dc.contributor.author | Coronado, Lorena M. | |
dc.contributor.author | De La Guardia, Carolina I. | |
dc.contributor.author | González, Yisett S. | |
dc.contributor.author | Restrepo, Carlos M. | |
dc.contributor.author | Tayler, Nicole M. | |
dc.date.accessioned | 2020-06-26T21:01:59Z | |
dc.date.available | 2020-06-26T21:01:59Z | |
dc.date.issued | 2011-07-01 | |
dc.identifier.issn | 2230-7303 | |
dc.identifier.uri | http://repositorio-indicasat.org.pa/handle/123456789/121 | |
dc.description | Nowadays, 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.abstract | Nowadays, 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.iso | eng | en_US |
dc.rights | info:eu-repo/semantics/openAccess | |
dc.subject | DNA damage | en_US |
dc.subject | antibiotic resistance | en_US |
dc.subject | SSB | en_US |
dc.subject | DSB | en_US |
dc.subject | antimicrobial drugs | en_US |
dc.subject | drug-resistant mutants | en_US |
dc.subject | BER | en_US |
dc.subject | NER | en_US |
dc.subject | HRR | en_US |
dc.subject | NHEJ | en_US |
dc.title | DNA Repair Mechanisms as Drug Targets in Prokaryotes | en_US |
dc.type | info:eu-repo/semantics/article | en_US |
dc.type | info:edu-repo/semantics/publishedVersion | |