Juan Carlos
Arévalo Martín

I set up my laboratory in May 2007 at the Institute for Neuroscience Castile and Leon (INCyL) at the University of Salamanca with a Ramón y Cajal contract after a postdoctoral stay at the laboratory of Dr. Moses Chao (2000-2007) at the Skirball Institute at New York University. I started applying for grants to different national and international funding agencies. I got a Marie Curie IRG (2008-2012), a NARSAD Young Investigator Grant (2007-2009) and a grant from the Spanish Ministry of Education and Science (2009-2011). In 2008, the first PhD student joined the lab and the following years additional PhD students have joined the lab, starting the defense of their thesis from 2012 and up to now 6 of them has been successfully defended their thesis. In 2012, I got a position as Associate Professor at the Department of Cell Biology and Pathology at the University of Salamanca. During this period, I have secured the funding of my laboratory with four national grants from the Spanish Government and one grant from the regional government. In addition, in July 2016 a grant from the SE Infraestructuras Científicas y Técnicas y Equipamiento was awarded. I have been a partner of a European Consortium funded by a grant from the European Commission FPVII program (PAINCAGE) from 2014-2017. Since I was established as independent investigator, my laboratory has published 25 papers in which I am the senior/corresponding author in 11 of them. Finally, I am coauthor of three patents licensed in 2015. The main aim of my laboratory is focused on the identification of molecular mechanisms governing neurotrophin actions, paying special attention to the ubiquitination of Trk receptors and pain. A brief summary of our research lines with the published papers is as follows: 1- Identification of the role of TrkA ubiquitination mediated by Nedd4-2 in the receptor trafficking and in the differentiation and survival in response to NGF (Yu, Traffic, 2011; Yu, Journal of Neuroscience, 2014; Anta, Journal of Biological Chemistry, 2016). 2- Generation of a mouse model with reduced levels of TrkA ubiquitination that has allowed to study in vivo the role of TrkA ubiquitination (Yu, Journal of Neuroscience, 2014). 3- Identification of Bex3 protein as a modulator of trkA gene transcription (Calvo, Journal of Neuroscience 2015). 4- Identification of deubiquitinases that regulate TrkA (Anta, Journal of Biological Chemistry, 2016) and TrkB receptor ubiquitination (Martín-Rodríguez, Journal of Cell Science, 2020). 5- Identification of ARMS protein on regulated secretion in response to neurotrophins and depolarization (López-Benito, Journal of Cell Science, 2016; López-Benito, Journal of Neuroscience, 2018). In addition, we have been collaborating with national and international laboratories in several different projects. The main focus of our research nowadays and the grants funding this research are as follows: 1- Studying the molecular mechanisms driven by NGF-TrkA in osteoarthritic pain (as part of PAINCAGE Consortium and BFU2017-82667-R). A collaboration with Marzia Malcangio (KCL), a world-wide expert in osteoarthrosis, is on-going. We are using the TrkA mouse model previously generated for this study. 2- Addressing the role of ARMS/Kidins220 in NGF-mediated functions in vivo (BFU2014-51486-R and BFU2017-82667-R grants). We have generated a transgenic mouse model to modulate ARMS/Kidins220 protein levels in a regulated way through Cre recombinase.