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Protein / target

Protein-lysine 6-oxidase

Encoded byLOXP28300Homo sapiensSwiss-Prot
UniProt: P28300Ensembl: ENSG00000113083HGNC: HGNC:6664NCBI Gene: 4015
Small-molecule tractable
Druggability
High-Quality Ligand
1
Research papers

Protein at a glance

Biological role

Protein-lysine 6-oxidase

Strongest disease association

Aortic Aneurysm

Via encoding gene LOX · Genetic literature evidence · score 0.76

Research activity

Emerging research

1 papers · latest 2023

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

Responsible for the post-translational oxidative deamination of peptidyl lysine residues in precursors to fibrous collagen and elastin.

View complete UniProt function annotation

Responsible for the post-translational oxidative deamination of peptidyl lysine residues in precursors to fibrous collagen and elastin (PubMed:26838787). Regulator of Ras expression. May play a role in tumor suppression. Plays a role in the aortic wall architecture (By similarity)

Subcellular location

SecretedSecreted, extracellular space
Domains and Gene Ontology detail (19)

Gene Ontology

  • Ccollagen trimer
  • Celastic fiber
  • Cextracellular matrix
  • Cextracellular region
  • Cextracellular space
  • Cmicrofibril
  • Fcollagen binding
  • Fcopper ion binding
  • Fmolecular adaptor activity
  • Fprotein-lysine 6-oxidase activity
  • Fsmall molecule binding
  • Pblood vessel morphogenesis

417 aa · 47 kDa

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 LOX

Gene-level evidence surfaced through the gene LOX 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.

Aortic Aneurysm
0.62Moderately supported

Genetic literature evidence dominant · Open Targets 0.47

Keratoconus
0.57Moderately supported

Genetic evidence dominant · Open Targets 0.33

Lymphohistiocytosis, Hemophagocytic
0.56Moderately supported

Genetic evidence dominant · Open Targets 0.34

View evidence synthesis (3)
Aortic AneurysmModerately supported
0.62
agreement 0.47–0.77
Genetic literature96%Literature4%

Open Targets aggregate 0.47 · 2 independent evidence families

KeratoconusModerately supported
0.57
agreement 0.43–0.71
Genetic80%Literature20%

Open Targets aggregate 0.33 · 2 independent evidence families

Lymphohistiocytosis, HemophagocyticModerately supported
0.56
agreement 0.44–0.68
Genetic100%

Open Targets aggregate 0.34 · 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
Aortic Aneurysm0.47
Lymphohistiocytosis, Hemophagocytic0.34
Keratoconus0.33

Tractability

Small molecules — Emerging

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

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

View underlying tractability evidence (6)
SM · 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

1 papers · to 2023

Papers linked directly to this protein. This is the protein's own literature — descriptor-derived papers are kept separate below.

Most cited

A first-in-class pan-lysyl oxidase inhibitor impairs stromal remodeling and enhances gemcitabine response and survival in pancreatic cancer.99 cites

Chitty JL · Nature cancer · 2023

Recent

A first-in-class pan-lysyl oxidase inhibitor impairs stromal remodeling and enhances gemcitabine response and survival in pancreatic cancer.

Chitty JL · Nature cancer · 2023

Europe PMC papers linked directly to this protein.