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During Shigella flexneri infection host protein Toca-1 precipitate not only the Shigella type 3 secreted effector protein IcsB, but also the type 3 secreted proteins OspC3, IpgD and IpaB. In infected cells, OspC3-mediated restriction of IL-18 production does not require the interaction with Toca-1.
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This suggests that TOCA1 binding to Cdc42 is an early step in the Cdc42-dependent pathways that govern actin dynamics, and the differential binding affinities of the effectors facilitate a handover from TOCA1 to N-WASP, which can then drive recruitment of the actin-modifying machinery.
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Loss of p53 tumor suppressor function in breast cancers leads to upregulation of Toca-1, and results in enhanced risk of developing metastatic disease.
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GWAS results show that the aggregate effects of common SNPs explain 22-46% of phenotypic variation in childhood intelligence in the three largest cohorts; FNBP1L was also significantly associated with childhood intelligence
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findings suggest that Toca-1 functions at an early step in the dissemination of metastatic breast tumor cells; taken together, results identify Toca-1 as a proinvasive protein in breast adenocarcinoma
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Toca-1 knockdown cells also display a significant defect in EGF-induced motility and invasiveness.
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Cdc42 may influence endocytic membrane trafficking by regulating the formation and activity of the Toca-1/N-WASP complex.
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Toca-1 promotes actin nucleation by activating the N-WASP-WIP/CR16 complex, the predominant form of N-WASP in cells.
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a vesicle trafficking regulator Toca-1 regulates different aspects of neuronal morphology from N-WASP
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We show that actin tail initiation by S. flexneri requires Toca-1 for the conversion of N-WASP from a closed inactive conformation to an open active one.
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the Toca-1-N-WASP complex can link filopodial formation to endocytosis
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Human FNBP1L binds the autophagy protein Atg3 and is required for autophagy of Salmonella Typhimurium in epithelial cells