Any feedback?
Please rate this page
(literature.php)
(0/150)

BRENDA support

Literature summary for 3.4.22.1 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
Search for more literature for 3.4.22.1

Protein Variants

Protein Variants Comment Organism
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

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

Localization

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

Organism

Organism UniProt Comment Textmining
Homo sapiens
-
-
-

Source Tissue

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

Synonyms

Synonyms Comment Organism
CatB
-
 Homo sapiens

General Information

General Information Comment Organism
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