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Protein / target

Neuromodulin

Encoded byGAP43P17677Homo sapiensSwiss-Prot
UniProt: P17677Ensembl: ENSG00000172020HGNC: HGNC:4140NCBI Gene: 2596
Antibody-tractable
Druggability
UniProt loc high conf
1
Research papers

Protein at a glance

Biological role

Phosphatidylinositol phosphate binding

Strongest disease association

Smoking initiation

Via encoding gene GAP43 · Genetic evidence · score 0.54

Research activity

Emerging research

1 papers · latest 2024

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

This protein is associated with nerve growth.

View complete UniProt function annotation

This protein is associated with nerve growth. It is a major component of the motile 'growth cones' that form the tips of elongating axons. Plays a role in axonal and dendritic filopodia induction

Subcellular location

Cell membraneCell projection, growth cone membraneSynapseCell projection, filopodium membranePerikaryonCell projection, dendriteCell projection, axonCytoplasm
Domains and Gene Ontology detail (22)

Domains & features

IQ

Gene Ontology

  • Ccytoplasm
  • Cdendrite
  • Cfilopodium membrane
  • CGABA-ergic synapse
  • Cgrowth cone membrane
  • Cperikaryon
  • Cplasma membrane
  • Cpostsynaptic density
  • Cpresynapse
  • Fcalmodulin binding
  • Flysophosphatidic acid binding
  • Fphosphatidylinositol phosphate binding

238 aa · 25 kDa · 2 isoforms

Biological roles

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

Synaptic signallingUniProt · GO
View supporting evidence

Synaptic signalling

  • ·Synapse
  • ·GABA-ergic synapse
  • ·postsynaptic density
  • ·presynapse

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 GAP43

Gene-level evidence surfaced through the gene GAP43 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.

Smoking initiation
0.54Moderately supported

Genetic evidence dominant · Open Targets 0.33

Cholelithiasis
0.54Moderately supported

Genetic evidence dominant · Open Targets 0.33

Neurodegenerative Diseases
0.30Preliminary

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

View evidence synthesis (3)
Smoking initiationModerately supported
0.54
agreement 0.42–0.66
Genetic100%

Open Targets aggregate 0.33 · 1 independent evidence family

CholelithiasisModerately supported
0.54
agreement 0.42–0.66
Genetic100%

Open Targets aggregate 0.33 · 1 independent evidence family

Neurodegenerative DiseasesPreliminary
0.30
agreement 0.12–0.48
Pathway90%Literature10%

Open Targets aggregate 0.43 · 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
Neurodegenerative Diseases0.43
Smoking initiation0.33
Cholelithiasis0.33

Tractability

Antibodies — Emerging

Feasibility evidence (uniprot loc high conf and go cc high 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.

View underlying tractability evidence (5)
AB · UniProt loc high confAB · GO CC high confAB · Human Protein Atlas locPR · Database UbiquitinationPR · Half-life Data

Raw Open Targets tractability assessment buckets, by modality.

Research activity

1 papers · to 2024

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

Most cited

Elevated CSF GAP-43 is associated with accelerated tau accumulation and spread in Alzheimer's disease.39 cites

Franzmeier N · Nature communications · 2024

Recent

Elevated CSF GAP-43 is associated with accelerated tau accumulation and spread in Alzheimer's disease.

Franzmeier N · Nature communications · 2024

Europe PMC papers linked directly to this protein.