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Journal of Nucleic AcidsVolume 2010 2010, Article ID 840768, 14 pages

Review ArticleDepartamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Avenida Antônio Carlos, 6627, Pampulha, 31270-901 Belo Horizonte, MG, Brazil

Received 17 June 2010; Revised 29 July 2010; Accepted 25 August 2010

Academic Editor: Ashis Basu

Copyright © 2010 Danielle Gomes Passos-Silva et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

A wide variety of DNA lesions arise due to environmental agents, normal cellular metabolism, or intrinsic weaknesses in the chemical bonds of DNA. Diverse cellular mechanisms have evolved to maintain genome stability, including mechanisms to repair damaged DNA, to avoid the incorporation of modified nucleotides, and to tolerate lesions translesion synthesis. Studies of the mechanisms related to DNA metabolism in trypanosomatids have been very limited. Together with recent experimental studies, the genome sequencing of Trypanosoma brucei, Trypanosoma cruzi, and Leishmania major, three related pathogens with different life cycles and disease pathology, has revealed interesting features of the DNA repair mechanism in these protozoan parasites, which will be reviewed here.





Autor: Danielle Gomes Passos-Silva, Matheus Andrade Rajão, Pedro Henrique Nascimento de Aguiar, João Pedro Vieira-da-Rocha, Carlos

Fuente: https://www.hindawi.com/



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