11 research outputs found
Balance between sympathetic response to head-up tilt and cardiac vagal factors in healthy humans
Training-induced increase in nitric oxide metabolites in chronic heart failure and coronary artery disease: an extra benefit of water-based exercises?
Sympathetic activity and early mobilization in patients in intensive and intermediate care with severe brain injuries: a preliminary prospective randomized study
Hypoglycemia Activates Orexin Neurons and Selectively Increases Hypothalamic Orexin-B Levels: Responses Inhibited by Feeding and Possibly Mediated by the Nucleus of the Solitary Tract
M-Cadherin Activates Rac1 GTPase through the Rho-GEF Trio during Myoblast Fusion
Cadherins are transmembrane glycoproteins that mediate Ca(2+)-dependent homophilic cell–cell adhesion and play crucial role during skeletal myogenesis. M-cadherin is required for myoblast fusion into myotubes, but its mechanisms of action remain unknown. The goal of this study was to cast some light on the nature of the M-cadherin–mediated signals involved in myoblast fusion into myotubes. We found that the Rac1 GTPase activity is increased at the time of myoblast fusion and it is required for this process. Moreover, we showed that M-cadherin–dependent adhesion activates Rac1 and demonstrated the formation of a multiproteic complex containing M-cadherin, the Rho-GEF Trio, and Rac1 at the onset of myoblast fusion. Interestingly, Trio knockdown efficiently blocked both the increase in Rac1-GTP levels, observed after M-cadherin–dependent contact formation, and myoblast fusion. We conclude that M-cadherin–dependent adhesion can activate Rac1 via the Rho-GEF Trio at the time of myoblast fusion