Carlos A. Matos
+351 916324139
c.matos@cnc.uc.pt
Research Fellow
Group at CNC
Education: 

I started studying Biology at the University of Coimbra in 2004, pursuing the strong interest I had in diverse life science fields. During my BSc I focused my attention and efforts into developing a deepened comprehension of the wide range of Biology-related disciplines, from biodiversity, taxonomy and ecology to cell biology and physiology. In 2007 I started my specialization in molecular cell biology with a MSc degree, that I finished in 2009. Since then I have been performing research at the Centre for Neuroscience and Cell Biology, and I obtained my graduation as a PhD in Cell Biology in 2015.

As a researcher I am interested in unravelling the mechanisms behind the neurodegeneration occurring in Machado-Joseph disease, a hereditary disease with an important prevalence in Portugal. At the same time, I am trying to elucidate the yet unknown biologic function of the protein that causes the disorder – ataxin-3. As part of my research I have employed a diverse array of techniques, ranging from enzymatic assays and immunodetection to the generation of animal models of disease. Until now the work I developed has conducted to the production of two theses and contributed to three scientific articles.

I am also very motivated to teach and communicate science and thus make a contribution to the scientific culture in our country.

Afiliation: 

CNC

Area of Research: 

My scientific activity has been focused on investigating several aspects related to Machado-Joseph disease, namely the way particular modifications of the causative protein (ataxin-3) may modulate the neurodegenerative events contributing to pathology. During my time as a PhD student I explored the way ataxin-3 post-translational modifications regulate the biochemical properties of the protein and how they contribute to its toxicity in cultured neurons and animal models.

My interest on this topic resides in the fact that the reason why ataxin-3 (an ubiquitous protein) is deleterious only in particular cellular contexts is still unknown. A deeper comprehension of the molecular and cellular mechanisms that are at the basis of the toxicity of ataxin-3 may be very important for the development of efficient therapeutic strategies.

Research Summary: 
orcid.org/0000-0002-9019-7569
Selected Publications: 

Matos, C.A., Nóbrega C., Louros S. R., Almeida B., de Almeida, L.P., Macedo-Ribeiro S., Carvalho A.L. (2015). Ataxin-3 phosphorylation decreases neuronal defects and toxicity in spinocerebellar ataxia type 3 disease models. J Cell Biol – Under 2nd revision. (IF 2014: 9,7)

Almeida, B.*, Abreu, I.*, Matos, C.A.*, Fraga, J., Fernandes, S., Macedo, M., Gutiérrez-Gallego, R., Pereira P., Carvalho, A.L., Ribeiro, S. (2015). SUMOylation of the brain-predominant Ataxin-3 isoform modulates its interaction with p97. Biochim Biophys Acta. Epub ahead of print. * - these authors share the first authorship. (IF 2014: 5,1)

Matos, C.A.,de Macedo-Ribeiro, S., and Carvalho, A.L. (2011). Polyglutamine diseases: the special case of ataxin-3 and Machado-Joseph disease. Prog Neurobiol 95, 26-48. (IF 2014: 10,0)

 
   
© 2017 CNC - Center for Neuroscience and Cell Biology powered by ponto.C