When lipid diacylglycerol (DAG) binds to the C1 domain, CHN1 is transferred to the plasma membrane and negatively regulates Rho-family small GTPases RAC1 and CDC42, thus causing the morphological change of axons by pruning the ends of axon dendrites.
mTORC2 has been shown to function as an important regulator of the cytoskeleton through its stimulation of F-actin stress fibers, paxillin, RhoA, Rac1, Cdc42, and protein kinase C α (PKCα).
E-cadherin binding to p120ctn may activate SRC leading to activation of Rac1 which results in phosphorylation of LIMK1 and LIMK2 to deactivate cofilin causing G-actin polymerization.