Camila Carriao Machado Garcia
From DNA Repair Lab
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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. |