NDR2 acts as the upstream kinase of ARK5 during insulin-like growth factor-1 signaling.

摘要: ARK5 is a tumor progression-associated factor that directly phosphorylated by AKT at serine 600 in the regulatory domain, but phosphorylation conserved threonine residue on active T loop has been found to be required for its full activation. In this study, we identified serine/threonine protein kinase NDR2 as phosphorylates and activates during insulin-like growth (IGF)-1 signaling. Upon stimulation with IGF-1, was phosphorylate 211 of promote cell survival invasion colorectal cancer lines through ARK5. During IGF-1 signaling, three residues (threonine 75, 282, 442) also Among these residues, 282 seemed most important activation (the same mouse homologue) because aspartic acid-converted mutant (NDR2/S282D) induced ARK5-mediated activities even absence IGF-1. As homologue, 75 interaction S100B, binding calcium ion- phospholipase C-γ-dependent manner. We PDK-1 plays an role especially 442. Based results report here upstream essential progression