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Literature summary for 3.4.22.1 extracted from

  • Oberle, C.; Huai, J.; Reinheckel, T.; Tacke, M.; Rassner, M.; Ekert, P.G.; Buellesbach, J.; Borner, C.
    Lysosomal membrane permeabilization and cathepsin release is a Bax/Bak-dependent, amplifying event of apoptosis in fibroblasts and monocytes (2010), Cell Death Differ., 17, 1167-1178.
    View publication on PubMed

Protein Variants

Protein Variants Comment Organism
additional information CTB knockout MEF cells are partially resistant to apoptosis induced by etoposide and IL-3 deprivation, but cannot be rescued from cell death in contrast to wild-type cells Mus musculus

Localization

Localization Comment Organism GeneOntology No. Textmining
lysosome
-
Mus musculus 5764
-

Organism

Organism UniProt Comment Textmining
Mus musculus
-
-
-

Source Tissue

Source Tissue Comment Organism Textmining
fibroblast
-
Mus musculus
-
monocyte
-
Mus musculus
-

Synonyms

Synonyms Comment Organism
CTB
-
Mus musculus

General Information

General Information Comment Organism
physiological function apoptotic stimuli, e.g. exposure to etoposide, ultraviolet light, FasL or deprivation of interleukin-3, trigger lysosomal membrane permeability, leading to the release of cathepsins, dependent on Bax/Bak and components of the apoptosome, which activate death signaling pathways in the cytosol, overview. Cathepsin B does not contribute to the commitment step of apoptosis, as Bax and Bak do, but enhances the efficiency of apoptosis through an amplification loop Mus musculus