Complement C1s serine protease
C1SgeneC1S genetic variants amplify complement-driven vascular inflammation increasing atherosclerotic instability risk.
Pathway placement
Cascade stepPlaque inflammation
Confidencemedium
RationaleClassical complement; genetic involvement in atherosclerotic plaque instability.
Druggability
DruggableYes
Known drugs / candidates2
Small-molecule tractableYes
Antibody tractableYes
EnsemblENSG00000182326
Type I vs non-Type I discrimination
ScoresLow-confidence (proxy)
R — rupture / Type-I50
C — non-Type-I62
A — assay feasibility52
E — evidence strength26
T1DI (composite)6
Specificity differential (R−C)-11.8
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
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
Literature evidence(2)
- Multi-omics data integration from patients with carotid stenosis illuminates key molecular signatures of atherosclerotic instability.Genome medicine · 2026 · PMID 41652626 · doi
- Proteomic insights into the associations between obesity, lifestyle factors, and coronary artery disease.BMC medicine · 2023 · PMID 38049831 · doi