Akt and PP2A Reciprocally Regulate the Guanine Nucleotide Exchange Factor Dock6 to Control Axon Growth of Sensory Neurons

Yuki Miyamoto, Tomohiro Torii, Natsuki Yamamori, Toru Ogata, Akito Tanoue, Junji Yamauchi*

*To whom correspondence should be addressed. E-mail: yamauchi-j{at}ncchd.go.jp or jyamauchi{at}nch.go.jp

This PDF file includes:

• Fig. S1. Estimation of the specificity of an anti-Dock6 antibody and efficiency of knockdown of various shRNAs in rat dorsal root ganglion neurons.
• Fig. S2. Generation of Dock6 shRNA transgenic mice.
• Fig. S3. Analysis of peripheral neuronal fibers and the number of CGRP-positive neurons in Dock6 shRNA transgenic mice.
• Fig. S4. Binding of the DHR-1 region of Dock6 to Akt, binding of the kinase region of Akt to Dock6, and identification of the phosphorylation site of Dock6 targeted by Akt.
• Fig. S5. Binding of the DHR-2 region of Dock6 to PP2Ac, the effect of PP2Ac on Dock6 binding to Rac1, and requirement of PP2 in axon growth and Dock6 dephosphorylation.
• Fig. S6. Reintroduction of Dock6 constructs into Dock6 shRNA transgenic mouse dorsal root ganglion neurons.
• Fig. S7. Attenuation of the GEF activity of Dock6 by phosphorylation of Ser¹¹⁹⁴ and the effect of active Rho GTPases in dorsal root ganglion neurons.

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