CV Lattes
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Universidade de São Paulo (USP). Instituto de Química (IQ) (Institutional affiliation from the last research proposal) Birthplace: Brazil
Undergraduate studies in Biomedicine at the Universidade Federal do Estado do Rio de Janeiro (Uni-Rio) (1988), masters in biophysics at the Universidade Federal do Rio de Janeiro (1992) e PhD obtained from The Weizmann Institute Of Science (1998). Pos-doctoral studies at Stanford University (1999-2005). Young Investigator (FAPESP) at the Heart Institue (InCor/ HCFMUSP) at the Laboratory of de Genetics and Molecular Cardiology (2005-2009). Has experience in biochemistry, emphasis in molecular and celular biology, working mainly with: signal transduction, proteomics, rational design of peptide modulators of protein-protein interactions and of conformational antibodies. Currently Associate Professor of the Chemistry Institute, Department of Biochemistry of the University of São Paulo. The main goal of the laboratory is to develop peptide modulators and conformation-specific antibodies to study signal transduction pathways involved in inflammatory pain identifying and validating new non-opioid targets for the treatment of pain (Source: Lattes Curriculum)
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The primary objective of this proposal is to identify the biological factors underlying the immunological and proinflammatory processes characteristic of chronic pain and specifically to establish whether the impact of chronic pain on gut mucosal homeostasis mediates systemic inflammation. Chronic pain is a refractory health disease that imposes significant economic burden on affected ind…
Opioides have an addictive effect generate tolerance upon prolonged use causing unwanted side effects. Thus, there is a great need to search for new analgesic substitutes. To this end, understanding the signaling pathways that lead to pain can help develop new non-opioid analgesics. Inflammatory pain begins with the secretion of nerve growth factor (NGF) and activation of its high affinit…
Physical pain can be subdivided into nociceptive and neuropathic. Nociceptive pain is due to the activation of nociceptors caused by a lesion or disease of the somatosensorial system, considered pathological pain. Both systems can lead to chronic pain, whose treatment is still a great challenge. Thus, it is necessaty to understand the signal transduction pathways that lead to pain to deve…
Data from the literature sugests that one of the problems to study the role of PKCs is the lack of tools that can distinguish specifically the inactive from active forms of the different protein kinase C (PKC) isoenzymes. Differently than other kinases, for example, ERK and JNK in which activation is determined by phosphorylation of the activation loop. Phosphorylations suffered in parti…
In the last years our lab has been characterizing the role of Protein kinase C (PKC) in undifferentiated murine embryonic stem cells (ESC). Our results suggest that most of the PKC²I substrates in undifferentiated ESC are nuclear proteins involved in the regulation of transcription of proteins involved in proliferaation/ diferentiation. Recent studies also have reported nuclear PKC²I i…
(Only some records are available in English at this moment)
Currently, the search for effective treatments for pain relief is a significant challenge, as many individuals do not experience significant improvements when resorting to anti-inflammatory analgesics and/or opioids available in the market. To address this therapeutic gap, we must have a better understanding of the pathways leading to pain signaling, with particular interest in the pathwa…
Pain plays a key protective role in maintaining tissue integrity and homeostasis, but it is also involved in pathological processes that makes the search for pain treatments of great relevance. Among the mediators secreted when there is tissue damage, the nerve growth factor (NGF) plays a significant role in pain perception through its interaction with its receptor, the tropomyosin recept…
(Only some records are available in English at this moment)
Chronic pain has become an important health issue for the last few decades, affecting nearly 30% of the population worldwide. The search for analgesics that may help with patient's treatment has increased. TrkA and its associated pathways have proven to be interesting targets for new drugs development. Previous studies from our group, analysed mutations that affect TrkA signaling and thes…
When a tissue injury is produced in the human body, there are several forms of cell signaling of pain. The research interest of our laboratory group is mediated by the dimerization of the TrkA receptor (Tropomyosin kinase A) and a consequent cascade of reactions until neuronal depolarization, through activation of the TRPV1 cation channel.In this inflammatory context, the first step is th…
(Only some records are available in English at this moment)
Following a nerve damage, T cells infiltrate the lesion site to allow tissue repair and homeostatic balance. Locally, T cells release various pro-inflammatory mediators for tissue repair that can influence local neuron activity. We therefore hypothesize that T cells may contribute to chronic pain development after nerve injury through communication with neurons at specific intersectional …
Pain signaling is conducted by nociceptors, which derive from the neural crest and reside in dorsal root ganglia. Inflammatory pain relies on activation of TrkA receptors by NGF, which initiates signaling pathways that trigger action potentials. TrkA activation by NGF also promotes neuronal survival and differentiation during development. Mutations in NTRK1, which encodes TrkA, cause cong…
The ongoing opioid crisis in developed countries has urged the importance of searching for new analgesics. Many pathways have been explored on the therapeutics of this area, but opioids are still the most potent class of drugs for this. Nevertheless, they have limited effects and may lead to addiction, tolerance, and even overdose. Our group, aiming to understand the genetics of a disease…
(Only some records are available in English at this moment)
| 2 / 2 | Ongoing grants |
| 5 / 5 | Completed research grants |
| 5 / 5 | Ongoing scholarships in Brazil |
| 17 / 12 | Completed scholarships in Brazil |
| 6 / 6 | Completed scholarships abroad |
| 35 / 30 | All research grants and scholarships |
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