CV Lattes
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Universidade de São Paulo (USP). Instituto de Química (IQ) (Institutional affiliation from the last research proposal) Birthplace: Brazil
Graduated with a B.Sc. in Biological Sciences from the State University of Campinas (1989), a M.Sc. in Biochemistry from the same university (1993) and a PhD in Biochemistry from the Federal University of São Paulo (1997). Holds full professor position at the Biochemistry Department, Chemistry Institute, University of São Paulo. Has experience in biochemistry and molecular biology, focusing on repair of oxidative DNA damage and mitochondrial DNA. Former President of the Brazilian Society of Mutagenesis and Environmental Genomics, MutaGen Brasil, for the 2014-2016 term, and current member of the General Council for the Society. Served as member of the Brazilian Technical Committee on Biosafety, CTNBio, from 2014-2020. (Source: Lattes Curriculum)
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The human and environmental cost of anthropogenic air pollution is enormous and, likely, still underestimated. Mitigating the environmental and human health effects of air pollution depends, primarily, on actions to reduce exposure, but also on a clear understanding of the biological targets and molecular effects of pollutants that could support strategies for monitoring, prevention, and …
Chemotherapy resistance arises from few remaining cells that behave differently from most cells in the population which are killed by chemotherapy.Thus, to better understand the molecular mechanisms leading to resistance it is paramount to investigate such processes in individual cells. Several experimental approaches have been used for that, including the use of fluorescently labeled pr…
Mitochondria are essential organelles in eukaryotic cells as they are involved in central pathways including energy metabolism and intracellular signaling. Besides being the main cellular site for ATP generation, they are involved in redox signaling, intracellular calcium homeostasis and cell fate after stress. Moreover, they contain their own independent genome. In humans, the mitochondr…
(Only some records are available in English at this moment)
All known cellular organisms have DNA repair pathways, essential for maintaining genomic stability. In biological contexts in which it is not possible to repair DNA lesions before transcription or replication events, tolerance mechanisms that allow the continuation of these processes are relevant. Among the damage tolerance mechanisms, the main one is translesion synthesis (TLS), which in…
XPC is a protein involved in the early stages of the global genome nucleotide excision repair pathway (GG-NER). However, deficient models of XPC have phenotypes that are not apparently related to DNA damage and therefore imply that XPC has functions other than those performed in the GG-NER pathway. Among the most evident phenotypes presented by XPC deficiency are apparent redox signaling …
So far, only a few studies have analysed the presence, pattern, and functional impacts of epigenetic alterations in the mitochondrial genome. However, the possibility that epigenetic alterations could impact mtDNA expression and several mitochondrial functions shouldnot be overlooked. Recent studies have found evidence of mitochondrial isoforms of DNA metiltransferases (DNMTs) and ten-ele…
Most organisms store their genetic information in DNA, which is constantly exposed to endogenous and exogenous physical and chemical agents that damage it. DNA lesions can block replication or transcription, leading to dysfunction and cell death, or can be potentially mutagenic. In addition to DNA repair pathways, cells have DNA damage tolerance mechanisms (DDT) that allow DNA replication…
The expression of key genes required for DNA repair by homology such as Brca1, Mre11, Rad51 and Atm decreases in oocytes during aging, resulting in a progressive increase in double-strand breaks (DSB) in DNA and infertility. In keeping with these findings, our data support that the conditional deletion of Rad51 in mouse oocytes results in subfertility characterized by a significant decrea…
(Only some records are available in English at this moment)
Only a few studies have analyzed the presence, pattern, and functional impacts of epigenetic alterations in the mitochondrial genome. Emerging data established correlations between mtDNA methylation patterns, mtDNA expression and alterations in mitochondrial respiration. Moreover, alterations in mitochondrial DNA have been associated with air pollution exposition, cardiopathies and cancer…
Mitochondrial dysfunction appears as an early event in Alzheimer's disease (AD) pathology and in other neurodegenerative diseases. AD individuals accumulate oxidized DNA lesions in the mitochondrial genome (mtDNA) when compared to age-matched control individuals, which is believed to play a causal role in the mitochondrial dysfunction observed in the AD pathology. However, it is not clear…
DNA is constantly exposed to damaging agents from both endogenous and exogenous sources. In the case of mitochondrial DNA (mtDNA), damage is thought to be more pronounced due to its physical proximity to the respiratory chain, where large amounts of reactive oxygen species (ROS) are generated. These species can react readily with both the bases as well as with the deoxyribose, resulting i…
| 1 / 1 | Ongoing grants |
| 10 / 8 | Completed research grants |
| 2 / 2 | Ongoing scholarships in Brazil |
| 23 / 22 | Completed scholarships in Brazil |
| 1 / 1 | Ongoing scholarships abroad |
| 2 / 2 | Completed scholarships abroad |
| 39 / 36 | All research grants and scholarships |
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