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Protein / target

Synaptophysin

Encoded bySYPP08247Homo sapiensSwiss-Prot
Antibody-tractable
Druggability
UniProt SigP or TMHMM
3
Research papers

Protein at a glance

Biological role

Identical protein binding

Strongest disease association

Genetic Diseases, Inborn

Via encoding gene SYP · Genetic evidence · score 0.31

Research activity

Emerging research

3 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

Possibly involved in structural functions as organizing other membrane components or in targeting the vesicles to the plasma membrane.

View complete UniProt function annotation

Possibly involved in structural functions as organizing other membrane components or in targeting the vesicles to the plasma membrane. Involved in the regulation of short-term and long-term synaptic plasticity (By similarity)

Subcellular location

Cytoplasmic vesicle, secretory vesicle, synaptic vesicle membraneSynapse, synaptosome
Domains and Gene Ontology detail (22)

Domains & features

MARVEL

Gene Ontology

  • Cexcitatory synapse
  • Cneuromuscular junction
  • Cneuron projection
  • Cperinuclear region of cytoplasm
  • Cpresynaptic active zone
  • Cpresynaptic membrane
  • CSchaffer collateral - CA1 synapse
  • Csynaptic vesicle
  • Csynaptic vesicle membrane
  • Cterminal bouton
  • Fcholesterol binding
  • Fidentical protein binding

313 aa · 34 kDa · 2 isoforms

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 SYP

Gene-level evidence surfaced through the gene SYPthat 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
0.31Limited support

Genetic evidence dominant · Open Targets 0.19

Neurodegenerative Diseases
0.27Preliminary

Pathway evidence dominant · Open Targets 0.38 · no direct causal or clinical evidence

Neoplasms
0.14Preliminary

Literature evidence dominant · Open Targets 0.11 · no direct causal or clinical evidence

Alzheimer's Disease
0.11Preliminary

Literature evidence dominant · Open Targets 0.09 · no direct causal or clinical evidence

Adenocarcinoma
0.11Preliminary

Literature evidence dominant · Open Targets 0.09 · no direct causal or clinical evidence

View evidence synthesis (5)
Genetic Diseases, InbornLimited support
0.31
agreement 0.190.43
Genetic100%

Open Targets aggregate 0.19 · 1 independent evidence family

Neurodegenerative DiseasesPreliminary
0.27
agreement 0.090.44
Pathway89%Literature11%

Open Targets aggregate 0.38 · 2 independent evidence families · no direct causal or clinical evidence

NeoplasmsPreliminary
0.14
agreement 0.000.41
Literature100%

Open Targets aggregate 0.11 · 1 independent evidence family · no direct causal or clinical evidence

Alzheimer's DiseasePreliminary
0.11
agreement 0.000.38
Literature100%

Open Targets aggregate 0.09 · 1 independent evidence family · no direct causal or clinical evidence

AdenocarcinomaPreliminary
0.11
agreement 0.000.38
Literature100%

Open Targets aggregate 0.09 · 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 Diseases0.38
Genetic Diseases, Inborn0.19
Neoplasms0.11
Alzheimer's Disease0.09
Adenocarcinoma0.09
Breast Neoplasms0.08
Schizophrenia0.08

Tractability

AntibodiesEmerging

Feasibility evidence (uniprot sigp or tmhmm) — no clinical-stage drug of this modality recorded.

Protein degradersEmerging

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

View underlying tractability evidence (3)
AB · UniProt SigP or TMHMMPR · UniProt UbiquitinationPR · Half-life Data

Raw Open Targets tractability assessment buckets, by modality.

Research activity

3 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

McClean PL · The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011

Morris M · Journal of neuropathology and experimental neurology · 2023

Angelin LG · International journal of molecular sciences · 2024

Recent

Hippocampal synaptic alterations associated with tau pathology in primary age-related tauopathy.

Morris M · Journal of neuropathology and experimental neurology · 2023

The diabetes drug liraglutide prevents degenerative processes in a mouse model of Alzheimer's disease.

McClean PL · The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011

Europe PMC papers linked directly to this protein.