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LDL Receptor
Pathway / Lipid retention & oxidation

LDL Receptor

LDLRgene

LDLR mediates LDL endocytosis; mutations impair LDL clearance, driving lipid retention and accelerated atherogenesis.

Pathway placement
Cascade stepLipid retention & oxidation
Confidencehigh
RationaleLDL clearance and uptake regulation; LDLR deficiency causes hypercholesterolemia and early atherosclerosis.
Druggability
DruggableYes
Known drugs / candidates0
Small-molecule tractableYes
Antibody tractableYes
EnsemblENSG00000130164

Type I vs Type II discrimination

ScoresType-II-associated
R — rupture / Type-I
0
C — confounder / Type-II
67
A — assay feasibility
52
E — evidence strength
42
T1DI (composite)
4
Specificity differential (R−C)-66.7
Confounder panel (Type-II drivers)
1sepsis / systemic inflammationmag 2
2anemia / acute blood lossn/a
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) · 15 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

0.689
Open Targets association (myocardial_infarction)
5
GWAS associations
Traits: myocardial infarction

Literature evidence(17)

Clinical trials(3)

Omics datasets(1)