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Literature summary extracted from

  • Pucer, A.; Castino, R.; Mirkovi?, B.; Falnoga, I.; Slejkovec, Z.; Isidoro, C.; Lah, T.T.
    Differential role of cathepsins B and L in autophagy-associated cell death induced by arsenic trioxide in U87 human glioblastoma cells (2010), Biol. Chem., 391, 519-531.
    View publication on PubMed

Protein Variants

EC Number Protein Variants Comment Organism
3.4.22.1 additional information downregulation of CatB by siRNA leads to 33% residual activity of CatB, but has no effect on caspase 3/7 activation Homo sapiens

Inhibitors

EC Number Inhibitors Comment Organism Structure
3.4.22.1 arsenite i.e. arsenic trioxide, inhibits CatB in glioblastoma cells, 20% inhibition at 0.022 mM, 50% at 0.020 mM Homo sapiens
3.4.22.1 CA-074-Me strong inhibition Homo sapiens
3.4.22.1 CLIK148
-
 Homo sapiens

Localization

EC Number Localization Comment Organism GeneOntology No. Textmining
3.4.22.1 lysosome
-
 Homo sapiens 5764
-

Organism

EC Number Organism UniProt Comment Textmining
3.4.22.1 Homo sapiens
-
-
-

Source Tissue

EC Number Source Tissue Comment Organism Textmining
3.4.22.1 glioblastoma cell upregulation of CatB Homo sapiens
-
3.4.22.1 U-87MG cell upregulation of CatB Homo sapiens
-

Synonyms

EC Number Synonyms Comment Organism
3.4.22.1 CatB
-
 Homo sapiens

General Information

EC Number General Information Comment Organism
3.4.22.1 malfunction arsenite treatment of human glioblastoma cells induces autophagosome formation and permeabilization of mitochondria, followed by caspase 3/7-mediated apoptosis. Arsenite toxicity involves a complex interplay between autophagy and apoptosis in human glioblastoma cells and is associated with inhibition of CatB, mechanism, overview Homo sapiens