Trypanosoma cruzi, the etiologic agent of Chagas diseases depends on an effective invasion of host cells, intracellular differentiation and proliferation for its survival inside the mammalian host. T. cruzi presents is characterized by two distinct forms in the mammalian host: the trypomastigotes, the infective form and the amastigote, the replicative form. The amastigogenesis, the differentiation process from trypomastigote to amastigote forms, is a fundamental step in the life cycle of the parasite. Currently, our group is interested in verify the possible role of nitric oxide signaling cascades during parasite amastigogenesis, with a main focus in the post-translational modifications of proteins mediated by NO*. S-nitrosylation modulates the biological activity of a large diversity of proteins and consequently, regulating process such as proliferation and differentiation. Accordingly, our group has been showing that both process- adhesion to Extracellular Matrix (ECM) and extracellular amastigogenesis- are able to change the protein S-nitrosylated profile. Therefore, this research project proposal aims to clarify the role of NO* on T. cruzi intracellular amastigogenesis.
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