Jun proto-oncogene, AP-1 transcription factor subunit

JUNgene

JUN orchestrates inflammatory gene programs destabilizing atherosclerotic plaques.

Pathway placement

Cascade stepPlaque inflammation

Confidencehigh

RationaleInflammatory transcription hub; regulates immune activation and vascular remodeling.

Also acts inCap degradation / rupture, Endothelial activation/erosion

Druggability

DruggableYes

Known drugs / candidates0

Small-molecule tractableYes

Antibody tractableNo

EnsemblENSG00000177606

Type I vs Type II discrimination

ScoresShared / rises in both

R — rupture / Type-I

C — confounder / Type-II

A — assay feasibility

E — evidence strength

T1DI (composite)

Specificity differential (R−C)0

Confounder panel (Type-II drivers)

1sepsis / systemic inflammationn/a

2anemia / acute blood lossn/a

3hypovolemia / dehydrationn/a

4tachyarrhythmian/a

5hypoxemia / respiratory failuren/a

6hypertensive emergencyn/a

7high-demand / peri-operative stressmag 2

Coverage: 1/7 confounders with evidence

Tier: deep-scored (abstract-extracted) · 2 supporting references. See the discrimination table for all markers.

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