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Protein / target

Apolipoprotein A-I

Encoded byAPOA1P02647Homo sapiensSwiss-Prot
Small-molecule tractable
Druggability
Structure with Ligand
4
Research papers

Protein at a glance

Biological role

Phosphatidylcholine-sterol O-acyltransferase activator

Strongest disease association

Amyloidosis

Via encoding gene APOA1 · Genetic literature evidence · score 0.61

Research activity

Emerging research

4 papers · latest 2025

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

Participates in the reverse transport of cholesterol from tissues to the liver for excretion by promoting cholesterol efflux from tissues and by acting as a cofactor for the lecithin cholesterol acyltransferase (LCAT).

View complete UniProt function annotation

Participates in the reverse transport of cholesterol from tissues to the liver for excretion by promoting cholesterol efflux from tissues and by acting as a cofactor for the lecithin cholesterol acyltransferase (LCAT). As part of the SPAP complex, activates spermatozoa motility

Subcellular location

Secreted
Domains and Gene Ontology detail (74)

Gene Ontology

  • Cblood microparticle
  • Cchylomicron
  • Ccytoplasmic vesicle
  • Ccytosol
  • Cearly endosome
  • Cendocytic vesicle
  • Cendocytic vesicle lumen
  • Cendoplasmic reticulum lumen
  • Cextracellular exosome
  • Cextracellular region
  • Cextracellular space
  • Cextracellular vesicle

267 aa · 31 kDa

Biological roles

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

Lipid & lipoprotein metabolismUniProt · GOCell migrationGOImmune signallingGOCell adhesionGO
View supporting evidence

Lipid & lipoprotein metabolism

  • ·Participates in the reverse transport of cholesterol from tissues to the liver for excre…
  • ·high-density lipoprotein particle
  • ·low-density lipoprotein particle
  • ·spherical high-density lipoprotein particle

Cell migration

  • ·negative chemotaxis

Immune signalling

  • ·negative regulation of cytokine production involved in immune response
  • ·negative regulation of inflammatory response
  • ·negative regulation of interleukin-1 beta production
  • ·negative regulation of response to cytokine stimulus

Cell adhesion

  • ·negative regulation of cell adhesion molecule production
  • ·negative regulation of heterotypic cell-cell adhesion

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 APOA1

Gene-level evidence surfaced through the gene APOA1that 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.

Amyloidosis
0.54Moderately supported

Genetic literature evidence dominant · Open Targets 0.39

Dengue
0.41Preliminary

Pathway evidence dominant · Open Targets 0.58 · no direct causal or clinical evidence

Immunoglobulin Light-chain Amyloidosis
0.32Preliminary

Pathway evidence dominant · Open Targets 0.47 · no direct causal or clinical evidence

View evidence synthesis (3)
AmyloidosisModerately supported
0.54
agreement 0.390.69
Genetic literature82%Literature18%

Open Targets aggregate 0.39 · 2 independent evidence families

DenguePreliminary
0.41
agreement 0.230.59
Pathway87%Literature13%

Open Targets aggregate 0.58 · 2 independent evidence families · no direct causal or clinical evidence

Immunoglobulin Light-chain AmyloidosisPreliminary
0.32
agreement 0.140.50
Pathway93%Literature7%

Open Targets aggregate 0.47 · 2 independent evidence families · 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
Dengue0.58
Immunoglobulin Light-chain Amyloidosis0.47
Amyloidosis0.39

Tractability

Small moleculesEmerging

Feasibility evidence (structure with ligand and med-quality pocket) — no clinical-stage drug of this modality recorded.

AntibodiesEmerging

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

Protein degradersEmerging

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

View underlying tractability evidence (7)
SM · Structure with LigandSM · Med-Quality PocketAB · GO CC high confAB · UniProt loc med confAB · UniProt SigP or TMHMMPR · Database UbiquitinationPR · Half-life Data

Raw Open Targets tractability assessment buckets, by modality.

Research activity

4 papers · to 2025

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

Most cited

Recent

Europe PMC papers linked directly to this protein.