Protein / target
Somatostatin
Protein at a glance
Biological role
Hormone
Strongest disease association
Placental abruption
Research activity
Emerging research
Derived from structured UniProt, Open Targets and literature data on this page.
Protein profile
Canonical identity and biological annotation from UniProt.
Function overview
Inhibits the secretion of pituitary hormones, including that of growth hormone/somatotropin (GH1), PRL, ACTH, luteinizing hormone (LH) and TSH.
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Inhibits the secretion of pituitary hormones, including that of growth hormone/somatotropin (GH1), PRL, ACTH, luteinizing hormone (LH) and TSH. Also impairs ghrelin- and GnRH-stimulated secretion of GH1 and LH; the inhibition of ghrelin-stimulated secretion of GH1 can be further increased by neuronostatin
Subcellular location
Domains and Gene Ontology detail (23)Hide
Gene Ontology
- Ccytosol
- Cextracellular region
- Cextracellular space
- CGABA-ergic synapse
- Cneuronal cell body
- Cneuronal dense core vesicle
- Fhormone activity
- Pcell surface receptor signaling pathway
- Pcell-cell signaling
- Pchemical synaptic transmission
- Pdigestion
- PG protein-coupled receptor signaling pathway
Biological roles
What this protein does, drawn together from its UniProt function, Gene Ontology terms and Reactome pathways.
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Synaptic signalling
- ·GABA-ergic synapse
- ·chemical synaptic transmission
- ·regulation of postsynaptic membrane neurotransmitter receptor levels
Cell proliferation & survival
- ·negative regulation of cell population proliferation
Cell migration
- ·regulation of cell migration
Concepts derived from UniProt GO Reactome — each badge above shows which sources supported that role.
Translational evidence
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 SST
Gene-level evidence surfaced through the gene SSTthat 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.
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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.
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Tractability
Small molecules — Emerging
Antibodies — Emerging
Protein degraders — Emerging
View underlying tractability evidence (5)Hide
Raw Open Targets tractability assessment buckets, by modality.
Research activity
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.