Overexpression of wild-type UNC5C causes low-grade death, intensified by an AD-linked mutation T835M inhibited by a AD-linked survival factor, calmodulin-like skin protein (CLSP), and a natural ligand of UNC5C, netrin1. T835M-UNC5C-induced neuronal cell death is mediated by an intracellular death-signaling cascade, consisting of DAPK1/protein kinase D/apoptosis signal-regulating kinase 1 (ASK1)/JNK/NADPH oxidase/caspases, which merges at ASK1 with a death-signaling cascade, mediated by amyloid ß precursor protein (APP).
Overexpression of UNC5B induces neuronal death by activating death-associated protein kinase (DAPK1) (19) via protein phosphatase 2A-mediated dephosphorylation of DAPK1 (20).
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If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.