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Protein / target

Beta-galactosidase

Encoded byGLB1P16278Homo sapiensSwiss-Prot
Small-molecule tractable
Druggability
Structure with Ligand
1
Research papers

Protein at a glance

Biological role

Protein homodimerization

Strongest disease association

Genetic Diseases, Inborn

Via encoding gene GLB1 · Genetic evidence · score 0.87

Research activity

Emerging research

1 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

Cleaves beta-linked terminal galactosyl residues from gangliosides, glycoproteins, and glycosaminoglycans

Subcellular location

LysosomeCytoplasm, perinuclear region
Domains and Gene Ontology detail (20)

Gene Ontology

  • Cazurophil granule lumen
  • Ccytoplasm
  • Cextracellular exosome
  • Cextracellular region
  • Cficolin-1-rich granule lumen
  • Clysosomal lumen
  • Clysosome
  • Cmembrane
  • Cperinuclear region of cytoplasm
  • Cvacuole
  • Fbeta-galactosidase activity
  • Fgalactoside binding

677 aa · 76 kDa · 3 isoforms

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 GLB1

Gene-level evidence surfaced through the gene GLB1 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
0.88Well supported

Genetic evidence dominant · Open Targets 0.53

Asthma
0.78Well supported

Genetic evidence dominant · Open Targets 0.48

Dermatitis, Atopic
0.67Moderately supported

Genetic evidence dominant · Open Targets 0.41

View evidence synthesis (3)
Genetic Diseases, InbornWell supported
0.88
agreement 0.741.00
Genetic99%Literature1%

Open Targets aggregate 0.53 · 2 independent evidence families

AsthmaWell supported
0.78
agreement 0.640.92
Genetic99%Literature1%

Open Targets aggregate 0.48 · 2 independent evidence families

Dermatitis, AtopicModerately supported
0.67
agreement 0.540.81
Genetic99%Literature1%

Open Targets aggregate 0.41 · 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
Genetic Diseases, Inborn0.53
Asthma0.48
Dermatitis, Atopic0.41

Tractability

Small moleculesEmerging

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

AntibodiesEmerging

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

Protein degradersEmerging

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

View underlying tractability evidence (8)
SM · Structure with LigandSM · High-Quality LigandSM · Druggable FamilyAB · GO CC high confAB · UniProt SigP or TMHMMPR · Database UbiquitinationPR · Half-life DataPR · Small Molecule Binder

Raw Open Targets tractability assessment buckets, by modality.

Research activity

1 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.