Literature summary for 3.4.22.63 extracted from

Mohr, A.; Deedigan, L.; Jencz, S.; Mehrabadi, Y.; Houlden, L.; Albarenque, S.M.; Zwacka, R.M.
Caspase-10 a molecular switch from cell-autonomous apoptosis to communal cell death in response to chemotherapeutic drug treatment (2018), Cell Death Differ., 25, 340-352 .

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Application

Application	Comment	Organism
medicine	the apoptosis-inducing complex FADDosome is driven by ATR-dependent caspase-10 upregulation. During FADDosome-induced apoptosis, FLICE-inhibitory protein cFLIPL is ubiquitinated by TRAF2, leading to its degradation and subsequent adaptor protein FADD-dependent caspase-8 activation. Cancer cells lacking caspase-10, TRAF2 or ATR switch from this cell-autonomous suicide to a more effective, autocrine/paracrine mode of apoptosis initiated by a different complex, the FLIPosome. It leads to processing of cFLIPL to cFLIPp43, TNF-alpha production and consequently, contrary to the FADDosome, p53-independent apoptosis	Homo sapiens

Organism

Organism	UniProt	Comment	Textmining
Homo sapiens	Q92851	-	-

Source Tissue

Source Tissue	Comment	Organism	Textmining
A-2780 cell	-	Homo sapiens	-
HCT-116 cell	-	Homo sapiens	-
HT-29 cell	-	Homo sapiens	-

General Information

General Information	Comment	Organism
physiological function	the apoptosis-inducing complex FADDosome is driven by ATR-dependent caspase-10 upregulation. During FADDosome-induced apoptosis, FLICE-inhibitory protein cFLIPL is ubiquitinated by TRAF2, leading to its degradation and subsequent adaptor protein FADD-dependent caspase-8 activation. Cancer cells lacking caspase-10, TRAF2 or ATR switch from this cell-autonomous suicide to a more effective, autocrine/paracrine mode of apoptosis initiated by a different complex, the FLIPosome. It leads to processing of cFLIPL to cFLIPp43, TNF-alpha production and consequently, contrary to the FADDosome, p53-independent apoptosis	Homo sapiens

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Release 2023.1 (January 2023)