Department of Biological Science and Technology, The University of Tokushima Graduate School, Tokushima 770-8506, Japan.
Biochem Biophys Res Commun. 2012 May 4;421(2):239-44. doi: 10.1016/j.bbrc.2012.03.143. Epub 2012 Apr 4.
Although the cGMP/cGMP-dependent protein kinase (cGK) signaling is involved in the regulation of neurite outgrowth, its mechanism remains to be clarified. In this study, we identified a Rho effector, rhotekin, as a cGK-I-interacting protein. Rhotekin was also a substrate for cGK-Iα. In neurite-extended Neuro2A neuroblastoma cells, cGK-Iα and rhotekin were colocalized in the plasma membrane and extended neurites, while treatment with cGMP resulted in translocation of rhotekin to the cytoplasm. In addition, we found that cGK-Iα and rhotekin synergistically suppressed Rho-induced neurite retraction. Our findings suggest that cGK-Iα interacts with and phosphorylates rhotekin, thereby contributing to neurite outgrowth regulation.
尽管环鸟苷酸（cGMP）/cGMP 依赖性蛋白激酶（cGK）信号通路参与了神经突生长的调控，但它的作用机制仍不清楚。在这项研究中，我们鉴定了 Rho 效应蛋白 rhotekin 是 cGK-I 的相互作用蛋白。rhotekin 也是 cGK-Iα 的底物。在神经突延伸的 Neuro2A 神经母细胞瘤细胞中，cGK-Iα 和 rhotekin 共定位于质膜和延伸的神经突中，而 cGMP 的处理导致 rhotekin 易位到细胞质中。此外，我们发现 cGK-Iα 和 rhotekin 协同抑制 Rho 诱导的神经突回缩。我们的研究结果表明，cGK-Iα 与 rhotekin 相互作用并磷酸化 rhotekin，从而有助于神经突生长的调控。
