Back to discover

Protein / target

Alpha-enolase

Encoded byENO1P06733Homo sapiensSwiss-Prot
UniProt: P06733Ensembl: ENSG00000074800HGNC: HGNC:3350NCBI Gene: 2023
Small-molecule tractable
Druggability
Structure with Ligand
1
Research papers

Protein at a glance

Biological role

Phosphopyruvate hydratase

Strongest disease association

Atrial Fibrillation

Via encoding gene ENO1 · Genetic evidence · score 0.68

Research activity

Emerging research

1 papers · latest 2025

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

Enolase that catalyzes the conversion of 2-phosphoglycerate to phosphoenolpyruvate in glycolysis and the reverse reaction in gluconeogenesis.

View complete UniProt function annotation

Enolase that catalyzes the conversion of 2-phosphoglycerate to phosphoenolpyruvate in glycolysis and the reverse reaction in gluconeogenesis (PubMed:1369209, PubMed:29775581). Also involved in various processes such as growth control, hypoxia tolerance and allergic responses (PubMed:10802057, PubMed:12666133, PubMed:2005901, PubMed:29775581). May also function in the intravascular and pericellular fibrinolytic system due to its ability to serve as a receptor and activator of plasminogen on the cell surface of several cell-types such as leukocytes and neurons (PubMed:12666133). Stimulates immunoglobulin production (PubMed:1369209)

Subcellular location

CytoplasmCell membraneCytoplasm, myofibril, sarcomere, M lineNucleus
Domains and Gene Ontology detail (34)

Gene Ontology

  • Ccell cortex
  • Ccell surface
  • Ccytoplasm
  • Ccytosol
  • Cextracellular exosome
  • Cextracellular space
  • CM band
  • Cmembrane
  • Cnuclear outer membrane
  • Cnucleus
  • Cphosphopyruvate hydratase complex
  • Cplasma membrane

434 aa · 47 kDa · 2 isoforms

Biological roles

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

Muscle contractionUniProt · GOTranscriptional regulationGO
View supporting evidence

Muscle contraction

  • ·Cytoplasm, myofibril, sarcomere, M line
  • ·positive regulation of muscle contraction

Transcriptional regulation

  • ·DNA-binding transcription repressor activity, RNA polymerase II-specific
  • ·RNA polymerase II transcription regulatory region sequence-specific DNA binding
  • ·transcription corepressor activity
  • ·transcription corepressor binding

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 ENO1

Gene-level evidence surfaced through the gene ENO1 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.

Atrial Fibrillation
0.69Moderately supported

Genetic evidence dominant · Open Targets 0.42

Tuberculosis
0.25Preliminary

Pathway evidence dominant · Open Targets 0.37 · no direct causal or clinical evidence

Melanoma
0.19Preliminary

Literature evidence dominant · Open Targets 0.17 · no direct causal or clinical evidence

Neurodegenerative Diseases
0.18Preliminary

Pathway evidence dominant · Open Targets 0.27 · no direct causal or clinical evidence

Neoplasms
0.15Preliminary

Literature evidence dominant · Open Targets 0.12 · no direct causal or clinical evidence

View evidence synthesis (5)
Atrial FibrillationModerately supported
0.69
agreement 0.55–0.82
Genetic97%Literature3%

Open Targets aggregate 0.42 · 2 independent evidence families

TuberculosisPreliminary
0.25
agreement 0.07–0.42
Pathway98%Literature2%

Open Targets aggregate 0.37 · 2 independent evidence families · no direct causal or clinical evidence

MelanomaPreliminary
0.19
agreement 0.02–0.37
Literature50%Pathway50%

Open Targets aggregate 0.17 · 2 independent evidence families · no direct causal or clinical evidence

Neurodegenerative DiseasesPreliminary
0.18
agreement 0.01–0.36
Pathway96%Literature4%

Open Targets aggregate 0.27 · 2 independent evidence families · no direct causal or clinical evidence

NeoplasmsPreliminary
0.15
agreement 0.00–0.42
Literature100%

Open Targets aggregate 0.12 · 1 independent evidence family · no direct causal or clinical evidence

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
Atrial Fibrillation0.42
Tuberculosis0.37
Neurodegenerative Diseases0.27
Melanoma0.17
Neoplasms0.12
Glioma0.11

Tractability

Small molecules — Emerging

Feasibility evidence (structure with ligand and high-quality ligand) — no clinical-stage drug of this modality recorded.

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 (uniprot ubiquitination and database ubiquitination) — no clinical-stage drug of this modality recorded.

View underlying tractability evidence (10)
SM · Structure with LigandSM · High-Quality LigandSM · High-Quality PocketAB · UniProt loc high confAB · GO CC high confAB · Human Protein Atlas locPR · UniProt UbiquitinationPR · Database UbiquitinationPR · Half-life DataPR · Small Molecule Binder

Raw Open Targets tractability assessment buckets, by modality.

Research activity

1 papers · to 2025

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

Most cited

Brain injury biomarkers and applications in neurological diseases.12 cites

Zhang H · Chinese medical journal · 2025

Recent

Brain injury biomarkers and applications in neurological diseases.

Zhang H · Chinese medical journal · 2025

Europe PMC papers linked directly to this protein.