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Dr. Ana Messias

Metabolic and neurodegenerative diseases

Messias' research focuses on basic molecular mechanisms in several human metabolic and neurodegenerative diseases. In particular, we are interested in how proteins perform their native functions and how diseases alter them. We do this by looking at the details of their 3D structure in an integrative structural biology approach combined with biochemical and biophysical techniques. This information is then used in the rational development of novel drugs to ameliorate disease conditions.

Current research centers around rare inherited disorders such as Neurodegenerative With Brain Iron Accumulation (NBIA) and Dilated Cardiomyopathy. Among NBIA diseases, we study MPAN (Mitochondrial-Membrane Protein-Associated Neurodegeneration), a fatal disease caused by mutations in C19orf12, a protein with no known biological function. The aim of our research is to understand the basic molecular and cellular mechanisms of C19orf12 and how mutations lead to MPAN by using structural biology, biochemistry, biophysics, combined with proteomics, and cellular biology. Our ultimate goal is to develop personalized drugs that will prolong and improve the lives of MPAN patients.

A second research area focuses on genetic and acquired metabolic diseases, in particular linked to diabetes and obesity. We unravel and exploit novel molecular features of the function of regulatory proteins in insulin- and leptin-based signalling, namely of protein tyrosine phosphatases (PTPs), and use it in structure-based drug discovery to identify and develop novel allosteric compounds in diabetes and obesity.

Messias' research focuses on basic molecular mechanisms in several human metabolic and neurodegenerative diseases. In particular, we are interested in how proteins perform their native functions and how diseases alter them. We do this by looking at the details of their 3D structure in an integrative structural biology approach combined with biochemical and biophysical techniques. This information is then used in the rational development of novel drugs to ameliorate disease conditions.

Current research centers around rare inherited disorders such as Neurodegenerative With Brain Iron Accumulation (NBIA) and Dilated Cardiomyopathy. Among NBIA diseases, we study MPAN (Mitochondrial-Membrane Protein-Associated Neurodegeneration), a fatal disease caused by mutations in C19orf12, a protein with no known biological function. The aim of our research is to understand the basic molecular and cellular mechanisms of C19orf12 and how mutations lead to MPAN by using structural biology, biochemistry, biophysics, combined with proteomics, and cellular biology. Our ultimate goal is to develop personalized drugs that will prolong and improve the lives of MPAN patients.

A second research area focuses on genetic and acquired metabolic diseases, in particular linked to diabetes and obesity. We unravel and exploit novel molecular features of the function of regulatory proteins in insulin- and leptin-based signalling, namely of protein tyrosine phosphatases (PTPs), and use it in structure-based drug discovery to identify and develop novel allosteric compounds in diabetes and obesity.

Team members

Fadime Stemmer

Bachelor's student

Publications

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2022 Scientific Article in eLife

Chora, A.F. ; Pedroso, D. ; Kyriakou, E. ; Pejanovic, N. ; Colaço, H. ; Gozzelino, R. ; Barros, A. ; Willmann, K. ; Velho, T.R. ; Moita, C. ; Santos, I. ; Pereira, P. ; Carvalho, S. ; Martins, F.B. ; Ferreira, J.A. ; de Almeida, S.F. ; Benes, V. ; Anrather, J. ; Weis, S. ; Soares, M.P. ; Geerlof, A. ; Neefjes, J.J. ; Sattler, M. ; Messias, A.C. ; Neves Costa, A. ; Moita, L.F.

DNA damage independent inhibition of NF-kB transcription by anthracyclines.

2018 Scientific Article in American Journal of Human Genetics, The

Iuso, A. ; Wiersma, M. ; Schüller, H.J. ; Pode-Shakked, B. ; Marek-Yagel, D. ; Grigat, M. ; Schwarzmayr, T. ; Berutti, R. ; Alhaddad, B. ; Kanon, B. ; Grzeschik, N.A. ; Okun, J.G. ; Perles, Z. ; Salem, Y. ; Barel, O. ; Vardi, A. ; Rubinshtein, M. ; Tirosh, T. ; Dubnov-Raz, G. ; Messias, A.C. ; Terrile, C. ; Barshack, I. ; Volkov, A. ; Avivi, C. ; Eyal, E. ; Mastantuono, E. ; Kumbar, M. ; Abudi, S. ; Braunisch, M. ; Strom, T.M. ; Meitinger, T. ; Hoffmann, G.F. ; Prokisch, H. ; Haack, T.B. ; Brundel, B.J.J.M. ; Haas, D. ; Sibon, O.C.M. ; Anikster, Y.

Mutations in PPCS, encoding phosphopantothenoylcysteine synthetase, cause autosomal-recessive dilated cardiomyopathy.

Previous and Current Funding

Michael J. Fox Foundation (US), NBIA-DA (US), Association NBIA Poland (Poland)

Contact

Dr. Ana Messias

Staff scientist, team leader