CV Lattes
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Universidade de São Paulo (USP). Instituto de Química (IQ) (Institutional affiliation for the last research proposal) Birthplace: Brazil
Bachelor of Pharmacy, UFRGS, Porto Alegre, Brazil (2007) PhD, St. Vincent's Institute, University of Melbourne, Australia (2013) Postdoctoral Research Fellow, Genome Damage and Stability Centre, University of Sussex, UK (2014-2018) Assistant Professor, Department of Biochemistry, University of São Paulo (from 2018) Studies cellular mechanisms of DNA repair and DNA damage signalling, with a special interest in human genetic disorders caused by mutations in these processes. Employs advanced molecular and cellular biology techniques, such as CRISP/Cas9 technology and high-content microscopy, as well as classic DNA damge and repair assays such as comet assays and sister chromatid exchanges. (Source: Lattes Curriculum)
The search for anti-coronaviral treatments is largely focused on inhibitors of the viral polymerase or one of the viral proteases. However, the viral macrodomain contained in non-structural protein 3 (Nsp3) is an attractive and underexplored target, as it has a druggable catalytic pocket, is required for viral replication and is part of an important mechanism of active viral repression of…
Genomic instability is the main driving force for cancer onset and progression, underlies the ageing process and is associated with neurodegenerative disease. Protein post-translational modification by NAD+-derived ADP-ribose moieties plays central roles in orchestrating the cellular DNA damage response, but most of the human enzymes that catalyse this modification, as well as the hydrola…
Genomic instability is the main driving force for cancer onset and progression, underlies the ageing process and is associated with neurodegenerative disease. Protein post-translational modification by NAD+-derived ADP-ribose moieties plays central roles in orchestrating the cellular DNA damage response, but most of the human enzymes that catalyze this modification, as well as the hydrola…
The SARS-CoV-2 Nsp3 macrodomain is a promising target for COVID-19 treatment. As part of an international effort to identify viral macrodomain inhibitors, this post-doctoral fellowship is aimed specifically at developing a cellular assay to detect the catalytic activity of the ectopically expressed viral macrodomain in human cells and use this assay to refine the list of candidate compoun…
Post-translational modification of proteins by ADP-ribosylation plays central roles in the cellular response to DNA damage. Few of the enzymes that catalyse this modification, and even fewer of the hydrolases that remove it, have been thoroughly characterised. The ADP-ribosyl hydrolase ARH3 has recently been shown to specifically remove ADP-ribose moieties attached to serines, which are t…
DNA damage signalling and repair, which are regulated by a variety of post-translational modifications including ubiquitination and ADP-ribosylation, prevent the genetic alterations that cause Cancer, neurodegeneration and aging. We have previously identified the ADP-ribosyl transferase PARP9 and the ubiquitin ligase DTX3L in an in vitro screen for factors that bind to a DNA damage-induce…
DNA damage activates pleiotropic cellular responses such as cell cycle arrest and senescence, but can also induce an inflammatory interferon response, which is an anti-viral pathway activated by the presence of DNA in the cytoplasm. We have identified PARP9 and DTX3L, two proteins that form a heterodimer in cells and are expressed from a shared interferon-responsive promoter, in a screen …
| 3 / 3 | Ongoing research grants |
| 3 / 3 | Ongoing scholarships in Brazil |
| 1 / 1 | Completed scholarships in Brazil |
| 7 / 7 | All research grants and scholarships |
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(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)
HOCH, NICOLAS C.; POLO, LUIS M.. ADP-ribosylation: from molecular mechanisms to human disease. GENETICS AND MOLECULAR BIOLOGY, v. 43, n. 1, 1, 2020. Web of Science Citations: 0. (18/18007-5)