Gustavo Satoru Kajitani

From Laboratório de Reparo de DNA

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-Estudante do curso Ciências Biológicas da Universidade de São Paulo (USP), cursando o terceiro ano da graduação. Atualmente está desenvolvendo um projeto de iniciação científica com co-orientação da doutoranda Carolina Quayle, com o apoio da FAPESP.+{|
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 +|Bsc,<b>Biological Sciences</b>, <b>Universidade de São Paulo ISP</b>, 2013 <br>Has experience in In vivo research, Cell Biology, Molecular Biology, Neuroinflammation, and DNA repair deficiencies<br><br> Gustavo Satoru is a <b>PhD student</b> in the DNA Repair Lab - <b>Institute of Biomedical Sciences</b> at <b>University of Sao Paulo</b> since 2013, having spent one year of his PhD as a <b>visiting scientist</b> in the [https://www.hsph.harvard.edu/james-mitchell/gustavo-satoru-kajitani/ Mitchell Lab] - <b>Harvard T.H. Chan School of Public Health</b>.<br><br>Research keywords: <b>DNA Repair</b>, <b> Photolesions</b>,<b>Aging and Inflammation</b>.<br><br>[http://buscatextual.cnpq.br/buscatextual/visualizacv.do?metodo=apresentar&id=K4331588Z6 Lattes] <br><br> Contato: gustkajitani[at]gmail.com
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-== Resumo do Projeto ==+== Current Project ==
 +=== Effects of DNA lesions on Nucleotide Excision Repair deficient mice ===
 +The Nucleotide Excision Repair (NER) pathway is responsible for the removal and repair of bulky DNA lesions capable of distorting the structure of the DNA double helix, such as cisplatin or UV induced lesions. Defects in genes related to the Nucleotide Excision Repair (NER) pathway lead to disorders in which patients display photosensitivity and/or neurological problems, such as Xeroderma Pigmentosum (XP), Cockayne Syndrome (CS). In order to study the impact of DNA damage in these genetic diseases, numerous knockout mice models have been developed, with several of them having similar characteristics to the human syndromes. In this project, we aim to study the impact of specific UV induced lesions (CPDs or 6-4PPs) on the induction of effects such as skin hyperplasia, cell death and inflammation on a XP mouse model. Moreover, we have used a Cockayne Syndrome mouse model in order to study the relationship between the molecular defects of CS and possible neuropathological phenotypes, namely vascular dysfunction and neuroinflammation.
-As principais lesões no DNA decorrentes de irradiação ultravioleta (UV) são os dímeros de pirimidina ciclobutano (CPDs) e os fotoprodutos 6-4 pirimidina pirimidona (6-4PPs). Tais lesões podem ser reparadas por diferentes vias de Reparo de DNA. Várias espécies contém genes para fotoliases, enzimas que utilizam energia de fótons para reparar cada uma dessas lesões especificamente. Porém, há grupos que não possuem genes para essas enzimas, como os mamíferos placentários, e que dependem então apenas da via de reparo por excisão de nucleotídeos (NER) para a remoção de fotolesões. Pretendemos estabelecer o cultivo de células obtidas a partir de camundongos transgênicos deficientes em diferentes proteínas da via NER e que expressam constitutivamente CPD-fotoliase ou 6-4PP-fotoliase, para observar o efeito específico de cada tipo de lesão in vitro após tratamento com irradiação UV.+== Publications ==
-<br><br>+Rocha, C.R.R., <b>Kajitani, G.S.</b>, Quinet, A., Fortunato, R.S. and Menck, C.F.M., 2016. NRF2 and glutathione are key resistance mediators to temozolomide in glioma and melanoma cells. <u>Oncotarget</u>, 7(30), p.48081.<br> [https://doi.org/10.18632/oncotarget.10129 Full Text]
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-<br>+de Oliveira Alves, N., Vessoni, A.T., Quinet, A., Fortunato, R.S., <b>Kajitani, G.S.</b>, Peixoto, M.S., de Souza Hacon, S., Artaxo, P., Saldiva, P., Menck, C.F.M. and de Medeiros, S.R.B., 2017. Biomass burning in the Amazon region causes DNA damage and cell death in human lung cells. <u>Scientific reports</u>, 7(1), p.10937. <br> [https://www.nature.com/articles/s41598-017-11024-3 Full Text]
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Revisão atual

Bsc,Biological Sciences, Universidade de São Paulo ISP, 2013
Has experience in In vivo research, Cell Biology, Molecular Biology, Neuroinflammation, and DNA repair deficiencies

Gustavo Satoru is a PhD student in the DNA Repair Lab - Institute of Biomedical Sciences at University of Sao Paulo since 2013, having spent one year of his PhD as a visiting scientist in the Mitchell Lab - Harvard T.H. Chan School of Public Health.

Research keywords: DNA Repair, Photolesions,Aging and Inflammation.

Lattes

Contato: gustkajitani[at]gmail.com



Current Project

Effects of DNA lesions on Nucleotide Excision Repair deficient mice

The Nucleotide Excision Repair (NER) pathway is responsible for the removal and repair of bulky DNA lesions capable of distorting the structure of the DNA double helix, such as cisplatin or UV induced lesions. Defects in genes related to the Nucleotide Excision Repair (NER) pathway lead to disorders in which patients display photosensitivity and/or neurological problems, such as Xeroderma Pigmentosum (XP), Cockayne Syndrome (CS). In order to study the impact of DNA damage in these genetic diseases, numerous knockout mice models have been developed, with several of them having similar characteristics to the human syndromes. In this project, we aim to study the impact of specific UV induced lesions (CPDs or 6-4PPs) on the induction of effects such as skin hyperplasia, cell death and inflammation on a XP mouse model. Moreover, we have used a Cockayne Syndrome mouse model in order to study the relationship between the molecular defects of CS and possible neuropathological phenotypes, namely vascular dysfunction and neuroinflammation.

Publications

Rocha, C.R.R., Kajitani, G.S., Quinet, A., Fortunato, R.S. and Menck, C.F.M., 2016. NRF2 and glutathione are key resistance mediators to temozolomide in glioma and melanoma cells. Oncotarget, 7(30), p.48081.
Full Text

de Oliveira Alves, N., Vessoni, A.T., Quinet, A., Fortunato, R.S., Kajitani, G.S., Peixoto, M.S., de Souza Hacon, S., Artaxo, P., Saldiva, P., Menck, C.F.M. and de Medeiros, S.R.B., 2017. Biomass burning in the Amazon region causes DNA damage and cell death in human lung cells. Scientific reports, 7(1), p.10937.
Full Text

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