Caspase cleavage of DCC

Stable Identifier
Homo sapiens
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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
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
9796814 The DCC gene product induces apoptosis by a mechanism requiring receptor proteolysis

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

Nature 1998
11248093 The dependence receptor DCC (deleted in colorectal cancer) defines an alternative mechanism for caspase activation

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

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
Catalyst Activity

aspartic-type endopeptidase activity of Caspase-3 [cytosol]

Orthologous Events
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