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RE1-silencing transcription factor
Pathway / Off-pathway / systemic markers

RE1-silencing transcription factor

RESTgene

Repressor element-1 silencing transcription factor; general chromatin remodeling, unrelated to atherothrombosis.

Pathway placement
Cascade stepOff-pathway / systemic markers
Confidencelow
RationaleChromatin regulator; neuronal/general transcription factor, no atherothrombotic mechanism.
Druggability
DruggableNo
Known drugs / candidates0
Small-molecule tractableNo
Antibody tractableNo
EnsemblENSG00000084093

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
5
T1DI (composite)
1
Specificity differential (R−C)-52
Confounder panel (Type-II drivers)
1sepsis / systemic inflammationn/a
2anemia / acute blood lossn/a
3hypovolemia / dehydrationn/a
4tachyarrhythmian/a
5hypoxemia / respiratory failuremag 2
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

0.531
Open Targets association (myocardial_infarction)
2
GWAS associations
Traits: myocardial infarction

Literature evidence(0)

No direct literature mentions harvested; included via genetic/target evidence.

Omics datasets(2)