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Protein / target

Procathepsin L

Encoded byCTSLP07711Homo sapiensSwiss-Prot
Small-molecule tractable
Druggability
Structure with Ligand
1
Research papers

Protein at a glance

Biological role

Cysteine-type endopeptidase

Strongest disease association

Neurodegenerative Diseases

Via encoding gene CTSL · Pathway evidence · score 0.56

Research activity

Emerging research

1 papers · latest 2021

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

Thiol protease important for the overall degradation of proteins in lysosomes (Probable).

View complete UniProt function annotation

Thiol protease important for the overall degradation of proteins in lysosomes (Probable). Plays a critical for normal cellular functions such as general protein turnover, antigen processing and bone remodeling. Involved in the solubilization of cross-linked TG/thyroglobulin and in the subsequent release of thyroid hormone thyroxine (T4) by limited proteolysis of TG/thyroglobulin in the thyroid follicle lumen (By similarity). In neuroendocrine chromaffin cells secretory vesicles, catalyzes the prohormone proenkephalin processing to the active enkephalin peptide neurotransmitter (By similarity). In thymus, regulates CD4(+) T cell positive selection by generating the major histocompatibility complex class II (MHCII) bound peptide ligands presented by cortical thymic epithelial cells. Also mediates invariant chain processing in cortical thymic epithelial cells (By similarity). Major elastin-degrading enzyme at neutral pH. Accumulates as a mature and active enzyme in the extracellular space of antigen presenting cells (APCs) to regulate degradation of the extracellular matrix in the course of inflammation (By similarity). Secreted form generates endostatin from COL18A1 (PubMed:10716919). Critical for cardiac morphology and function. Plays an important role in hair follicle morphogenesis and cycling, as well as epidermal differentiation (By similarity). Required for maximal stimulation of steroidogenesis by TIMP1 (By similarity)

Subcellular location

LysosomeApical cell membraneCytoplasmic vesicle, secretory vesicle, chromaffin granuleSecreted, extracellular spaceSecretedNucleus
Domains and Gene Ontology detail (38)

Gene Ontology

  • Capical plasma membrane
  • Cchromaffin granule
  • Cendocytic vesicle lumen
  • Cendolysosome lumen
  • Cextracellular exosome
  • Cextracellular matrix
  • Cextracellular region
  • Cextracellular space
  • Clysosomal lumen
  • Clysosome
  • Cmultivesicular body
  • Cnucleus

333 aa · 38 kDa · 2 isoforms

Biological roles

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

Immune signallingUniProt · GOProteolysisUniProt · GOCell adhesionUniProt · GO
View supporting evidence

Immune signalling

  • ·Thiol protease important for the overall degradation of proteins in lysosomes (Probable)…
  • ·adaptive immune response
  • ·antigen processing and presentation
  • ·antigen processing and presentation of exogenous peptide antigen via MHC class II

Proteolysis

  • ·Thiol protease important for the overall degradation of proteins in lysosomes (Probable)…
  • ·cysteine-type endopeptidase activity
  • ·cysteine-type peptidase activity
  • ·proteolysis

Cell adhesion

  • ·Thiol protease important for the overall degradation of proteins in lysosomes (Probable)…
  • ·extracellular matrix

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 CTSL

Gene-level evidence surfaced through the gene CTSL 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.

Neurodegenerative Diseases
0.38Preliminary

Pathway evidence dominant · Open Targets 0.56 · no direct causal or clinical evidence

COVID-19
0.33Preliminary

Pathway evidence dominant · Open Targets 0.39 · no direct causal or clinical evidence

Parkinson's Disease
0.31Preliminary

Pathway evidence dominant · Open Targets 0.39 · no direct causal or clinical evidence

Alzheimer's Disease
0.31Preliminary

Pathway evidence dominant · Open Targets 0.39 · no direct causal or clinical evidence

Severe Acute Respiratory Syndrome
0.26Preliminary

Pathway evidence dominant · Open Targets 0.37 · no direct causal or clinical evidence

View evidence synthesis (5)
Neurodegenerative DiseasesPreliminary
0.38
agreement 0.200.56
Pathway96%Literature5%

Open Targets aggregate 0.56 · 2 independent evidence families · no direct causal or clinical evidence

COVID-19Preliminary
0.33
agreement 0.150.51
Pathway68%Literature32%

Open Targets aggregate 0.39 · 2 independent evidence families · no direct causal or clinical evidence

Parkinson's DiseasePreliminary
0.31
agreement 0.130.49
Pathway73%Literature27%

Open Targets aggregate 0.39 · 2 independent evidence families · no direct causal or clinical evidence

Alzheimer's DiseasePreliminary
0.31
agreement 0.130.49
Pathway73%Literature27%

Open Targets aggregate 0.39 · 2 independent evidence families · no direct causal or clinical evidence

Severe Acute Respiratory SyndromePreliminary
0.26
agreement 0.090.44
Pathway91%Literature9%

Open Targets aggregate 0.37 · 2 independent evidence families · 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
Neurodegenerative Diseases0.56
COVID-190.39
Parkinson's Disease0.39
Alzheimer's Disease0.39
Severe Acute Respiratory Syndrome0.37
Lysosomal Storage Diseases0.37
Multiple Sclerosis0.37
Neoplasms0.12

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 loc med conf) — 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 (9)
SM · Structure with LigandSM · High-Quality LigandSM · Druggable FamilyAB · GO CC high confAB · UniProt loc med 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 2021

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.