Please use this identifier to cite or link to this item: https://repositorio.unifesp.br/handle/11600/33176
Title: The challenge of Chagas' disease Has the human pathogen, Trypanosoma cruzi, learned how to modulate signaling events to subvert host cells?
Authors: Lima, F. M. [UNIFESP]
Oliveira, P. [UNIFESP]
Mortara, R. A. [UNIFESP]
Silveira, J. F. [UNIFESP]
Bahia, Daniella Marcia Maranhão [UNIFESP]
Universidade Federal de São Paulo (UNIFESP)
Issue Date: 31-Dec-2010
Publisher: Elsevier B.V.
Citation: New Biotechnology. Amsterdam: Elsevier B.V., v. 27, n. 6, p. 837-843, 2010.
Abstract: Chagas' disease, caused by Trypanosoma cruzi, is an urgent and highly prevalent danger that is endemic to Latin America, and which the research community continues to ignore Each year, Chagas' disease kills more people in Latin America compared to any other parasite-borne disease, including malaria in addition, between 15 and 18 million people worldwide are afflicted with this potentially lethal disease Despite these devastating numbers, less than 0 5% of worldwide research and development for neglected diseases was aimed at Chagas' disease the aim of this review is to draw the attention of biotechnologists to the intriguing parasite that causes Chagas' disease, which is T cruzi Additionally, we would also like to convince the community that basic science research can have a profound impact on the diagnosis and treatment of Chagas' disease in this review, we introduce distinct features of T cruzi such as its complex life cycle (e g the potentially infective extracellular amastigote form), its genome and genomics, as well as proteomic analysis of this parasite Notably, the PIK pathway has been widely acknowledged as an excellent target for drug discovery to combat this pathogen Furthermore we also describe how the identification and characterization of PIK genes can aid in neutralizing Trypanosoma infections
URI: http://repositorio.unifesp.br/handle/11600/33176
ISSN: 1871-6784
Other Identifiers: http://dx.doi.org/10.1016/j.nbt.2010.02.003
Appears in Collections:Em verificação - Geral

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