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Suppression Of Rhog Activity Is Mediated By A Syndecan 4–Synectin–Rhogdi1 Complex And Is Reversed By Pkcα In A Rac1 Activation Pathway, Arye Elfenbein, John M. Rhodes, Julia Meller, Martin A. Schwartz, Michiyuki Matsuda, Michael Simons
Suppression Of Rhog Activity Is Mediated By A Syndecan 4–Synectin–Rhogdi1 Complex And Is Reversed By Pkcα In A Rac1 Activation Pathway, Arye Elfenbein, John M. Rhodes, Julia Meller, Martin A. Schwartz, Michiyuki Matsuda, Michael Simons
Dartmouth Scholarship
Fibroblast growth factor 2 (FGF2) is a major regulator of developmental, pathological, and therapeutic angiogenesis. Its activity is partially mediated by binding to syndecan 4 (S4), a proteoglycan receptor. Angiogenesis requires polarized activation of the small guanosine triphosphatase Rac1, which involves localized dissociation from RhoGDI1 and association with the plasma membrane. Previous work has shown that genetic deletion of S4 or its adapter, synectin, leads to depolarized Rac activation, decreased endothelial migration, and other physiological defects. In this study, we show that Rac1 activation downstream of S4 is mediated by the RhoG activation pathway. RhoG is maintained in an inactive …