Graduated from Universidade Estadual de Londrina (1986) with a degree in Pharmacy. Completed a master's degree and a PhD degree in Biochemistry from Universidade de São Paulo (1993). Postdoctoral training at the Harvard Medical School and Washington University at Saint Louis (1998). Is the Principal Investigator of the Laboratory of Molecular Biology of Leishmanias at the Department of Cell Biology of the Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo. Coordinates projects that are focused on the study of the DNA damage response and its role in genome plasticity in the protozoan parasite Leishmania. (Source: Lattes Curriculum)
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The protozoan Leishmania, etiological agent of diseases of indisputable medical importance, has peculiar forms of genome organization and expression. The aim of this proposal is to investigate key elements of genetic variability and post-transcriptional regulation of gene expression. In specific lines of investigation, we will study genome variation in response to DNA replication stress; …
Leishmaniasis is a devastating parasitic disease that targets the poorest of society and is the 9th largest global infectious disease burden (WHO). It is truly a Neglected Infectious Disease as the combined financial support of basic and clinical research equates to <2% of infectious disease R&D resources available. Consequently, there are no vaccines available currently and the limited a…
Pathogenic trypanosomatids such as Leishmania spp. and Trypanosoma cruzi are the causative agents of leishmaniosis and Chagas disease, a group of neglected diseases endemic in the tropical and subtropical belt of the planet and the Americas, respectively. The therapeutic approaches against these diseases are largely unsatisfactory due to toxicity and emergence of resistance. Thus, new dru…
Our laboratory has contributed to the understanding of DNA damage signaling pathways in the protozoan parasite Leishmania. The study of the detection and signaling of DNA damage in an early-diverging eukaryote can further our understanding of how DNA Damage Response (DDR) has been established in the eukaryotic line. Based on the identification and characterization of checkpoint proteins R…
(Only some records are available in English at this moment)
Leishmaniasis is a parasitic disease of undeniable medical importance. The etiological agent, Leishmania, possesses mechanisms of adaptation frequently associated with genomic plasticity, including variation in the number of chromosome and gene copies. These adaptions may arise as a consequence of DNA replication stress and activation of DNA damage repair pathways. Our laboratory studies …
Leishmania adaptability to different environmental conditions is often correlated to genome plasticity and general chromosome and gene copy number variations. The mechanisms by which DNA Replication Stress modulates genome plasticity in Leishmania are complex and involve multiple DNA Damage Repair pathways. Understanding these mechanisms will provide valuable insights into the biology of …
The genome of Leishmania is characterized by a remarkable plasticity that has been associated with the acquisition of drug resistance and with host adaptation. Here, we will explore if the parasite's signaling of replication 'stress' may underlie genome plasticity and diversity. The analysis of the ATR pathway, which is central to the detection and signaling DNA replication stress and dam…
Considering that DNA damage is an important modulator of chromatin states, our aim is not only to evaluate the existence of genomic sites of recurrent replication stress or DNA damage, but also characterize the chromatin environment associated to these sites in Trypanosoma cruzi and Leishmania major. (AU)
(Only some records are available in English at this moment)
The eukaryotic cell has developed mechanisms to maintain genome integrity, which are constantly challenged by DNA damage and replication impediments. The protein kinase Ataxia-Telangiectasia and Rad3-related (ATR), a member of the phosphatidylinositol 3-kinase-like family, is a master regulator of the eukaryotic response to DNA injuries to ensure genome maintenance and stability. In this …
Eukaryote cells have developed mechanisms to coordinate DNA damage sensing, cell cycle arrest and DNA damage repair in order to grant genome stability. In higher eukaryotes, the 9-1-1 checkpoint complex, composed by the proteins Rad9, Rad1 and Hus1, participates in the early steps of the DNA damage response. We have identified possible homologues of each one of the three subunits of the 9…
| 1 / 1 | Ongoing grants |
| 12 / 9 | Completed research grants |
| 2 / 2 | Ongoing scholarships in Brazil |
| 23 / 9 | Completed scholarships in Brazil |
| 2 / 2 | Completed scholarships abroad |
| 40 / 23 | All research grants and scholarships |
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CV Lattes
ORCID