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Protein / target

Folate receptor beta

Encoded byFOLR2P14207Homo sapiensSwiss-Prot
Small-molecule tractable
Druggability
Structure with Ligand
2
Research papers

Protein at a glance

Biological role

Folic acid receptor

Strongest disease association

Neoplasms

Via encoding gene FOLR2 · Literature evidence · score 0.12

Research activity

Emerging research

2 papers · latest 2024

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

Binds to folate and reduced folic acid derivatives and mediates delivery of 5-methyltetrahydrofolate and folate analogs into the interior of cells.

View complete UniProt function annotation

Binds to folate and reduced folic acid derivatives and mediates delivery of 5-methyltetrahydrofolate and folate analogs into the interior of cells. Has high affinity for folate and folic acid analogs at neutral pH. Exposure to slightly acidic pH after receptor endocytosis triggers a conformation change that strongly reduces its affinity for folates and mediates their release

Subcellular location

Cell membraneSecreted
Domains and Gene Ontology detail (14)

Gene Ontology

  • Ccell surface
  • Cexternal side of plasma membrane
  • Cextracellular region
  • Cplasma membrane
  • Ffolic acid binding
  • Ffolic acid receptor activity
  • Fsignaling receptor activity
  • Pcell adhesion
  • Pfolic acid metabolic process
  • Pfolic acid transport
  • Pfusion of sperm to egg plasma membrane involved in single fertilization
  • Pinflammatory response

255 aa · 29 kDa

Biological roles

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

Cell proliferation & survivalGO
View supporting evidence

Cell proliferation & survival

  • ·positive regulation of cell population proliferation

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 FOLR2

Gene-level evidence surfaced through the gene FOLR2that 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.

Neoplasms
0.14Preliminary

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

Arthritis, Rheumatoid
0.12Preliminary

Literature evidence dominant · Open Targets 0.09 · no direct causal or clinical evidence

Leukemia, Myeloid, Acute
0.12Preliminary

Literature evidence dominant · Open Targets 0.10 · no direct causal or clinical evidence

Carcinoma, Non-Small-Cell Lung
0.10Preliminary

Literature evidence dominant · Open Targets 0.08 · no direct causal or clinical evidence

Kidney Failure, Chronic
0.09Preliminary

Literature evidence dominant · Open Targets 0.07 · no direct causal or clinical evidence

View evidence synthesis (5)
NeoplasmsPreliminary
0.14
agreement 0.000.41
Literature100%

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

Arthritis, RheumatoidPreliminary
0.12
agreement 0.000.31
Literature95%RNA expression5%

Open Targets aggregate 0.09 · 2 independent evidence families · no direct causal or clinical evidence

Leukemia, Myeloid, AcutePreliminary
0.12
agreement 0.000.39
Literature100%

Open Targets aggregate 0.10 · 1 independent evidence family · no direct causal or clinical evidence

Carcinoma, Non-Small-Cell LungPreliminary
0.10
agreement 0.000.37
Literature100%

Open Targets aggregate 0.08 · 1 independent evidence family · no direct causal or clinical evidence

Kidney Failure, ChronicPreliminary
0.09
agreement 0.000.36
Literature100%

Open Targets aggregate 0.07 · 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
Neoplasms0.12
Leukemia, Myeloid, Acute0.10
Arthritis, Rheumatoid0.09
Carcinoma, Non-Small-Cell Lung0.08
Kidney Failure, Chronic0.07
Colorectal Neoplasms0.07
Stomach Neoplasms0.07
Lung carcinoma0.06
Lung Neoplasms0.06

Tractability

Small moleculesEmerging

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

AntibodiesEmerging

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

Protein degradersEmerging

Feasibility evidence (small molecule binder) — no clinical-stage drug of this modality recorded.

View underlying tractability evidence (7)
SM · Structure with LigandSM · High-Quality LigandAB · UniProt loc high confAB · GO CC high confAB · UniProt loc med confAB · UniProt SigP or TMHMMPR · Small Molecule Binder

Raw Open Targets tractability assessment buckets, by modality.

Research activity

2 papers · to 2024

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.