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Protein / target

Myelin P2 protein

Encoded byPMP2P02689Homo sapiensSwiss-Prot
Small-molecule tractable
Druggability
Structure with Ligand
1
Research papers

Protein at a glance

Biological role

Cholesterol binding

Strongest disease association

Genetic Diseases, Inborn

Via encoding gene PMP2 · Genetic evidence · score 0.55

Research activity

Emerging research

1 papers · latest 1999

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

May play a role in lipid transport protein in Schwann cells.

View complete UniProt function annotation

May play a role in lipid transport protein in Schwann cells. May bind cholesterol

Subcellular location

Cytoplasm
Domains and Gene Ontology detail (8)

Gene Ontology

  • Ccytosol
  • Cextracellular exosome
  • Cmyelin sheath
  • Cnucleus
  • Fcholesterol binding
  • Ffatty acid binding
  • Pfatty acid transport
  • Pmembrane organization

132 aa · 15 kDa

Biological roles

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

Lipid & lipoprotein metabolismUniProt · GO
View supporting evidence

Lipid & lipoprotein metabolism

  • ·May play a role in lipid transport protein in Schwann cells. May bind cholesterol
  • ·cholesterol binding
  • ·fatty acid binding
  • ·fatty acid transport

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 PMP2

Gene-level evidence surfaced through the gene PMP2 that 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.

Genetic Diseases, Inborn
0.55Moderately supported

Genetic evidence dominant · Open Targets 0.33

Charcot-Marie-Tooth Disease
0.27Limited support

Genetic literature evidence dominant · Open Targets 0.19

Schizophrenia
0.20Preliminary

Animal model evidence dominant · Open Targets 0.06 · no direct causal or clinical evidence

Hashimoto's Disease
0.14Preliminary

Genetic evidence dominant · Open Targets 0.08

View evidence synthesis (4)
Genetic Diseases, InbornModerately supported
0.55
agreement 0.430.67
Genetic100%

Open Targets aggregate 0.33 · 1 independent evidence family

Charcot-Marie-Tooth DiseaseLimited support
0.27
agreement 0.120.42
Genetic literature87%Literature13%

Open Targets aggregate 0.19 · 2 independent evidence families

SchizophreniaPreliminary
0.20
agreement 0.020.37
Animal model99%Literature1%

Open Targets aggregate 0.06 · 2 independent evidence families · no direct causal or clinical evidence

Hashimoto's DiseasePreliminary
0.14
agreement 0.020.26
Genetic100%

Open Targets aggregate 0.08 · 1 independent evidence family

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
Genetic Diseases, Inborn0.33
Charcot-Marie-Tooth Disease0.19
Hashimoto's Disease0.08
Schizophrenia0.06

Tractability

Small moleculesEmerging

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

View underlying tractability evidence (2)
SM · Structure with LigandSM · Med-Quality Pocket

Raw Open Targets tractability assessment buckets, by modality.

Research activity

1 papers · to 1999

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

Most cited

Kersten S · The Journal of clinical investigation · 1999

Recent

Europe PMC papers linked directly to this protein.