Carlos Farinha


Departamento de Química e Bioquímica

Sala/Gabinete 8.3.67
Ext. Principal 28363 / 28367
Telefone Direto 217500904
Página Pessoal

Carreira Docente Universitário
Categoria Professor Associado com Agregação



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Currículo Resumido

Carlos M Farinha is Associate Professor with Habilitation at Faculty of Sciences, University of Lisboa and PI at the BioISI research centre (Functional Genomics and Proteostasis Unit). His research focuses on the molecular mechanisms of cystic fibrosis (CF), in particular the endoplasmic reticulum retention and early degradation of CFTR’s most common mutant as well as its rescue strategies, through modified folding or circumvention of quality control mechanisms and elucidation of the role of novel CFTR interactions. He received the 2012 ERS Romain Pauwels Research Award from the European Respiratory Society for “research into the different aspects of CFTR biology”. He has authored over 50 refereed international papers and was PI in several competitive grants.

Scientific Interests

Understanding the molecular mechanisms that are responsible for ER retention of CFTR protein (the protein that is in the basis of the autosomic recessive disease cystic fibrosis) and that signal its targeting to the degradative pathway is the main goal of my research work. Our current research interests focus mainly in the following aspects of CFTR biology:

1. Mechanisms of rescue and ER quality control for F508del-CFTR (and for rare trafficking mutants)

2. Characterization of novel CFTR interactors and their role in CFTR membrane stability

3. Disease associated mRNA and protein expression patterns for CF-causing mutations

The expected results will contribute to new advances in CFTR traffic and cell biology, in general, but also to the potential identification of novel therapeutic targets for the treatment of CF patients.

Publicações selecionadas
  • Santos JD, Pinto FR, Amaral MD, Zaccolo M, Farinha CM (2020) “Cytoskeleton regulators CAPZA2 and INF2 associate with CFTR to control its membrane levels under EPAC1 activation”. Biochem J 477, 2561-2580.
  • Canato S, Santos JD, Carvalho AS, Aloria K, Amaral MD, Matthiesen R, Falcao AO, Farinha CM (2018) “Proteomic interaction profiling reveals KIFC1 as a factor involved in early targeting of F508del-CFTR to degradation”. Cell Mol Life Sci 75, 4495-4509.
  • Lobo MJ, Amaral MD, Zaccolo M, Farinha CM (2016) "EPAC1 activation by cAMP stabilizes CFTR at the membrane by promoting its interaction with NHERF1". J Cell Sci 129, 2599-2612.
  • Farinha CM, King-Underwood J, Sousa M, Correia AR, Henriques MJ, Roxo-Rosa M, Da Paula AC, Williams J, Hirst S, Gomes CM, Amaral MD (2013) “Revertants, low temperature, and correctors reveal the mechanism of F508del-CFTR rescue by VX-809 and suggest multiple agents for full correction”. Chem Biol. 20, 943-955.
  • Farinha CM, Amaral MD (2005) “Most F508del-CFTR is targeted to degradation at an early folding checkpoint and independently of calnexin”. Mol Cell Biol 25, 5242-5252.

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