Lack of C3G triggers embryonic lethality in mice and mutant fibroblasts show impaired cell adhesion, delayed spreading and enhanced cell migration. Nevertheless the mechanisms through which C3G regulates these cellular functions are poorly understood. Cell adhesion and migration are essentially dependent on modulation of actin dynamics in reaction to extracellular signals, and on inside out signaling influencing integrin bioactive small molecule library function. The Rho family GTPases have been implicated as mediators of actin rearrangements through their capability to activateWasp meats, assisting Arp2/3 induced nucleation of actin polymerization. These molecular events are responsible for morphological changes in the cells like lamellipodia and filopodia formation, needed for navigation and exploration. Rap1, the main effector of C3G activation, has demonstrated an ability to regulate adhesion and motility dependent cellular functions by controlling actin dynamics. Rap1 is activated by a variety of stimuli including adhesion, growth facets, neurotransmitters and cytokines. Rap1 may stimulate other GTPases resulting in cytoskeletal reorganization, though its downstream effectors are not very well understood. TC10, another substrate of C3G induces actin rich cellular processes. Ena/VASP family of proteins increase filopodial dynamics through their ability to generate profilin and present actin filament anticapping property. Formins are another type of molecules able to triggering actin nucleation and making similar linear filaments resulting in filopodia formation. Filopodia are skinny Mitochondrion actin rich protrusions put forth by cells under various physiological conditions for example epithelial cell migration during embryonic development, neuronal growth cone extension, immune cell migration, phagocytosis and host?pathogen connections. The molecular effectors of signaling pathways leading to filopodia development have yet to be defined. The c Abl tyrosine kinase regulates F actin dependent cytoskeletal changes to affect migration, cell adhesion, virus contamination, neurite outgrowth and apoptosis. In a kinase dependent fashion, h Abl influences filopodia Crizotinib PF-2341066 in cells spreading on fibronectin and this property has been linked to its role in cell migration. The mechanisms involved in d Abl activation and the molecular effectors involved by these kinases in promoting filopodial actin assembly remain to be described. Since the signals that mediate cell adhesion and migration converge on actin regulatory compounds, we investigated whether C3G performs a in actin cytoskeletal reorganization. In today’s study, we have uncovered a novel purpose of C3G in its ability to regulate actin reorganization to cause filopodia. Using equally overexpression and knockdown methods, we define a pathway involving C3G in filopodia formation.