Back to discover

Protein / target

Pro-epidermal growth factor

Encoded byEGFP01133Homo sapiensSwiss-Prot
UniProt: P01133Ensembl: ENSG00000138798HGNC: HGNC:3229NCBI Gene: 1950
Antibody-tractable
Druggability
GO CC high conf
1
Research papers

Protein at a glance

Biological role

Guanyl-nucleotide exchange factor

Strongest disease association

Atrial Fibrillation

Via encoding gene EGF · Genetic evidence · score 0.63

Research activity

Emerging research

1 papers · latest 2007

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

EGF stimulates the growth of various epidermal and epithelial tissues in vivo and in vitro and of some fibroblasts in cell culture.

View complete UniProt function annotation

EGF stimulates the growth of various epidermal and epithelial tissues in vivo and in vitro and of some fibroblasts in cell culture. Magnesiotropic hormone that stimulates magnesium reabsorption in the renal distal convoluted tubule via engagement of EGFR and activation of the magnesium channel TRPM6. Can induce neurite outgrowth in motoneurons of the pond snail Lymnaea stagnalis in vitro (PubMed:10964941)

Subcellular location

Membrane
Domains and Gene Ontology detail (49)

Domains & features

EGF-like 1EGF-like 2; calcium-bindingEGF-like 3EGF-like 4EGF-like 5EGF-like 6EGF-like 7; calcium-bindingEGF-like 8; calcium-bindingEGF-like 9

Gene Ontology

  • Cclathrin-coated endocytic vesicle membrane
  • Cextracellular exosome
  • Cextracellular region
  • Cextracellular space
  • Clysosomal membrane
  • Cplasma membrane
  • Cplatelet alpha granule lumen
  • Fcalcium ion binding
  • Fepidermal growth factor receptor binding
  • Fgrowth factor activity
  • Fguanyl-nucleotide exchange factor activity
  • Freceptor ligand activity

1207 aa · 134 kDa · 3 isoforms

Biological roles

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

Receptor tyrosine kinase signallingGOGrowth-factor signallingGOCell migrationGOCell proliferation & survivalGOLipid & lipoprotein metabolismGOTranscriptional regulationGO
View supporting evidence

Receptor tyrosine kinase signalling

  • ·transmembrane receptor protein tyrosine kinase activator activity
  • ·ERBB2-EGFR signaling pathway

Growth-factor signalling

  • ·epidermal growth factor receptor binding
  • ·epidermal growth factor receptor signaling pathway

Cell migration

  • ·positive regulation of cell migration
  • ·positive regulation of endothelial cell migration

Cell proliferation & survival

  • ·positive regulation of cell population proliferation

Lipid & lipoprotein metabolism

  • ·negative regulation of cholesterol efflux

Transcriptional regulation

  • ·positive regulation of DNA-templated transcription
  • ·positive regulation of gene expression

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 EGF

Gene-level evidence surfaced through the gene EGF 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
0.68Moderately supported

Genetic evidence dominant · Open Targets 0.41

Neoplasms
0.48Preliminary

Pathway evidence dominant · Open Targets 0.63 · no direct causal or clinical evidence

Cholangiocarcinoma
0.25Preliminary

Genetic evidence dominant · Open Targets 0.13

Carcinoma, Hepatocellular
0.16Preliminary

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

Enterocolitis, Necrotizing
0.14Preliminary

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

View evidence synthesis (5)
Atrial FibrillationModerately supported
0.68
agreement 0.54–0.81
Genetic84%Literature17%

Open Targets aggregate 0.41 · 2 independent evidence families

NeoplasmsPreliminary
0.48
agreement 0.31–0.66
Pathway73%Literature27%

Open Targets aggregate 0.63 · 2 independent evidence families · no direct causal or clinical evidence

CholangiocarcinomaPreliminary
0.25
agreement 0.11–0.39
Genetic70%Literature30%

Open Targets aggregate 0.13 · 2 independent evidence families

Carcinoma, HepatocellularPreliminary
0.16
agreement 0.00–0.35
Literature87%RNA expression13%

Open Targets aggregate 0.12 · 2 independent evidence families · no direct causal or clinical evidence

Enterocolitis, NecrotizingPreliminary
0.14
agreement 0.00–0.41
Literature100%

Open Targets aggregate 0.11 · 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
Neoplasms0.63
Atrial Fibrillation0.41
Cholangiocarcinoma0.13
Carcinoma, Hepatocellular0.12
Enterocolitis, Necrotizing0.11

Tractability

Antibodies — Emerging

Feasibility evidence (go cc high conf and uniprot sigp or tmhmm) — 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 (3)
AB · GO CC high confAB · UniProt SigP or TMHMMPR · Database Ubiquitination

Raw Open Targets tractability assessment buckets, by modality.

Safety-related annotations

regulation of transcription factor activityToxCast

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 2007

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

Most cited

Expression of epiregulin and amphiregulin and K-ras mutation status predict disease control in metastatic colorectal cancer patients treated with cetuximab.852 cites

Khambata-Ford S · Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2007

Recent

Expression of epiregulin and amphiregulin and K-ras mutation status predict disease control in metastatic colorectal cancer patients treated with cetuximab.

Khambata-Ford S · Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2007

Europe PMC papers linked directly to this protein.