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Study of protein kinases pathways involved in the invasion process of HeLa cells by Trypanosoma cruzi extracellular amastigotes (EAs)

Grant number: 13/04249-3
Support type:Scholarships in Brazil - Scientific Initiation
Effective date (Start): June 01, 2013
Effective date (End): December 31, 2013
Field of knowledge:Biological Sciences - Parasitology - Protozoology of Parasites
Principal researcher:Renato Arruda Mortara
Grantee:Bianca Rodrigues Lima Ferreira
Home Institution: Escola Paulista de Medicina (EPM). Universidade Federal de São Paulo (UNIFESP). Campus São Paulo. São Paulo , SP, Brazil
Associated research grant:11/51475-3 - Molecular and cellular biology of the parasitism by Trypanosoma cruzi, AP.TEM

Abstract

Trypanosoma cruzi, a flagellate protozoan of the Trypanosomatidae family, is the causative agent of Chagas' disease, which currently affects about 10 million people worldwide. This parasite has distinct developmental stages: bloodstream and metacyclic trypomastigotes, epimastigotes, and amastigotes. The classic infective forms are trypomastigotes, but there is an alternative pathway of cell invasion used by extracellular amastigotes (EAs) forms. EA cellular invasion depends on adhesion, recognition, and activation of several cell proteins which culminates in host actin cytoskeleton mobilization, essential for the cell entry by these forms. Signaling pathways that control this process, however, are still poorly characterized. Protein kinases, key mediators of signaling pathways, regulate cell responses to external stimuli by modifying other proteins by chemically adding phosphate groups to them. This process is fundamental to most signaling and regulatory processes in the eukaryotic cell. Few studies have shown the participation of PKs during the cellular invasion by EAs, however, the pathways associated with these proteins have not been fully described. In this context, this project aims to characterize the role of Src and phosphatidylinositol kinase (PIK) pathways - essential for many cellular functions - during the EA-host cell interaction. The results obtained can support the future development of chemotherapeutic targets and new therapeutic approaches. (AU)

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Scientific publications
(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)
FERREIRA, BIANCA LIMA; FERREIRA, EDEN RAMALHO; BONFIM-MELO, ALEXIS; MORTARA, RENATO ARRUDA; BAHIA, DIANA. Trypanosoma cruzi extracellular amastigotes selectively trigger the PI3K/Akt and Erk pathways during HeLa cell invasion. Microbes and Infection, v. 21, n. 10, p. 485-489, . (13/04249-3, 11/51475-3)

Please report errors in scientific publications list by writing to: cdi@fapesp.br.