CV Lattes
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Universidade de São Paulo (USP). Instituto de Ciências Biomédicas (ICB) (Institutional affiliation from the last research proposal) Birthplace: Brazil
He holds a degree in Biological Sciences from the University of São Paulo (1977) and a PhD in Biochemistry from the University of São Paulo (1982). He is currently a full professor at the Institute of Biomedical Sciences, University of São Paulo. He has experience in the area of Genetics, with an emphasis on Molecular Genetics and Mutagenesis, working mainly on the following topics: DNA repair, mutagenesis, ultraviolet radiation and gene transfer in human cells. As a model, he basically uses cells from patients with DNA repair deficiency syndromes. His work seeks to understand the processes of carcinogenesis and aging. This knowledge has also been used in the search for better therapeutic processes for cancer. (Source: Lattes Curriculum)
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The world population is getting older and older. Unfortunately, this increased life expectancy is generally associated by so-called age-related vascular diseases, such as dementia, heart infarct, and stroke, which profoundly compromise the quality of life of the elderly. Age-related disorders are generally viewed as necessary evil. Our project challenges this dogma, as we propose that the…
The world population is getting older and older. Unfortunately, this increased life expectancy is generally associated by so-called age-related vascular diseases, such as dementia, heart infarct, and stroke, which profoundly compromise the quality of life of the elderly. Age-related disorders are generally viewed as necessary evil. Our project challenges this dogma, as we propose that the…
The circadian clock is an internal timing mechanism, orchestrating diurnal variations in behavior, physiology and metabolism, aimed to best prepare us for daily recurring changes in our environment (i,e. the light/dark cycle). Evidence is increasing that uptake, metabolization and detoxification of chemicals is under control of the circadian clock and that, accordingly, the severity of to…
(Only some records are available in English at this moment)
The ERCC2/XPD gene encodes a protein of the same name that takes part in the nucleotide excision DNA repair pathway (NER). Individuals with a mutation in this gene, such as patients with Xeroderma Pigmentosum group D, experience symptoms related to lesions on the genetic material caused by ultraviolet radiation from sunlight. In some cases, signs of neurodegeneration are also observed, wh…
(Only some records are available in English at this moment)
Cockayne Syndrome (CS) is a genetic neurodegenerative disease related to the impairment of the transcription-coupled repair sub-pathway (TCR-NER). The CSB protein acts directly on this repair subpathway and, therefore, CSB mutant cells are more sensitive to agents that cause DNA damage. The greater sensitivity of these cells to UV light, an agent that damage DNA, is well known, however, e…
Genetic defects in nucleotide excision repair (NER) result in syndromes whose patients have a high frequency of cancer and/or symptoms related to premature aging and neurodegeneration. In the case of mutations in the ERCC2/XPD gene, for example, mutations can lead to different pathologies, such as Xeroderma Pigmentosum (XP), Cockayne syndrome (CS) and Trichothiodystrophy (TTD), in which t…
The DNA molecule is injured by exogenous and endogenous factors, and the Nucleotide Excision Repair (NER) pathway is one of the cells' mechanisms that remove some of those lesions and help to maintain the genome integrity. The TFIIH complex is one of the NER components and is involved in both DNA repair and transcription. Among other proteins, the XPD and XPB helicases are core components…
(Only some records are available in English at this moment)
DNA is constantly exposed to endogenous and exogenous agents that cause its damage. Such damage can lead to transient slowing or stalling of replication forks, a process known as "replication stress". To solve replication stress and, therefore, keep genome stability and cell viability, cells present defense mechanisms of DNA damage tolerance, including translesion synthesis (TLS), templat…
Temozolomide (TMZ) is the most used antitumoral drug in Glioblastoma Multiforme (GBM). However, chemotherapy-resistant cells are recurrent due to many factors, and one of them is the Translesion Synthesis (TLS) mechanism, which allows tumor cells to tolerate genomic damage by bypassing DNA lesions. Specifically, TLS DNA polymerases Kappa (Polº) and Iota (Pol¹) are associated with chemothe…
Trichothiodystrophy is a progeroid syndrome related to Nucleotide Excision Repair deficiency, derived from a mutation in the ERCC2/XPD gene. Considering that the most important and more complex clinical feature of TTD is the neurodegeneration process and that the available cells we have are patients' fibroblasts in monolayer culture, the possibility to use a more appropriate and complete …
Temozolomide (TMZ) is the main drug used to treat gliomas, which causes DNA damage leading to cell death mainly as a consequence of processing of the primary damage O6-methylguanine (O6meG). Several mechanisms of resistance were described, and the ability of MGMT (O-6-methylguanine-DNA methyltransferase) to directly reverse O6meG in the DNA molecule is the most significant. Moreover, the …
(Only some records are available in English at this moment)
| 2 / 2 | Ongoing grants |
| 55 / 21 | Completed research grants |
| 10 / 10 | Ongoing scholarships in Brazil |
| 126 / 46 | Completed scholarships in Brazil |
| 1 / 1 | Ongoing scholarships abroad |
| 12 / 12 | Completed scholarships abroad |
| 206 / 92 | All research grants and scholarships |
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