Protein / target

Prolow-density lipoprotein receptor-related protein 1

Encoded byLRP1Q07954Homo sapiensSwiss-Prot

UniProt: Q07954 Ensembl: ENSG00000123384 HGNC: HGNC:6692 NCBI Gene: 4035

Clinical-stage

Therapeutic maturity

Clinical candidates

Antibody-tractable

Druggability

GO CC high conf

Research papers

Protein at a glance

Biological role

Low-density lipoprotein particle receptor

Strongest disease association

Neurodegenerative Diseases

Via encoding gene LRP1 · Pathway evidence · score 0.51

Therapeutic position

Clinically advancing target

Research activity

Emerging research

2 papers · latest 2012

Derived from structured UniProt, Open Targets and literature data on this page.

Protein profile

UniProt 2026_02

Canonical identity and biological annotation from UniProt.

Function overview

Endocytic receptor involved in endocytosis and in phagocytosis of apoptotic cells.

View complete UniProt function annotation

Endocytic receptor involved in endocytosis and in phagocytosis of apoptotic cells (PubMed:11907044, PubMed:12713657). Required for early embryonic development (By similarity). Involved in cellular lipid homeostasis. Involved in the plasma clearance of chylomicron remnants and activated LRPAP1 (alpha 2-macroglobulin), as well as the local metabolism of complexes between plasminogen activators and their endogenous inhibitors. Acts as an LRPAP1 alpha-2-macroglobulin receptor (PubMed:1702392, PubMed:26142438). Acts as TAU/MAPT receptor and controls the endocytosis of TAU/MAPT as well as its subsequent spread (PubMed:32296178). May modulate cellular events, such as APP metabolism, kinase-dependent intracellular signaling, neuronal calcium signaling as well as neurotransmission (PubMed:12888553). Also acts as a receptor for IGFBP3 to mediate cell growth inhibition (PubMed:9252371)

Subcellular location

Cell membraneMembrane, coated pitCytoplasmNucleusGolgi outpostCytoplasm, cytoskeleton, microtubule organizing center

Domains and Gene Ontology detail (114)

Domains & features

LDL-receptor class A 1LDL-receptor class A 2EGF-like 1EGF-like 2; calcium-bindingEGF-like 3EGF-like 4LDL-receptor class A 3LDL-receptor class A 4LDL-receptor class A 5LDL-receptor class A 6LDL-receptor class A 7LDL-receptor class A 8LDL-receptor class A 9LDL-receptor class A 10EGF-like 5EGF-like 6

Gene Ontology

Cbasolateral plasma membrane
Cclathrin-coated pit
Ccytosol
Cearly endosome
Cendocytic vesicle membrane
Cfocal adhesion
Clysosomal membrane
Cmembrane
Cmicrotubule organizing center
Cnucleolus
Cplasma membrane
Cplasma membrane protein complex

4544 aa · 505 kDa · 2 isoforms

Biological roles

What this protein does, drawn together from its UniProt function, Gene Ontology terms and Reactome pathways.

Lipid & lipoprotein metabolismGOCell migrationGOCell adhesionGO

View supporting evidence

Lipid & lipoprotein metabolism

·apolipoprotein binding
·apolipoprotein receptor activity
·lipoprotein particle receptor binding
·low-density lipoprotein particle receptor activity

Cell migration

·negative regulation of smooth muscle cell migration

Cell adhesion

·regulation of extracellular matrix disassembly
·regulation of extracellular matrix organization

Concepts derived from UniProt GO Reactome — each badge above shows which sources supported that role.

Translational evidence

Open Targets 26

Why this target matters therapeutically, strongest evidence first. Disease associations are gene-level (via the gene that encodes this protein) and open into the full confidence synthesis; the development universe, tractability and safety annotations are target-level, from Open Targets.

Strongest disease associations · via encoding gene LRP1

Gene-level evidence surfaced through the gene LRP1that encodes this protein — not a direct protein–disease relationship. Ranked by Forefront's causal-directness weighting, so genetically- and clinically-evidenced diseases lead over ones that merely share the literature.

Alzheimer's Disease

0.39Preliminary

Pathway evidence dominant · Open Targets 0.46 · no direct causal or clinical evidence

Neurodegenerative Diseases

0.35Preliminary

Pathway evidence dominant · Open Targets 0.51 · no direct causal or clinical evidence

Parkinson's Disease

0.32Preliminary

Pathway evidence dominant · Open Targets 0.44 · no direct causal or clinical evidence

Multiple Sclerosis

0.30Preliminary

Pathway evidence dominant · Open Targets 0.44 · no direct causal or clinical evidence

Lysosomal Storage Diseases

0.28Preliminary

Pathway evidence dominant · Open Targets 0.43 · no direct causal or clinical evidence

View evidence synthesis (5)

Alzheimer's DiseasePreliminary

0.39

agreement 0.21–0.56

Pathway67%Literature33%

Open Targets aggregate 0.46 · 2 independent evidence families · no direct causal or clinical evidence

Neurodegenerative DiseasesPreliminary

0.35

agreement 0.17–0.53

Pathway95%Literature5%

Open Targets aggregate 0.51 · 2 independent evidence families · no direct causal or clinical evidence

Parkinson's DiseasePreliminary

0.32

agreement 0.14–0.50

Pathway86%Literature14%

Open Targets aggregate 0.44 · 2 independent evidence families · no direct causal or clinical evidence

Multiple SclerosisPreliminary

0.30

agreement 0.12–0.47

Pathway94%Literature6%

Open Targets aggregate 0.44 · 2 independent evidence families · no direct causal or clinical evidence

Lysosomal Storage DiseasesPreliminary

0.28

agreement 0.06–0.51

Pathway100%

Open Targets aggregate 0.43 · 1 independent evidence family · no direct causal or clinical evidence

This ranking differs from Open Targets' own: re-weighting moves genetically-evidenced diseases above more heavily co-mentioned ones. The evidence agreement range shows how closely the independent evidence families agree — it is not a statistical confidence interval, and nothing here is fitted to outcome data. Derived from Open Targets evidence types under Forefront weighting; the per-type scores above show the calculation.

Show all associations

Neurodegenerative Diseases0.51

Alzheimer's Disease0.46

Parkinson's Disease0.44

Multiple Sclerosis0.44

Lysosomal Storage Diseases0.43

Drug development

1 compounds recorded · 1 in clinical development

Open Targets' development universe — every compound recorded against the target at any stage, not all approved medicines.

View all recorded compounds (1)

ANG1005Phase 3

Open Targets known-drugs universe. Drug name and highest clinical stage only — the disease relationship is NOT read from this slice (it carries trial-context noise); approved indications come from the canonical graph above.

Tractability

Antibodies — Emerging

Feasibility evidence (go cc high conf and uniprot loc med conf) — no clinical-stage drug of this modality recorded.

Protein degraders — Emerging

Feasibility evidence (database ubiquitination and half-life data) — no clinical-stage drug of this modality recorded.

Other modalities — Strong

Advanced Clinical support this modality.

View underlying tractability evidence (7)

AB · GO CC high confAB · UniProt loc med confAB · UniProt SigP or TMHMMAB · Human Protein Atlas locPR · Database UbiquitinationPR · Half-life DataOC · Advanced Clinical

Raw Open Targets tractability assessment buckets, by modality.

Research activity

2 papers · to 2012

Papers linked directly to this protein. This is the protein's own literature — descriptor-derived papers are kept separate below.

Most cited

Apolipoprotein E and apolipoprotein E receptors: normal biology and roles in Alzheimer disease.606 cites

Holtzman DM · Cold Spring Harbor perspectives in medicine · 2012

Reelin and ApoE receptors cooperate to enhance hippocampal synaptic plasticity and learning.481 cites

Weeber EJ · The Journal of biological chemistry · 2002

Recent

Apolipoprotein E and apolipoprotein E receptors: normal biology and roles in Alzheimer disease.

Holtzman DM · Cold Spring Harbor perspectives in medicine · 2012

Reelin and ApoE receptors cooperate to enhance hippocampal synaptic plasticity and learning.

Weeber EJ · The Journal of biological chemistry · 2002

Europe PMC papers linked directly to this protein.