Reactome | Caspase cleavage of DCC

Caspase cleavage of DCC

Stable Identifier

R-HSA-373705

Type

Reaction [transition]

Species

Homo sapiens

Compartment

cytosol, plasma membrane

ReviewStatus

5/5

Locations in the PathwayBrowser

Expand all

General

SBML | | PDF

SVG | | PPTX | SBGN

Click the image above or here to open this reaction in the Pathway Browser
The layout of this reaction may differ from that in the pathway view due to the constraints in pathway layout

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 Mehlen, P, Rabizadeh, S, Snipas, SJ, Assa-Munt, N, Salvesen, GS, Bredesen, DE	Nature	1998
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