Back to discover

Protein / target

Semaphorin-3A

Encoded bySEMA3AQ14563Homo sapiensSwiss-Prot
Antibody-tractable
Druggability
GO CC high conf
1
Research papers

Protein at a glance

Biological role

Semaphorin receptor binding

Strongest disease association

Alcohol drinking

Via encoding gene SEMA3A · Genetic evidence · score 0.68

Research activity

Emerging research

1 papers · latest 2018

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

Involved in the development of the olfactory system and in neuronal control of puberty.

View complete UniProt function annotation

Involved in the development of the olfactory system and in neuronal control of puberty. Induces the collapse and paralysis of neuronal growth cones. Could serve as a ligand that guides specific growth cones by a motility-inhibiting mechanism. Binds to the complex neuropilin-1/plexin-1

Subcellular location

Secreted
Domains and Gene Ontology detail (34)

Domains & features

SemaIg-like C2-type

Gene Ontology

  • Caxon
  • Cextracellular region
  • Cextracellular space
  • Cglutamatergic synapse
  • Cplasma membrane
  • Fchemorepellent activity
  • Fneuropilin binding
  • Fsemaphorin receptor binding
  • Paxon extension involved in axon guidance
  • Paxon guidance
  • Paxonogenesis involved in innervation
  • Pbasal dendrite arborization

771 aa · 89 kDa

Biological roles

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

Cell migrationGOImmune signallingGOMotor controlGO
View supporting evidence

Cell migration

  • ·negative chemotaxis
  • ·neural crest cell migration
  • ·neural crest cell migration involved in autonomic nervous system development
  • ·positive regulation of cell migration

Immune signalling

  • ·neural crest cell migration
  • ·neural crest cell migration involved in autonomic nervous system development

Motor control

  • ·branchiomotor neuron axon guidance
  • ·motor neuron axon guidance

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 SEMA3A

Gene-level evidence surfaced through the gene SEMA3Athat 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.

Alcohol drinking
0.68Moderately supported

Genetic evidence dominant · Open Targets 0.42

Glaucoma, Open-Angle
0.66Moderately supported

Genetic evidence dominant · Open Targets 0.40

Brugada syndrome
0.62Moderately supported

Genetic evidence dominant · Open Targets 0.38

Kallmann syndrome
0.61Moderately supported

Genetic evidence dominant · Open Targets 0.53

Glaucoma
0.56Moderately supported

Genetic evidence dominant · Open Targets 0.34

View evidence synthesis (5)
Alcohol drinkingModerately supported
0.68
agreement 0.560.80
Genetic100%

Open Targets aggregate 0.42 · 1 independent evidence family

Glaucoma, Open-AngleModerately supported
0.66
agreement 0.540.78
Genetic100%

Open Targets aggregate 0.40 · 1 independent evidence family

Brugada syndromeModerately supported
0.62
agreement 0.480.76
Genetic94%Literature6%

Open Targets aggregate 0.38 · 2 independent evidence families

Kallmann syndromeModerately supported
0.61
agreement 0.470.74
Genetic96%Literature4%Genetic literaturedup

Open Targets aggregate 0.53 · 2 independent evidence families · 1 not counted as duplicate

GlaucomaModerately supported
0.56
agreement 0.420.70
Genetic100%Literature0%

Open Targets aggregate 0.34 · 2 independent evidence families

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
Kallmann syndrome0.53
Alcohol drinking0.42
Glaucoma, Open-Angle0.40
Brugada syndrome0.38
Heart Defects, Congenital0.37
Glaucoma0.34

Tractability

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) — no clinical-stage drug of this modality recorded.

View underlying tractability evidence (4)
AB · GO CC high confAB · UniProt loc med confAB · UniProt SigP or TMHMMPR · Database Ubiquitination

Raw Open Targets tractability assessment buckets, by modality.

Research activity

1 papers · to 2018

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.