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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 0.54–0.81
Genetic100%Literature1%

Open Targets aggregate 0.41 · 2 independent evidence families

Neurodevelopmental DisordersModerately supported
0.56
agreement 0.42–0.70
Genetic98%Literature2%Genetic literaturedup

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

EpilepsyModerately supported
0.50
agreement 0.35–0.66
Genetic literature94%Literature6%

Open Targets aggregate 0.38 · 2 independent evidence families

HypotensionLimited support
0.43
agreement 0.31–0.55
Genetic100%

Open Targets aggregate 0.26 · 1 independent evidence family

Placental retentionLimited support
0.27
agreement 0.15–0.39
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

Antibodies — Emerging

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.