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Protein / target

Endothelin-1

Encoded byEDN1P05305Homo sapiensSwiss-Prot
UniProt: P05305Ensembl: ENSG00000078401HGNC: HGNC:3176NCBI Gene: 1906
Antibody-tractable
Druggability
GO CC high conf
1
Research papers

Protein at a glance

Biological role

Endothelin A receptor binding

Strongest disease association

Alcohol drinking

Via encoding gene EDN1 · Genetic evidence · score 0.48

Research activity

Emerging research

1 papers · latest 2019

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

Endothelins are endothelium-derived vasoconstrictor peptides.

View complete UniProt function annotation

Endothelins are endothelium-derived vasoconstrictor peptides (By similarity). Probable ligand for G protein-coupled receptors EDNRA and EDNRB which activates PTK2B, BCAR1, BCAR3 and, GTPases RAP1 and RHOA cascade in glomerular mesangial cells (PubMed:19086031). Also binds the DEAR/FBXW7-AS1 receptor (PubMed:17446437). Promotes mesenteric arterial wall remodeling via activation of ROCK signaling and subsequent colocalization of NFATC3 with F-actin filaments (By similarity). NFATC3 then translocates to the nucleus where it subsequently promotes the transcription of the smooth muscle hypertrophy and differentiation marker ACTA2 (By similarity)

Subcellular location

Secreted
Domains and Gene Ontology detail (116)

Gene Ontology

  • Cbasal part of cell
  • Ccytoplasm
  • Cextracellular region
  • Cextracellular space
  • Crough endoplasmic reticulum lumen
  • Ctransport vesicle
  • CWeibel-Palade body
  • Fcytokine activity
  • Fendothelin A receptor binding
  • Fendothelin B receptor binding
  • Fhormone activity
  • Partery smooth muscle contraction

212 aa · 24 kDa

Biological roles

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

Cell migrationGOIon channel gatingGOCell proliferation & survivalGOLipid & lipoprotein metabolismGOTranscriptional regulationUniProt · GOG protein-coupled signallingUniProt · GO
View supporting evidence

Cell migration

  • ·cardiac neural crest cell migration involved in outflow tract morphogenesis
  • ·positive regulation of cell migration
  • ·positive regulation of endothelial cell migration
  • ·positive regulation of neutrophil chemotaxis

Ion channel gating

  • ·calcium ion transmembrane transport
  • ·positive regulation of cation channel activity

Cell proliferation & survival

  • ·positive regulation of cell population proliferation

Lipid & lipoprotein metabolism

  • ·cellular response to fatty acid

Transcriptional regulation

  • ·Endothelins are endothelium-derived vasoconstrictor peptides (By similarity). Probable l…
  • ·negative regulation of gene expression
  • ·negative regulation of transcription by RNA polymerase II
  • ·positive regulation of transcription by RNA polymerase II

G protein-coupled signalling

  • ·Endothelins are endothelium-derived vasoconstrictor peptides (By similarity). Probable l…
  • ·G protein-coupled receptor signaling pathway

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 EDN1

Gene-level evidence surfaced through the gene EDN1 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.

Alcohol drinking
0.48Limited support

Genetic evidence dominant · Open Targets 0.29

Genetic Diseases, Inborn
0.31Limited support

Genetic evidence dominant · Open Targets 0.19

Dementia
0.31Limited support

Genetic evidence dominant · Open Targets 0.18

Aortic Valve Stenosis
0.30Limited support

Genetic evidence dominant · Open Targets 0.17

View evidence synthesis (4)
Alcohol drinkingLimited support
0.48
agreement 0.36–0.60
Genetic100%

Open Targets aggregate 0.29 · 1 independent evidence family

Genetic Diseases, InbornLimited support
0.31
agreement 0.19–0.43
Genetic100%

Open Targets aggregate 0.19 · 1 independent evidence family

DementiaLimited support
0.31
agreement 0.17–0.45
Genetic83%Literature17%

Open Targets aggregate 0.18 · 2 independent evidence families

Aortic Valve StenosisLimited support
0.30
agreement 0.16–0.43
Genetic89%Literature11%

Open Targets aggregate 0.17 · 2 independent evidence families

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
Alcohol drinking0.29
Genetic Diseases, Inborn0.19
Dementia0.18
Aortic Valve Stenosis0.17

Tractability

Antibodies — Emerging

Feasibility evidence (go cc high conf and uniprot loc med conf) — no clinical-stage drug of this modality recorded.

Protein degraders — Emerging

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.

Safety-related annotations

edemaClinPGx

Terms indexed against this target in Open Targets' safety data, with their datasource. These are annotations, not causal claims: the direction of effect (whether activation or inhibition is implicated), species and evidence strength are not captured here, so an entry does not mean that modulating this target is known to cause that condition.

Research activity

1 papers · to 2019

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

Most cited

Amyloid β oligomers constrict human capillaries in Alzheimer's disease via signaling to pericytes.577 cites

Nortley R · Science (New York, N.Y.) · 2019

Recent

Amyloid β oligomers constrict human capillaries in Alzheimer's disease via signaling to pericytes.

Nortley R · Science (New York, N.Y.) · 2019

Europe PMC papers linked directly to this protein.