Caspase cleavage of DCC

Stable Identifier
R-HSA-373705
Type
Reaction [transition]
Species
Homo sapiens
Compartment
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DCC exerts its pro-apoptotic effect when netrin ligand is absent. When unbound to its ligand, DCC is cleaved roughly in the middle of its intracellular domain (aspartic acid residue 1290) by caspase-3 (Mehlen et al. 1998). The cleavage releases DCC's inhibitory C-terminal domain and exposes the addiction/dependence domain (ADD), which is sufficient for cell death induction.

Literature References
PubMed ID Title Journal Year
9796814 The DCC gene product induces apoptosis by a mechanism requiring receptor proteolysis

Mehlen, P, Rabizadeh, S, Snipas, SJ, Assa-Munt, N, Salvesen, GS, Bredesen, DE

Nature 1998
16158190 Netrin-1: when a neuronal guidance cue turns out to be a regulator of tumorigenesis

Mehlen, P, Furne, C

Cell Mol Life Sci 2005
11248093 The dependence receptor DCC (deleted in colorectal cancer) defines an alternative mechanism for caspase activation

Forcet, C, Ye, X, Granger, L, Corset, V, Shin, H, Bredesen, DE, Mehlen, P

Proc Natl Acad Sci U S A 2001
15310786 Role of the dependence receptor DCC in colorectal cancer pathogenesis

Mehlen, P, Fearon, ER

J Clin Oncol 2004
Participants
Participant Of
Catalyst Activity
Catalyst Activity
Title
aspartic-type endopeptidase activity of Caspase-3 [cytosol]
Physical Entity
Activity
Orthologous Events
Authored
Reviewed
Created