Kank regulates RhoA-dependent formation of actin stress fibers and cell migration via 14-3-3 in PI3K–Akt signaling

• DOI: 10.1083/jcb.200707022
• Publication Date: 2008-05-05T20:35:20Z
• Authors: Naoto Kakinuma; Badal Chandra Roy; Yun Zhu; Yong Wang; Ryoiti Kiyama
• Keywords: Stress fiber; Proto-Oncogene Proteins c-akt; Actin remodeling

Phosphoinositide-3 kinase (PI3K)/Akt signaling is activated by growth factors such as insulin and epidermal factor (EGF) regulates several functions cell cycling, apoptosis, growth, migration. Here, we find that Kank an Akt substrate located downstream of PI3K a 14-3-3–binding protein. The interaction between 14-3-3 regulated EGF mediated through phosphorylation Akt. In NIH3T3 cells expressing Kank, the amount actin stress fibers reduced, coexpression disrupted this effect. also inhibits insulin-induced migration via binding. Furthermore, active Akt-dependent activation RhoA binding to 14-3-3. Based on these findings, hypothesize negatively formation inhibition activity, which controlled in PI3K–Akt signaling.