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dc.contributor.authorCoronado, Lorena M.
dc.contributor.authorDe La Guardia, Carolina I.
dc.contributor.authorGonzález, Yisett S.
dc.contributor.authorRestrepo, Carlos M.
dc.contributor.authorTayler, Nicole M.
dc.date.accessioned2020-06-26T21:01:59Z
dc.date.available2020-06-26T21:01:59Z
dc.date.issued2011-07-01
dc.identifier.issn2230-7303
dc.identifier.urihttp://repositorio-indicasat.org.pa/handle/123456789/121
dc.descriptionNowadays, a great amount of pathogenic bacteria has been identified such as Mycobacterium sp. and Helicobacter pylori and have become a serious health problem around the world. These bacteria have developed several DNA repair mechanisms as a strategy to neutralize the effect of the exposure to endogenous and exogenous agents that will lead to two different kinds of DNA damage: single strand breaks (SSBs) and double strand breaks (DSBs). For SSBs repair, bacteria use the base excision repair (BER) and nucleotide excision repair (NER) mechanisms, which fix the damaged strand replacing the damaged base or nucleotide. DSBs repair in bacteria is performed by homologous recombination repair (HRR) and non-homologous end-joining (NHEJ). HRR uses the homologous sequence to fix the two damaged strand, while NHEJ repair does not require the use of its homologous sequence. The use of unspecific antibiotics to treat bacterial infections has caused a great deal of multiple resistant strains making less effective the current therapies with antibiotics. In this review, we emphasized the mechanisms mentioned above to identify molecular targets that can be used to develop novel and more efficient drugs in future.en_US
dc.description.abstractNowadays, a great amount of pathogenic bacteria has been identified such as Mycobacterium sp. and Helicobacter pylori and have become a serious health problem around the world. These bacteria have developed several DNA repair mechanisms as a strategy to neutralize the effect of the exposure to endogenous and exogenous agents that will lead to two different kinds of DNA damage: single strand breaks (SSBs) and double strand breaks (DSBs). For SSBs repair, bacteria use the base excision repair (BER) and nucleotide excision repair (NER) mechanisms, which fix the damaged strand replacing the damaged base or nucleotide. DSBs repair in bacteria is performed by homologous recombination repair (HRR) and non-homologous end-joining (NHEJ). HRR uses the homologous sequence to fix the two damaged strand, while NHEJ repair does not require the use of its homologous sequence. The use of unspecific antibiotics to treat bacterial infections has caused a great deal of multiple resistant strains making less effective the current therapies with antibiotics. In this review, we emphasized the mechanisms mentioned above to identify molecular targets that can be used to develop novel and more efficient drugs in future.en_US
dc.language.isoengen_US
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectDNA damageen_US
dc.subjectantibiotic resistanceen_US
dc.subjectSSBen_US
dc.subjectDSBen_US
dc.subjectantimicrobial drugsen_US
dc.subjectdrug-resistant mutantsen_US
dc.subjectBERen_US
dc.subjectNERen_US
dc.subjectHRRen_US
dc.subjectNHEJen_US
dc.titleDNA Repair Mechanisms as Drug Targets in Prokaryotesen_US
dc.typeinfo:eu-repo/semantics/articleen_US
dc.typeinfo:edu-repo/semantics/publishedVersion


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