Cathepsin C

CTSC
Available structures
PDBOrtholog search: PDBe RCSB
Identifiers
AliasesCTSC, CPPI, DPP-I, DPP1, DPPI, HMS, JP, JPD, PALS, PDON1, PLS, cathepsin C
External IDsOMIM: 602365; MGI: 109553; HomoloGene: 1373; GeneCards: CTSC; OMA:CTSC - orthologs
Orthologs
SpeciesHumanMouse
Entrez

1075

13032

Ensembl

ENSG00000109861

ENSMUSG00000030560

UniProt

P53634

P97821

RefSeq (mRNA)

NM_148170
NM_001114173
NM_001814

NM_009982
NM_001311790

RefSeq (protein)

NP_001107645
NP_001805
NP_680475

NP_001298719
NP_034112

Location (UCSC)Chr 11: 88.27 – 88.36 MbChr 7: 87.93 – 87.96 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse
Cathepsin C exclusion domain
re-determination of the native structure of human dipeptidyl peptidase i (cathepsin c)
Identifiers
SymbolCathepsinC_exc
PfamPF08773
InterProIPR014882
SCOP21k3b / SCOPe / SUPFAM
Available protein structures:
PDB  IPR014882 PF08773 (ECOD; PDBsum)  
AlphaFold

Cathepsin C (CTSC) also known as dipeptidyl peptidase I (DPP-I or DPP1) is a lysosomal exo-cysteine protease belonging to the peptidase C1 protein family, a subgroup of the cysteine cathepsins. In humans, it is encoded by the CTSC gene.[5][6]

Function

Cathepsin C appears to be a central coordinator for activation of many serine proteases in immune/inflammatory cells.

Cathepsin C catalyses excision of dipeptides from the N-terminus of protein and peptide substrates, except if (i) the amino group of the N-terminus is blocked, (ii) the site of cleavage is on either side of a proline residue, (iii) the N-terminal residue is lysine or arginine, or (iv) the structure of the peptide or protein prevents further digestion from the N-terminus.

Inflammatory response

Particularly, it is involved in activation of neutrophil serine proteases (NSPs; i.e., cathepsin G, proteinase 3 and neutrophil elastase) as they are synthesised as inactive proenzymes during neutrophil maturation. Then, they are released during degranulation.[7][8] Other enzymes activated by cathepsin C are: chymase and tryptase in mast cells and granzymes A and B, cathepsin G, and elastase in lymphocytes and natural killer cells (NK cells).[9]

Overactivation of NSPs causes a cascade of processess that result in excessive lung inflammation and reduced pathogen clearance. They involve reduced secretion of antileukoproteinase, extracellular matrix degradation, activation of IL-1β, IL-8 and TNF-α as well as inhibition of alpha-1 antitrypsin, an enzyme involved in NSP degradation.[8]

Structure

The cDNAs encoding rat, human, murine, bovine, dog and two Schistosome cathepsin Cs have been cloned and sequenced and show that the enzyme is highly conserved.[10] The human and rat cathepsin C cDNAs encode precursors (prepro-cathepsin C) comprising signal peptides of 24 residues, pro-regions of 205 (rat cathepsin C) or 206 (human cathepsin C) residues and catalytic domains of 233 residues which contain the catalytic residues and are 30–40% identical to the mature amino acid sequences of papain and a number of other cathepsins including cathepsins, B, H, K, L, and S.[11]

The translated prepro-cathepsin C is processed into the mature form by at least four cleavages of the polypeptide chain. The signal peptide is removed during translocation or secretion of the pro-enzyme (pro-cathepsin C) and a large N-terminal proregion fragment (also known as the exclusion domain),[12] which is retained in the mature enzyme, is separated from the catalytic domain by excision of a minor C-terminal part of the pro-region, called the activation peptide. A heavy chain of about 164 residues and a light chain of about 69 residues are generated by cleavage of the catalytic domain.

Unlike the other members of the papain family, mature cathepsin C consists of four subunits, each composed of the N-terminal proregion fragment, the heavy chain and the light chain. Both the pro-region fragment and the heavy chain are glycosylated.

Clinical significance

Defects in the encoded protein have been shown to be a cause of Papillon-Lefevre disease,[13][14] an autosomal recessive disorder characterized by palmoplantar keratosis and periodontitis.

Inhibition of DPP-I addresses the inflammatory response that is thought to be responsible for one of many aspects of degenerative lung diseases, including bronchiectasis[15], chronic obstructive pulmonary disease (COPD), asthma and asthma-COPD overlap [16].

Brensocatib, a DPP-I inhibitor, was approved in 2025 by the FDA[17] and the EMA[18] to treat bronchiectasis.

References

  1. ^ a b c GRCh38: Ensembl release 89: ENSG00000109861Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000030560Ensembl, May 2017
  3. ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. ^ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  5. ^ "Entrez Gene: CTSC cathepsin C".
  6. ^ Paris A, Strukelj B, Pungercar J, Renko M, Dolenc I, Turk V (August 1995). "Molecular cloning and sequence analysis of human preprocathepsin C". FEBS Letters. 369 (2–3): 326–330. Bibcode:1995FEBSL.369..326P. doi:10.1016/0014-5793(95)00777-7. PMID 7649281. S2CID 45737414.
  7. ^ Korkmaz B, Horwitz MS, Jenne DE, Gauthier F (December 2010). "Neutrophil elastase, proteinase 3, and cathepsin G as therapeutic targets in human diseases". Pharmacological Reviews. 62 (4): 726–759. doi:10.1124/pr.110.002733. PMC 2993259. PMID 21079042.
  8. ^ a b Chalmers JD, Kettritz R, Korkmaz B (2023-12-14). "Dipeptidyl peptidase 1 inhibition as a potential therapeutic approach in neutrophil-mediated inflammatory disease". Frontiers in Immunology. 14 1239151. doi:10.3389/fimmu.2023.1239151. PMC 10755895. PMID 38162644.
  9. ^ McGuire M, Lipsky P, Thiele D (February 1993). "Generation of active myeloid and lymphoid granule serine proteases requires processing by the granule thiol protease dipeptidyl peptidase I." Journal of Biological Chemistry. 268 (4): 2458–2467. doi:10.1016/S0021-9258(18)53798-4.
  10. ^ Hola-Jamriska L, Tort JF, Dalton JP, Day SR, Fan J, Aaskov J, et al. (August 1998). "Cathepsin C from Schistosoma japonicum--cDNA encoding the preproenzyme and its phylogenetic relationships". European Journal of Biochemistry. 255 (3): 527–534. doi:10.1046/j.1432-1327.1998.2550527.x. PMID 9738890.
  11. ^ Kominami E, Ishido K, Muno D, Sato N (July 1992). "The primary structure and tissue distribution of cathepsin C". Biological Chemistry Hoppe-Seyler. 373 (7): 367–373. doi:10.1515/bchm3.1992.373.2.367. PMID 1515062.
  12. ^ Turk D, Janjić V, Stern I, Podobnik M, Lamba D, Dahl SW, et al. (December 2001). "Structure of human dipeptidyl peptidase I (cathepsin C): exclusion domain added to an endopeptidase framework creates the machine for activation of granular serine proteases". The EMBO Journal. 20 (23): 6570–6582. doi:10.1093/emboj/20.23.6570. PMC 125750. PMID 11726493.
  13. ^ Wani AA, Devkar N, Patole MS, Shouche YS (February 2006). "Description of two new cathepsin C gene mutations in patients with Papillon-Lefèvre syndrome". Journal of Periodontology. 77 (2): 233–237. doi:10.1902/jop.2006.050124. PMID 16460249.
  14. ^ Meade JL, de Wynter EA, Brett P, Sharif SM, Woods CG, Markham AF, et al. (May 2006). "A family with Papillon-Lefevre syndrome reveals a requirement for cathepsin C in granzyme B activation and NK cell cytolytic activity". Blood. 107 (9): 3665–3668. doi:10.1182/blood-2005-03-1140. PMID 16410452.
  15. ^ Johnson E, Gilmour A, Chalmers JD (April 2025). "Dipeptidyl peptidase-1 inhibitors in bronchiectasis". European Respiratory Review. 34 (176): 240257. doi:10.1183/16000617.0257-2024. PMC 12175074. PMID 40533102.
  16. ^ Tanabe N, Matsumoto H, Kogo M, Morimoto C, Nomura N, Hayashi Y, et al. (May 2025). "Exploring the roles of airway dipeptidyl peptidase 1 in obstructive airway disease". ERJ Open Research. 11 (3): 00841–02024. doi:10.1183/23120541.00841-2024. PMC 12086829. PMID 40391061.
  17. ^ Research CF (2026-01-02). "Novel Drug Approvals for 2025". FDA.
  18. ^ "First treatment for serious chronic lung disease | European Medicines Agency (EMA)". www.ema.europa.eu. 2025-10-17. Retrieved 2026-01-10.

Further reading