Camila Carriao Machado Garcia

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-== Resumo do Projeto ==+== Research Project ==
The most studied repair pathway as the nucleotide excision repair (NER) that removes a wide variety of lesions that distort the double helix. The NER is divided into two subways: global genome repair (GGR) is responsible for removal the lesions present in any area of ​​the genome, and the transcription coupled repair (TCR) that removes damages present in transcriptionally active genes. Many proteins are associated with this route, performing functions from the recognition of the injury, its removal and insertion of a new DNA strand. The XPA protein, for example, is recruited at the stage of removal of adducts and, therefore, cells deficient in this protein does not exhibit any of the repair of two NER subways. While proteins XPC and CSA are involved in the recognition mechanisms associated with GGR and TCR, respectively. It is known that patients with mutations in some genes that encode proteins involved in NER pathways, such as XPA and XPC, xeroderma pigmentosum have a syndrome that among the many features is the high incidence of skin cancer. However patients with mutations in CSA and CSB, Cockayne syndrome, which is characterized by neurodegeneration and premature ageing, accompanied by the absence of tumors. For this reason, studying the effect of radiation and redox stress-inducing substances in NER proteins cells and animals deficient is an important tool to understand the mechanisms of diseases progression, tumors incidence, neurodegeneration and ageing. It is in this context that this project, to investigate the mechanisms of cell death that may be associated with redox imbalance in human cells and NER deficient animals, in order to clarify the importance of oxidative stress and lipid peroxidation in the mechanisms of disease progression. We also hope to contribute to understanding the possible association of the NER proteins in the repair of DNA adducts caused by redox imbalance and the involvement of CSA and CSB proteins in response to oxidative stress. The most studied repair pathway as the nucleotide excision repair (NER) that removes a wide variety of lesions that distort the double helix. The NER is divided into two subways: global genome repair (GGR) is responsible for removal the lesions present in any area of ​​the genome, and the transcription coupled repair (TCR) that removes damages present in transcriptionally active genes. Many proteins are associated with this route, performing functions from the recognition of the injury, its removal and insertion of a new DNA strand. The XPA protein, for example, is recruited at the stage of removal of adducts and, therefore, cells deficient in this protein does not exhibit any of the repair of two NER subways. While proteins XPC and CSA are involved in the recognition mechanisms associated with GGR and TCR, respectively. It is known that patients with mutations in some genes that encode proteins involved in NER pathways, such as XPA and XPC, xeroderma pigmentosum have a syndrome that among the many features is the high incidence of skin cancer. However patients with mutations in CSA and CSB, Cockayne syndrome, which is characterized by neurodegeneration and premature ageing, accompanied by the absence of tumors. For this reason, studying the effect of radiation and redox stress-inducing substances in NER proteins cells and animals deficient is an important tool to understand the mechanisms of diseases progression, tumors incidence, neurodegeneration and ageing. It is in this context that this project, to investigate the mechanisms of cell death that may be associated with redox imbalance in human cells and NER deficient animals, in order to clarify the importance of oxidative stress and lipid peroxidation in the mechanisms of disease progression. We also hope to contribute to understanding the possible association of the NER proteins in the repair of DNA adducts caused by redox imbalance and the involvement of CSA and CSB proteins in response to oxidative stress.

Revision as of 12:30, 28 November 2011

120px-CamilaCarriao.jpg PhD in Sciences with emphasis in Biochemistry by the University of São Paulo (2010), interested in: DNA repair and DNA damage, oxidative stress, lipid peroxidation and cell death. Currently develops the postdoctoral project   entitled: “Association between oxidative stress and syndromes associated with nucleotide excision repair”, funded by Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP).



Research Project

The most studied repair pathway as the nucleotide excision repair (NER) that removes a wide variety of lesions that distort the double helix. The NER is divided into two subways: global genome repair (GGR) is responsible for removal the lesions present in any area of ​​the genome, and the transcription coupled repair (TCR) that removes damages present in transcriptionally active genes. Many proteins are associated with this route, performing functions from the recognition of the injury, its removal and insertion of a new DNA strand. The XPA protein, for example, is recruited at the stage of removal of adducts and, therefore, cells deficient in this protein does not exhibit any of the repair of two NER subways. While proteins XPC and CSA are involved in the recognition mechanisms associated with GGR and TCR, respectively. It is known that patients with mutations in some genes that encode proteins involved in NER pathways, such as XPA and XPC, xeroderma pigmentosum have a syndrome that among the many features is the high incidence of skin cancer. However patients with mutations in CSA and CSB, Cockayne syndrome, which is characterized by neurodegeneration and premature ageing, accompanied by the absence of tumors. For this reason, studying the effect of radiation and redox stress-inducing substances in NER proteins cells and animals deficient is an important tool to understand the mechanisms of diseases progression, tumors incidence, neurodegeneration and ageing. It is in this context that this project, to investigate the mechanisms of cell death that may be associated with redox imbalance in human cells and NER deficient animals, in order to clarify the importance of oxidative stress and lipid peroxidation in the mechanisms of disease progression. We also hope to contribute to understanding the possible association of the NER proteins in the repair of DNA adducts caused by redox imbalance and the involvement of CSA and CSB proteins in response to oxidative stress.

Publicações

1.Angeli, José Pedro F.; Garcia, Camila Carrião M. ; Sena, Fernanda ; Freitas, Florencio P. ; Miyamoto, Sayuri ; Medeiros, Marisa Helena G. ; Di Mascio, Paolo . Lipid hydroperoxide-induced and hemoglobin-enhanced oxidative damage to colon cancer cells. Free Radical Biology & Medicine, v. 51, p. 503-515, 2011.
2.Garcia, Camila Carrião M. ; Angeli, José Pedro F. ; Freitas, Florêncio Porto ; Gomes, Osmar Francisco ; de Oliveira, Tiago Franco ; Loureiro, Ana Paula Melo ; Di Mascio, Paolo; Medeiros, Marisa Helena Gennari de . [13C2]- Acetaldehyde promotes unequivocal formation of 1,N2-propano-2 -deoxyguanosine in human cells.. Journal of the American Chemical Society. V. 133, p. 1140-1143, 2011.
3.Garcia, Camila C.M.; Freitas, Florencio P.; Di Mascio, Paolo; Medeiros, Marisa H.G. Ultra-sensitive simultaneous quantification of 1,N2-etheno-2´-deoxyguanosine and 1,N2-propano-2´-deoxyguanosine in DNA by an on-line liquid chromatography-electrospray tandem mass spectrometry assay. Chemical Research in Toxicology, v.23, p. 1245-1255, 2010.
4.Barbosa, Livea F.; Cerqueira, Fernanda M.; Macedo, Antero F.A.; Garcia, Camila C.M.; Angeli, José Pedro F.; Schumacher, Robert I.; Sogayar, Mari Cleide; Augusto, Ohara ; Carrì, Maria Teresa; Di Mascio, Paolo; Medeiros, Marisa H.G..Biochimica et Biophysica Acta. Molecular Basis of Disease, v. 1802, p. 462-471, 2010.
5.Barbosa, Livea F.; Garcia, Camila C.M. ; Di Mascio, Paolo ; Medeiros, Marisa H.G.. Dalton Transactions, p. 1450-1459, 2009.

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