Deborah Schechtman, obtained her BA in Biological Sciences (Biomedidine) from the Universidade Federal do Estado do Rio de Janeiro (Uni-Rio), masters in Biological Siences  Biológicas (Biophysics) from the Universidade Federal do Rio de Janeiro, and PhD in the department of Chemical Immunology at The  Weizmann Institute of Science. Accomplished her Post doctoral studies at the  University of Stanford. Was a Young Investigator (FAPESP) at the Heart Institute  (InCor/ HCFMUSP) at the Laboratory  of Genetics and Molecular Cardiology.  Presently is an associate  Professor  at the Chemistry  Instituto Biochemistry Department of the Universidade de São Paulo, working on signal transduction pathways leading to pain.

The Laboratory of  Biochemistry of Cell  Signaling is localized at LAPIC, Chemistry Institute of the University of São Paulo and has as a main goal  understand the signal transduction pathways involved in pain for the development of new non-opioid analgesics.

Analyzing mutations in TrkA the  tyrosine kinase coupled e high affinity NGF receptor, in patients with congenital insensitivity to pain with anhidrosis (CIPA), and thus these patients don't feel pain, we identified the PLCg pathway activated by  TrkA as a key pathway for pain signaling.  We developed a peptide that inhibits this signaling pathway. This peptide has an analgesic effect in animal models of inflammatory pain. Using multidisciplinary approaches that involve  structural biology, physiology, embryology, biochemistry, chemistry and  cell biology and  several collaborators in Brazil and world wide  we are looking at the effects of this peptide in other animal pain models, understanding how mutations in TrkA can affect the development of the peripheral nociceptive nervous system and identifying other signaling pathways that may be affected by the peptide, and characterizing the effect of this pathway in pain. We are also developing strategies to find small molecules that can act like the peptide and can serve as leads to develop new analgesics.

We are a laboratory that values diversity, working together to achieve our goals.
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PhD Students

The role of PLCg in experimental acute and chronic pain induced hypersensitivity

Recently our lab developed a peptide, TAT-pQYP, that acts by inibiting the  PLCg pathway via  TrkA and that has an analgesic effect in acute inflammatory pain in animals. Continuing the project developed during my masters, my PhD's project goal is to characterize the effect of the inhibition of specific  signaling pathways activated by  TrkA in chronic pain models, mainly the role of PLCg in the development of chronic pain in animals, using beahvioural assays  biochemical and molecular biology techniques to elucidate the role of  the modulation of these pathways and the interaction between pathways, in this complex disease model affecting millions of people worldwide. 


Msc. Beatriz C. de Moraes
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Masters Students

Undergraduate Students

My project aims to find proteins that bind to the peptide TAT-pQYP, besides PLCg that may contribute to the analgesic effect of the peptide. To this end, we used affinity columns with the biotinilated peptide followed by  mass spectrometry, to identify binding proteins. Binding proteins are then validated as potential targets and characterized as well as the signaling pathways involved in the analgesic effect of  TAT-pQYP, and potential side effects caused by the peptide.

Heloisa Espreáfico Guelerman Ramos 
Heloisa Ramos
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Technicians

Some publications from our group