Gustavo Satoru Kajitani

From Laboratório de Reparo de DNA

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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. 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.
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 +== Publications ==

Revisão de 20:25, 24 Abril 2018

Bacharel em Ciências Biológicas pela Universidade de São Paulo (2013)
Doutorando pelo curso Interunidades em Biotecnologia da Universidade de São Paulo (USP), com estágio na Harvard University sob orientação do Prof. James Mitchell.</b>

Seu projeto atual visa relacionar, in vivo, danos no DNA relacionados à via de reparo por excisão de nucleotídeos (NER) com a ativação de vias relacionadas a morte/sobrevivência celular e inflamação.



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

Ferramentas pessoais