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Overview of DNA Repair in Trypanosoma cruzi, Trypanosoma brucei, and Leishmania major

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...

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Detalles Bibliográficos
Autores principales: Passos-Silva, Danielle Gomes, Rajão, Matheus Andrade, Nascimento de Aguiar, Pedro Henrique, Vieira-da-Rocha, João Pedro, Machado, Carlos Renato, Furtado, Carolina
Formato: Texto
Lenguaje:English
Publicado: SAGE-Hindawi Access to Research 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2952945/
https://www.ncbi.nlm.nih.gov/pubmed/20976268
http://dx.doi.org/10.4061/2010/840768
Descripción
Sumario: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.