CV Lattes
Universidade Federal de São Paulo (UNIFESP). Campus São Paulo. Escola Paulista de Medicina (EPM) (Institutional affiliation from the last research proposal) Birthplace: Brazil
PhD in Sciences and Master in Microbiology and Immunology both in Dept. of Micro, Immunology and Parasitology of Federal University of São Paulo (UNIFESP). Bachelor in Marine Biology at State University of São Paulo (UNESP). In recent years I studied the role of host cell signaling pathways responsible for the regulation of actin dynamics during invasion of Trypanosoma cruzi extracellular amastigotes (EAs). I am used to techniques such as confocal microscopy, western blotting and overexpression / depletion of proteins by lentiviral transduction. Currently, i am seeking new mediators of actin cytoskeleton during EA host invasion using biochemical techniques coupled to mass spectrometry. Keywords: Trypanosoma cruzi, extracellular amastigotes, actin cytoskeleton, host cell invasion, host cell signaling (Source: Lattes Curriculum)
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The etiologic agent of Chagas Disease, Trypanosoma cruzi is able to infect professional and non-professional phagocytic cells by mechanisms that depend, among other factors, on the parasite form. While bloodstream trypomastigotes rely on host cell lysosome exocytosis, extracellular amastigotes (AEs), object of our study, mainly depend on the actin cytoskeleton to invade mammalian host cel…
Chagas' disease is caused by the flagellated protozoan Trypanosoma cruzi. The extracellular amastigotes (EA) cellular invasion is highly dependent on the actin cytoskeleton of the host cell whose regulation during this specific interaction remains poorly characterized. The Cdc42 and Rac1 GTPases are involved in a variety of in various cellular processes, but mainly in the regulation of th…
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