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Protein / target

Platelet endothelial cell adhesion molecule

Encoded byPECAM1P16284Homo sapiensSwiss-Prot
UniProt: P16284Ensembl: ENSG00000261371HGNC: HGNC:8823NCBI Gene: 5175
Antibody-tractable
Druggability
UniProt loc high conf
3
Research papers

Protein at a glance

Biological role

Transmembrane signaling receptor

Strongest disease association

Coronary Artery Disease

Via encoding gene PECAM1 · Genetic evidence · score 0.69

Research activity

Emerging research

3 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

Cell adhesion molecule which is required for leukocyte transendothelial migration (TEM) under most inflammatory conditions.

View complete UniProt function annotation

Cell adhesion molecule which is required for leukocyte transendothelial migration (TEM) under most inflammatory conditions (PubMed:17580308, PubMed:19342684). Tyr-690 plays a critical role in TEM and is required for efficient trafficking of PECAM1 to and from the lateral border recycling compartment (LBRC) and is also essential for the LBRC membrane to be targeted around migrating leukocytes (PubMed:19342684). Trans-homophilic interaction may play a role in endothelial cell-cell adhesion via cell junctions (PubMed:27958302). Heterophilic interaction with CD177 plays a role in transendothelial migration of neutrophils (PubMed:17580308). Homophilic ligation of PECAM1 prevents macrophage-mediated phagocytosis of neighboring viable leukocytes by transmitting a detachment signal (PubMed:12110892). Promotes macrophage-mediated phagocytosis of apoptotic leukocytes by tethering them to the phagocytic cells; PECAM1-mediated detachment signal appears to be disabled in apoptotic leukocytes (PubMed:12110892). Modulates bradykinin receptor BDKRB2 activation (PubMed:18672896). Regulates bradykinin- and hyperosmotic shock-induced ERK1/2 activation in endothelial cells (PubMed:18672896). Induces susceptibility to atherosclerosis (By similarity)

Subcellular location

Cell membraneMembrane raftCell junction
Domains and Gene Ontology detail (44)

Domains & features

Ig-like C2-type 1Ig-like C2-type 2Ig-like C2-type 3Ig-like C2-type 4Ig-like C2-type 5Ig-like C2-type 6

Gene Ontology

  • Ccell-cell contact zone
  • Ccell-cell junction
  • Cexternal side of plasma membrane
  • Cextracellular exosome
  • Cextracellular space
  • Cmembrane raft
  • Cplasma membrane
  • Cplatelet alpha granule membrane
  • Cprotein-containing complex
  • Csecretory granule membrane
  • Csmooth muscle contractile fiber
  • Fprotein homodimerization activity

738 aa · 83 kDa · 6 isoforms

Biological roles

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

Cell migrationGOCell adhesionUniProt · GOImmune signallingGO
View supporting evidence

Cell migration

  • ·positive regulation of cell migration

Cell adhesion

  • ·Cell adhesion molecule which is required for leukocyte transendothelial migration (TEM)…
  • ·Cell junction
  • ·cell-cell junction
  • ·bicellular tight junction assembly

Immune signalling

  • ·immune response
  • ·T cell activation

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 PECAM1

Gene-level evidence surfaced through the gene PECAM1that 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.

Coronary Artery Disease
0.71Moderately supported

Genetic evidence dominant · Open Targets 0.43

Alzheimer's Disease
0.63Moderately supported

Genetic evidence dominant · Open Targets 0.37

Hypertension
0.57Moderately supported

Genetic evidence dominant · Open Targets 0.34

Myocardial Infarction
0.56Moderately supported

Genetic evidence dominant · Open Targets 0.34

Essential Hypertension
0.41Limited support

Genetic evidence dominant · Open Targets 0.25

View evidence synthesis (5)
Coronary Artery DiseaseModerately supported
0.71
agreement 0.57–0.85
Genetic90%Literature10%

Open Targets aggregate 0.43 · 2 independent evidence families

Alzheimer's DiseaseModerately supported
0.63
agreement 0.52–0.74
Genetic57%Pathway24%Literature17%RNA expression2%

Open Targets aggregate 0.37 · 4 independent evidence families

HypertensionModerately supported
0.57
agreement 0.43–0.71
Genetic90%Literature10%

Open Targets aggregate 0.34 · 2 independent evidence families

Myocardial InfarctionModerately supported
0.56
agreement 0.43–0.70
Genetic88%Literature12%

Open Targets aggregate 0.34 · 2 independent evidence families

Essential HypertensionLimited support
0.41
agreement 0.27–0.55
Genetic99%Literature2%

Open Targets aggregate 0.25 · 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
Coronary Artery Disease0.43
Alzheimer's Disease0.37
Hypertension0.34
Myocardial Infarction0.34
Parkinson's Disease0.30
Multiple Sclerosis0.30
Neurodegenerative Diseases0.29
Lysosomal Storage Diseases0.29
Essential Hypertension0.25

Tractability

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

View underlying tractability evidence (5)
AB · UniProt loc high confAB · GO CC high confAB · UniProt SigP or TMHMMPR · Database UbiquitinationPR · Half-life Data

Raw Open Targets tractability assessment buckets, by modality.

Research activity

3 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

Cellular and developmental control of O2 homeostasis by hypoxia-inducible factor 1 alpha.1,888 cites

Iyer NV · Genes & development · 1998

Type H blood vessels in bone modeling and remodeling.387 cites

Peng Y · Theranostics · 2020

Pathological angiogenesis was associated with cerebrovascular lesion and neurodegeneration in Alzheimer's disease.12 cites

Gao F · Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025

Recent

Pathological angiogenesis was associated with cerebrovascular lesion and neurodegeneration in Alzheimer's disease.

Gao F · Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025

Type H blood vessels in bone modeling and remodeling.

Peng Y · Theranostics · 2020

Cellular and developmental control of O2 homeostasis by hypoxia-inducible factor 1 alpha.

Iyer NV · Genes & development · 1998

Europe PMC papers linked directly to this protein.