Back to discover

Protein / target

Claudin-5

Encoded byCLDN5O00501Homo sapiensSwiss-Prot
Antibody-tractable
Druggability
GO CC high conf
1
Research papers

Protein at a glance

Biological role

Structural molecule

Strongest disease association

Genetic Diseases, Inborn

Via encoding gene CLDN5 · Genetic evidence · score 0.67

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

Plays a major role in tight junction-specific obliteration of the intercellular space

Subcellular location

Cell junction, tight junctionCell membrane
Domains and Gene Ontology detail (32)

Gene Ontology

  • Capicolateral plasma membrane
  • Cbicellular tight junction
  • Ccell junction
  • Ccell-cell junction
  • Clateral plasma membrane
  • Cmembrane
  • Cparanode region of axon
  • Cplasma membrane
  • CSchmidt-Lanterman incisure
  • Ctight junction
  • Fidentical protein binding
  • Fstructural molecule activity

218 aa · 23 kDa

Biological roles

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

Cell proliferation & survivalGOCell migrationGOCell adhesionUniProt · GOTranscriptional regulationGO
View supporting evidence

Cell proliferation & survival

  • ·positive regulation of cell population proliferation

Cell migration

  • ·negative regulation of cell migration

Cell adhesion

  • ·Plays a major role in tight junction-specific obliteration of the intercellular space
  • ·Cell junction, tight junction
  • ·bicellular tight junction
  • ·cell junction

Transcriptional regulation

  • ·negative regulation of gene expression
  • ·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 CLDN5

Gene-level evidence surfaced through the gene CLDN5 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.

Genetic Diseases, Inborn
0.68Moderately supported

Genetic evidence dominant · Open Targets 0.41

Neurodevelopmental Disorders
0.56Moderately supported

Genetic evidence dominant · Open Targets 0.34

Epilepsy
0.50Moderately supported

Genetic literature evidence dominant · Open Targets 0.38

Hypotension
0.43Limited support

Genetic evidence dominant · Open Targets 0.26

Placental retention
0.27Limited support

Genetic evidence dominant · Open Targets 0.16

View evidence synthesis (5)
Genetic Diseases, InbornModerately supported
0.68
agreement 0.540.81
Genetic100%Literature1%

Open Targets aggregate 0.41 · 2 independent evidence families

Neurodevelopmental DisordersModerately supported
0.56
agreement 0.420.70
Genetic98%Literature2%Genetic literaturedup

Open Targets aggregate 0.34 · 2 independent evidence families · 1 not counted as duplicate

EpilepsyModerately supported
0.50
agreement 0.350.66
Genetic literature94%Literature6%

Open Targets aggregate 0.38 · 2 independent evidence families

HypotensionLimited support
0.43
agreement 0.310.55
Genetic100%

Open Targets aggregate 0.26 · 1 independent evidence family

Placental retentionLimited support
0.27
agreement 0.150.39
Genetic100%

Open Targets aggregate 0.16 · 1 independent evidence family

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
Genetic Diseases, Inborn0.41
Epilepsy0.38
Neurodevelopmental Disorders0.34
Hypotension0.26
Placental retention0.16
Osteoarthritis, Hip0.12
Heart Diseases0.12
Alzheimer's Disease0.10

Tractability

AntibodiesEmerging

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

View underlying tractability evidence (3)
AB · GO CC high confAB · UniProt loc med confAB · UniProt SigP or TMHMM

Raw Open Targets tractability assessment buckets, by modality.

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

Recent

Europe PMC papers linked directly to this protein.

Related family literature

9

Papers about “Claudins” — a broader family this protein belongs to. Shown as context; not counted as papers specifically about this protein.

Global prevalence of claudin 18 isoform 2 in tumors of patients with locally advanced unresectable or metastatic gastric or gastroesophageal junction adenocarcinoma.

Shitara K · Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2024

via Claudins

Heterogeneity of claudin 18.2 expression in metastatic gastric cancer.

Choi E · Scientific reports · 2024

via Claudins

ILUSTRO: Phase II Multicohort Trial of Zolbetuximab in Patients with Advanced or Metastatic Claudin 18.2-Positive Gastric or Gastroesophageal Junction Adenocarcinoma.

Klempner SJ · Clinical cancer research : an official journal of the American Association for Cancer Research · 2023

via Claudins

CT041 CAR T cell therapy for Claudin18.2-positive metastatic pancreatic cancer.

Qi C · Journal of hematology & oncology · 2023

via Claudins

Europe PMC literature, reached through curated HGNC family membership. Membership is a taxonomic relationship — it does not imply this protein participates in every mechanism these papers discuss.