gene

LDLR

Entity Detail — Knowledge Graph Node

Understanding Entity Pages

This page aggregates everything SciDEX knows about LDLR: its mechanistic relationships (Knowledge Graph edges), hypotheses targeting it, analyses mentioning it, and supporting scientific papers. The interactive graph below shows its immediate neighbors. All content is AI-synthesized from peer-reviewed literature.

1318Connections

4Hypotheses

4Analyses

50Outgoing

50Incoming

0Experiments

4Debates

Summary

LDLR is a gene implicated in neurodegeneration research. Key relationships include: associated with, inhibits, regulates. Associated with ADH, ALS, ALZHEIMER'S DISEASE. Connected to 499 entities in the SciDEX knowledge graph.

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🧬 Gene Info

Gene Symbol	LDLR
Chromosome	19p13.2
Protein Type	Receptor
Target Class	Receptor
Function	LDL Binding: Extracellular domain binds circulating LDL (containing cholesterol and triglycerides)
Mechanism of Action	Upregulation through PCSK9 inhibition or direct receptor modulation
Druggability	High (0.75)
Clinical Stage	Approved
Amino Acids	860 aa
Exons	18
Pathways	Cholesterol, Cholesterol Metabolism, Complement, EGFR_signaling, Endocytosis
UniProt ID	H0YMD1
Ensembl ID	ENSG00000130164
GeneCards	LDLR
Human Protein Atlas	LDLR
Associated Diseases	ADH, Aging, Als, Alzheimer, Alzheimer's disease
Known Drugs/Compounds	25-Hydroxycholesterol, lipid_lowering_medications, statins
Interactions	AB, ABCA1, abca2, ABCA2, ACETYL-COA, Actin
SciDEX Target	View Target Profile (8 clinical trials)
SciDEX Hypotheses	FcRn Transport Bypass Strategy
KG Connections	1318 knowledge graph edges
Databases	GeneCards NCBI Gene HPA STRING

🔮 Predicted Structure: LDLR — AlphaFold H0YMD1 Click to expand

AI-predicted structure from AlphaFold | Powered by Mol*

Wiki Pages (4)

Knowledge base pages for this entity

Canonical Page

Pathway Diagram

graph TD
    LDLR["LDLR"] -->|"interacts"| ABCA1["ABCA1"]
    LDLR["LDLR"] -->|"interacts"| SREBF2["SREBF2"]
    LDLR["LDLR"] -->|"studied in"| neurodegeneration["neurodegeneration"]
    LDLR["LDLR"] -->|"associated"| neurodegeneration_1["neurodegeneration"]
    LDLR["LDLR"] -->|"interacts"| APOE["APOE"]
    LDLR["LDLR"] -->|"interacts"| LRP1["LRP1"]
    ABCA1_2["ABCA1"] -->|"interacts"| LDLR["LDLR"]
    SREBF2_3["SREBF2"] -->|"interacts"| LDLR["LDLR"]
    APOE_4["APOE"] -->|"interacts"| LDLR["LDLR"]
    LRP1_5["LRP1"] -->|"interacts"| LDLR["LDLR"]
    style LDLR fill:#4a1a6b,stroke:#4fc3f7,stroke-width:2px,color:#e0e0e0

Outgoing (803)

Target	Relation	Type	Str
LDL	regulates	protein	0.97
familial hypercholesterolemia	causes	disease	0.95
Familial Hypercholesterolemia	associated_with	disease	0.95
Autosomal Dominant Hypercholesterolemia	risk_factor_for	disease	0.95
Variant Classification	involved_in	process	0.90
LDL Cholesterol Metabolism	involved_in	process	0.90
lipid metabolism	participates_in	pathway	0.90
Lipid Metabolism	regulates	pathway	0.90
oxidative stress response	participates_in	pathway	0.90
MICROGLIA	regulates_activation	cell_type	0.90
Brain Apoe Levels	downregulates	biomarker	0.90
Tau Pathology	suppresses	phenotype	0.90
Cholesterol Transport	involved_in	process	0.90
cholesterol metabolism	participates_in	pathway	0.90
cardiovascular disease	contributes_to	disease	0.90
LDL cholesterol	regulates	phenotype	0.90
APOE	activates	gene	0.90
Tau Pathology	inhibits	phenotype	0.85
LIPID METABOLISM	regulates	entity	0.85
Pulmonary Arterial Hypertension	implicated_in	disease	0.85
Pulmonary Arterial Hypertension	involved_in	disease	0.85
Neurodegeneration	protects_against	process	0.85
Als	inhibits	disease	0.85
Microglial Activation	suppresses	process	0.85
Endothelial Dysfunction	contributes_to	phenotype	0.80
Vascular Remodeling	contributes_to	process	0.80
Interleukin-17C	interacts_with	protein	0.80
coronary artery disease	associated_with	disease	0.80
Microglial Immunometabolism	modulates	process	0.80
Microglial Activation	inhibits	process	0.80
cholesterol	regulates	protein	0.80
Cholesterol	regulates	pathway	0.80
hypercholesterolemia	associated_with	disease	0.79
FAMILIAL_HYPERCHOLESTEROLEMIA	associated_with	disease	0.76
neurodegeneration	inhibits	phenotype	0.75
OXIDATIVE STRESS	regulates	entity	0.75
Atherosclerosis	activates	disease	0.75
Oligodendrocyte Progenitor Cell Expansion	upregulates	process	0.75
Myelin Integrity	protects_against	phenotype	0.75
Als	associated_with	disease	0.75
Neurodegeneration	inhibits	disease	0.75
Inflammatory Pathway	interacts_with	pathway	0.75
Als	activates	disease	0.75
Aging	associated_with	disease	0.75
Reactive Astrocyte Activation	suppresses	process	0.75
Cardiovascular	regulates	disease	0.75
Atherosclerosis	regulates	disease	0.75
Cardiovascular	activates	disease	0.75
Oligodendrocyte Progenitor Cells	modulates	cell_type	0.75
ADH	causes	disease	0.72

Incoming (515)

Source	Relation	Type	Str
TDP-43	binds	protein	1.00
PCSK9	inhibits	protein	0.95
MAFF	regulates	protein	0.90
statins	activates	drug	0.90
TNF	upregulates	protein	0.90
h-9d29bfe5	targets_gene	hypothesis	0.90
h-a87702b6	targets_gene	hypothesis	0.90
h-9d16afa0	targets_gene	hypothesis	0.90
h-b948c32c	targets_gene	hypothesis	0.90
APOE	co_mentioned_with	gene	0.90
h-64d92165	targets_gene	hypothesis	0.90
IDOL	inhibits	protein	0.85
GOLIATH	inhibits	protein	0.85
RNF130	inhibits	protein	0.85
BACH1	inhibits	protein	0.85
SREBF1	regulates	protein	0.85
25-Hydroxycholesterol	modulates	compound	0.85
NTS	correlates_with	gene	0.80
h-9d29bfe5	targets	hypothesis	0.80
γ-secretase	modifies	protein	0.80
APOE4	binds	protein	0.80
h-b948c32c	targets	hypothesis	0.80
CSF2	correlates_with	gene	0.80
ASGR1	regulates	protein	0.80
BMP1	modifies	protein	0.80
MT1-MMP	modifies	protein	0.80
APOE2	binds_weakly	protein	0.80
IL13RA1	correlates_with	gene	0.80
CCR9	correlates_with	gene	0.80
EGFR	interacts_with	gene	0.80
TMEM55B	regulates	protein	0.80
inflammation	inhibits	phenotype	0.80
APOE3	binds	protein	0.80
GPX4	transports	gene	0.70
GFAP	disrupts	gene	0.70
BMP	inhibits	gene	0.70
IDE	regulates	gene	0.70
CREB	regulates	gene	0.70
APOE	expresses	gene	0.70
ABCA1	protects_against	gene	0.70
CD2AP	activates	gene	0.70
APOE	targets	gene	0.70
ABCA1	targets	gene	0.70
ABCA1	expresses	gene	0.70
CHAT	mediates	gene	0.70
ENDOTHELIAL	activates	cell_type	0.70
LDL	activates	gene	0.70
CHOLESTEROL	causes	phenotype	0.70
CHOLESTEROL	destabilizes	phenotype	0.70
NEURODEGENERATION	inhibits	gene	0.70

Targeting Hypotheses (4)

Hypotheses where this entity is a therapeutic target

Hypothesis	Score	Disease	Analysis
LDLR Ligand-Binding Domain A Fusion for Receptor-Mediated Tr	0.650	neurodegeneration	Blood-brain barrier antibody transport m
APOE4 preferentially signals through LRP1 over LDLR, alterin	0.610	neuroscience	APOE4-driven lipid metabolism dysregulat
FcRn Transport Bypass Strategy	0.583	neuropharmacology	What is the actual quantitative contribu
Poorly lipidated APOE4 particles are preferentially routed t	0.340	molecular biology	Does APOE4's reduced lipid-binding direc

Mentioning Analyses (4)

Scientific analyses that reference this entity

Experiments (0)

Experimental studies targeting or related to this entity

Experiment	Type	Disease	Score	Feasibility	Model	Status	Est. Cost
No experiments found

Related Papers (0)

Scientific publications cited in analyses involving this entity

Title & PMID	Authors	Journal	Year	Citations
No papers found

Debates (4)

Multi-agent debates referencing this entity

LDLR

Understanding Entity Pages

Summary

Wiki Pages (4)

LDLR Gene

LDLRAD3 (LDLR Adapter Protein 1) Protein

LDLRAP1 — Low Density Lipoprotein Receptor Adaptor Protein 1

LDLR Protein (Low-Density Lipoprotein Receptor)

Pathway Diagram

Outgoing (803)

Incoming (515)

Targeting Hypotheses (4)

Mentioning Analyses (4)

What is the actual quantitative contribution of FcRn-mediated transcytosis to BB

CRISPR-based therapeutic approaches for neurodegenerative diseases

Blood-brain barrier transport mechanisms for antibody therapeutics

Lipid raft composition changes in synaptic neurodegeneration

Experiments (0)

Related Papers (0)

Debates (4)

What is the actual quantitative contribution of FcRn-mediated transcytosis to BB

Investigate how lipid raft composition (cholesterol metabolism, sphingolipids) c

Anti-amyloid antibodies (lecanemab, donanemab) have ~0.1% brain penetrance. Engi

Evaluate the potential of CRISPR/Cas9 and related gene editing technologies for