammation

FES Proto-Oncogene, Tyrosine Kinase

FESgene

Tyrosine kinase modulating vascular smooth-muscle and endothelial inflammation; CAD and hypertension risk via arterial remodeling.

Pathway placement
Cascade stepPlaque inflammation
Confidencemedium
RationaleVascular smooth-muscle and endothelial signaling; inflammatory remodeling; pleiotropic CAD/hypertension.
Also acts inEndothelial activation/erosion
Druggability
DruggableYes
Known drugs / candidates0
Small-molecule tractableYes
Antibody tractableYes
EnsemblENSG00000182511

Type I vs Type II discrimination

ScoresType-II-associated
R — rupture / Type-I
—
C — confounder / Type-II
67
A — assay feasibility
52
E — evidence strength
95
T1DI (composite)
12
Specificity differential (R−C)-51.7
Confounder panel (Type-II drivers)
1sepsis / systemic inflammationn/a
2anemia / acute blood lossmag 2
3hypovolemia / dehydrationn/a
4tachyarrhythmian/a
5hypoxemia / respiratory failuren/a
6hypertensive emergencyn/a
7high-demand / peri-operative stressn/a
Coverage: 1/7 confounders with evidence
Tier: deep-scored (abstract-extracted) · 1 supporting references. 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
Whole blood — gene is not a circulating analyte; measure protein product or genotype
Collection tube
K2-EDTA whole blood (lavender-top)
Method / principle
SNP genotyping / sequencing; or immunoassay of encoded protein
Reagent / substrate
Allele-specific primers/probes (TaqMan) or NGS panel; or antibody for protein
Platform
qPCR / NGS / array
Turnaround · availability
Send-out · Genotyping widely available; protein assay variable

Human genetic evidence

0.539
Open Targets association (myocardial_infarction)
5
GWAS associations
Traits: myocardial infarction

Literature evidence(4)