Masato Nakafuku

TL;DR: Rho appears to inhibit myosin phosphatase through the action of Rho-kinase, which is activated by GTP·RhoA, phosphorylation of MBS and MLC in NIH 3T3 cells.

TL;DR: It is shown that activation of endogenous progenitors leads to massive regeneration of hippocampal pyramidal neurons after ischemic brain injury, expanding the possibility of novel neuronal cell regeneration therapies for stroke and other neurological diseases.

TL;DR: P purified a Rho‐interacting protein with a molecular mass of approximately 164 kDa (p164) from bovine brain that bound to GTPgammaS (a non‐hydrolyzable GTP analog) and is likely to be a putative target serine/threonine kinase for Rho and serves as a mediator of the RHo‐dependent signaling pathway.

TL;DR: In transgenic mouse embryos, N-terminally truncated Gli2, unlike the full length protein, activates a Shh target gene, HNF3beta, in the dorsal neural tube, thus mimicking the effect of Shh signal, which suggests that unmasking of the strong activation potential of Gli 2 through modulation of the N-Terminal repression domain is one of the key mechanisms of the Shh signaling.

TL;DR: Findings suggest that Gli, and probably also Gli2, are good candidates for transcriptional activators of the HNF-3beta floor plate enhancer, and the binding site for Gli proteins is a key element for response to Shh signalling.