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. 2017 Feb 15;8:159. doi: 10.3389/fimmu.2017.00159

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Copyright © 2017 Peng, Zhu, Zhang, Shi, Feng, Liu, Huang and Zheng.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Non-canonical signaling pathway of Shh. By coupling of G protein-coupled receptors, Smo modulates the activation of RhoA/ROCK (MYPT1) signaling through increasing/decreasing MLCP level to enhance/weaken traction force, which results in promoting/reducing rheumatoid arthritis (RA)-fibroblast-like synoviocytes (FLSs) migration. On the other side, Rac1 induces actin polymerization to promote RA-FLSs migration through its downstream protein such as WAVE/ARP2/3 complex. It is likely that Smo serves as a principal mediator of cytoskeletal tension in the process of cell migration.