Journal
JOURNAL OF NUCLEIC ACIDS
Volume 2010, Issue -, Pages -Publisher
HINDAWI LTD
DOI: 10.4061/2010/840768
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Funding
- CNPq
- Fundacao de Amparo a Pesquisa do Estado de Minas Gerais-FAPEMIG (Brazil)
- Howard Hughes Medical Institute
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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.
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