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Literature summary for 3.4.22.15 extracted from

  • Pranjol, M.Z.I.; Gutowski, N.J.; Hannemann, M.; Whatmore, J.L.
    Cathepsin L induces proangiogenic changes in human omental microvascular endothelial cells via activation of the ERK1/2 pathway (2019), Curr. Cancer Drug Targets, 19, 231-242 .
    View publication on PubMed

Inhibitors

Inhibitors Comment Organism Structure
FY-CHO
-
Homo sapiens

Localization

Localization Comment Organism GeneOntology No. Textmining
extracellular the enzyme is secreted Homo sapiens
-
-
lysosome
-
Homo sapiens 5764
-

Organism

Organism UniProt Comment Textmining
Homo sapiens P07711
-
-

Source Tissue

Source Tissue Comment Organism Textmining
epithelial ovarian cancer cell
-
Homo sapiens
-

Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
Z-Val-Val-Arg-AMC + H2O a cathepsin L-specific substrate Homo sapiens Z-Val-Val-Arg + 7-amino-4-methylcoumarin
-
?

Synonyms

Synonyms Comment Organism
cathepsin L1
-
Homo sapiens
CathL
-
Homo sapiens

General Information

General Information Comment Organism
metabolism CathL acts as an extracellular ligand and plays an important pro-angiogenic, and thus pro-metastatic, role during epithelial ovarian cancer metastasis to the omentum, by activating the omental microvasculature Homo sapiens
physiological function cathepsin L (CathL) is a cysteine endopeptidase, that physiologically plays an important role in degrading endocytosed proteins as well as intracellular proteins. Cathepsin L induces proangiogenic changes in human omental microvascular endothelial cells via activation of the ERK1/2 pathway. Epithelial ovarian cancer (EOC) cells secrete a range of factors with potential pro-angiogenic activity, in disease-relevant human omental microvascular endothelial cells (HOMECs), including the lysosomal protease cathepsin L (CathL), potential pro-proliferative and pro-migratory effects of CathL in HOMECs and the activated signalling pathways. CathL activates the proliferative kinases ERK1/2 and AKT Homo sapiens