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.
Mehlen, P, Rabizadeh, S, Snipas, SJ, Assa-Munt, N, Salvesen, GS, Bredesen, DE
Mehlen, P, Furne, C
Forcet, C, Ye, X, Granger, L, Corset, V, Shin, H, Bredesen, DE, Mehlen, P
Mehlen, P, Fearon, ER
aspartic-type endopeptidase activity of Caspase-3 [cytosol]
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