Abp1 has been shown to interact with aproline rich domain in the N-terminus of Piccolo.Abp1 binds to both F-actin and the GTPase Dynamin and has been implicated in linking the actin cytoskeleton to Clathrin-mediated endocytosis. The cAMP-binding guanidine nucleotide exchange factor Epac2 has also been shown to bind to Piccolo through the PDZ domain in Piccolo. Through interactions with Rim2, the Piccolo-Epac2 complex confers cAMP-dependence to evoked vesicle exocytosis in pancreatic ��-cells. Our current and previous Benserazide hydrochloride experiments demonstrate that one function of Piccolo, not shared by the structurally related active zone protein Bassoon, is to regulate the dynamic assembly of presynaptic F-actin. This function appears crucial both for the activity-dependent recruitment of plasticity molecules such as CaMKII, as well as for the regulation of SV exocytosis during neuro transmission. The ability of Piccolo to associate with multiple Actin associated proteins implies that it may spatially NSC 207895 restrict the activities of these proteins, a concept consistent with data presented here demonstrating that Piccolo can spatially control Daam1-mediated F-actin assembly. In this regard, it will be important to elucidate how upstream signaling pathways including Wnt signaling temporally control this and other Actin regulatory mechanisms and how presynaptic F-actin assembly and disassembly are modulated to influence presynaptic function. Previous researches have demonstrated the mechanism of synergism against FLC-resistant C. albicans such as: increasing reactive oxygen species to promote apoptosis, and inhibiting drug efflux pumps to increase intracellular drug concentration. For the synergism of FLC and BBR, our previous comparative proteomic analysis suggested that mitochondrial aerobic respiration shift and endogenous ROS augmentation contributed to the synergistic effect of FLC and BBR in FLC-resistant C. albicans. Based on the above findings, we further investigated the synergistic mechanism of FLC and B-7b against FLC-resistant C.albicans.