Leonardo Carmo de Andrade Lima

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-|[[Image:Leo Lima.jpg|150px|left]]+|[[Image:Leo_Lima3.jpg|150px|left]]
-|I Am an undergrad student of Biology at University of Sao Paulo, currently in third year. I develop a Scientific Iniciation project, supported by FAPESP, entitled: '''Effects of expression modulation of ATR and polη in clelular responses induced by UVB.'''+
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-== Resumo do Projeto ==+
-Com o potencial que a luz ultravioleta tem em lesionar o DNA nos seres vivos, foram selecionados evolutivamente mecanismos celulares, como reparo e tolerância a danos no DNA, além de maquinarias de checagem que coordenam a progressão do ciclo celular e mantém a estabilidade e manutenção do material genético.+
-A proteína ATR possui papel central e coordena essa sinalização de checagem de danos no DNA, sendo ativada por simples quebras e forquilhas de replicação bloqueadas, eventos comumente encontrados após UV, o que resulta em atraso ou parada do ciclo celular possibilitando tempo para reparo adequado desses danos. Para esse reparo, a via mais flexível e versátil é o reparo por excisão de nucleotídeos (NER), o qual reconhece lesões que promovem distorções na dupla hélice do DNA. Outro mecanismo que a célula utiliza em conjunto ao reparo é a tolerância aos danos, através de DNA polimerases, que conseguem ultrapassar as lesões devido a sítios catalíticos mais abertos acomodando grandes lesões, fazendo a síntese translesão (TLS). Com destaque para polη, a qual é expressa pelo gene XPV.+
-Desta forma, pretendemos neste projeto empregar o mecanismo de RNAi para induzir o silenciamento dos genes ATR e XPV, com vista a obter informações de como células humanas, principalmente aquelas com deficiência em NER, se comportam após irradiação UVB. Para isso, utilizaremos ensaios de sobrevivência e de citometria de fluxo para investigar a sensibilidade dessas células.+
-==Publicações==+ 
-|}+I Am a graduate student of Biology at University of Sao Paulo, supported by FAPESP.
 + 
 + 
 +== Project Abstract ==
 +With all the potential that ultraviolet (UV) radiation has to damage DNA, cellular mechanisms have been selected evolutionarily, such as repair and tolerance to DNA damage, besides checkpoint machinery which coordinates cell-cycle progression and maintains genome stability and maintenance.
 +The ATR protein has a central role by coordinating this DNA damage checking signaling. It is activated by single strand breaks and arrested replication forks. These events are normally triggered by UV radiation and results in stalled or halted cell-cycle, which gives time to appropriate lesion repair. The more flexible and versable repair path is the nucleotide excision repair (NER), which recognizes bulky DNA lesions. Cells also possess a mechanism where specialized DNA polymerases help to overcome replication blocks when occasional unrepaired DNA lesions stall the replication machinery, accomplishing a translesion synthesis (TLS). The DNA polymerase η (polη), expressed by XPV gene, has a great significance in this context.
 +Therefore, we intend in this project to apply the RNA interference (RNAi) technology to induce ATR and XPV silencing, in order to obtain information of how human fibroblast cells, mainly deficient in NER, behave after UVB irradiation. To achieve this, we will perform survival and cytometry assays to investigate these cells sensibility.
 + 
 +==Publications==
 + 
 +1.'''Andrade-Lima, L. C.'''; Jogo da Resposta ao Dano no DNA. Revista Genética na Escola. Vol IX, artigo 6. 2014 (http://geneticanaescola.com.br/vol-ix1-artigo-06/)
 + 
 +2. Veloso A, Biewen B, Paulsen MT, Berg N, '''Carmo de Andrade Lima L''', Prasad J, Bedi K, Magnuson B, Wilson TE, Ljungman M.; Genome-wide transcriptional effects of the anti-cancer agent camptothecin. PLoS One. 2013 Oct 23;8(10) (http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0078190)
 + 
 +3.Kobayashi GS, Alvizi L, Sunaga DY, Francis-West P, Kuta A, Almada BV, Ferreira SG, '''de Andrade-Lima LC''', Bueno DF, Raposo-Amaral CE, Menck CF, Passos-Bueno MR.; Susceptibility to DNA damage as a molecular mechanism for non-syndromic cleft lip and palate. PLoS One. 2013 Jun 12;8(6) (http://dx.plos.org/10.1371/journal.pone.0065677)
 + 
 +4.Maria Berra C, de Oliveira CS, Machado Garcia CC, Reily Rocha CR, Koch Lerner L, '''de Andrade Lima LC''', da Silva Baptista M, Martins Menck CF.; Nucleotide excision repair activity on DNA damage induced by photoactivated methylene blue. Free Radic Biol Med. 2013 Apr 6;61C:343-356 (http://www.sciencedirect.com/science/article/pii/S0891584913001317)

Current revision

Image:Leo Lima3.jpg


I Am a graduate student of Biology at University of Sao Paulo, supported by FAPESP.


[edit]

Project Abstract

With all the potential that ultraviolet (UV) radiation has to damage DNA, cellular mechanisms have been selected evolutionarily, such as repair and tolerance to DNA damage, besides checkpoint machinery which coordinates cell-cycle progression and maintains genome stability and maintenance. The ATR protein has a central role by coordinating this DNA damage checking signaling. It is activated by single strand breaks and arrested replication forks. These events are normally triggered by UV radiation and results in stalled or halted cell-cycle, which gives time to appropriate lesion repair. The more flexible and versable repair path is the nucleotide excision repair (NER), which recognizes bulky DNA lesions. Cells also possess a mechanism where specialized DNA polymerases help to overcome replication blocks when occasional unrepaired DNA lesions stall the replication machinery, accomplishing a translesion synthesis (TLS). The DNA polymerase η (polη), expressed by XPV gene, has a great significance in this context. Therefore, we intend in this project to apply the RNA interference (RNAi) technology to induce ATR and XPV silencing, in order to obtain information of how human fibroblast cells, mainly deficient in NER, behave after UVB irradiation. To achieve this, we will perform survival and cytometry assays to investigate these cells sensibility.

[edit]

Publications

1.Andrade-Lima, L. C.; Jogo da Resposta ao Dano no DNA. Revista Genética na Escola. Vol IX, artigo 6. 2014 (http://geneticanaescola.com.br/vol-ix1-artigo-06/)

2. Veloso A, Biewen B, Paulsen MT, Berg N, Carmo de Andrade Lima L, Prasad J, Bedi K, Magnuson B, Wilson TE, Ljungman M.; Genome-wide transcriptional effects of the anti-cancer agent camptothecin. PLoS One. 2013 Oct 23;8(10) (http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0078190)

3.Kobayashi GS, Alvizi L, Sunaga DY, Francis-West P, Kuta A, Almada BV, Ferreira SG, de Andrade-Lima LC, Bueno DF, Raposo-Amaral CE, Menck CF, Passos-Bueno MR.; Susceptibility to DNA damage as a molecular mechanism for non-syndromic cleft lip and palate. PLoS One. 2013 Jun 12;8(6) (http://dx.plos.org/10.1371/journal.pone.0065677)

4.Maria Berra C, de Oliveira CS, Machado Garcia CC, Reily Rocha CR, Koch Lerner L, de Andrade Lima LC, da Silva Baptista M, Martins Menck CF.; Nucleotide excision repair activity on DNA damage induced by photoactivated methylene blue. Free Radic Biol Med. 2013 Apr 6;61C:343-356 (http://www.sciencedirect.com/science/article/pii/S0891584913001317)

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