Thread View: bionet.molbio.evolution
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Started by Isabell Witt
Mon, 24 Jan 2011 13:33
PhD project in axonal degeneration
Author: Isabell Witt
Date: Mon, 24 Jan 2011 13:33
Date: Mon, 24 Jan 2011 13:33
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6411 bytes
PhD Student position available in the group of Elena Rugarli, University of Cologne-Biocenter Our group studies the mechanisms underlying axonal degeneration, a process that occurs in several common neurodegenerative diseases, and correlates with the onset of symptoms. We focus on the pathogenic mechanisms underlying hereditary spastic paraplegia and spinocerebellar ataxias, two model diseases to study axonal degeneration. Mitochondrial proteases involved in protein quality control have been linked to these diseases. The project aims at identifying the pathogenic mechanism leading from impaired mitochondrial proteolysis to axonal and neuronal degeneration using already available mouse models. The successful candidate must have a degree (master/diploma) in science (e.g. biology, biochemistry or chemistry) and a strong research interest in neuroscience. Candidates with previous experience in neurobiology and/or mouse genetics are strongly encouraged to apply. For application, please send your complete CV and the contact details of two potential referees by email to Elena Rugarli (elena.rugarli@uni-koeln.de). Web site: http://www.uni-koeln.de/math-nat-fak/zoologie/tierphysiologie/rugarli/Welcom e.html Relevant bibliography: Ehses S., Raschke I., Mancuso M., Bernacchia A., Geimer S., Tondera D., Martinou J-C., Westermann B., Rugarli E.I., Langer T. Regulation of mitochondrial fusion and OPA1 processing by m-AAA protease isoenzymes and OMA1. J. Cell Biol., 187, 1023-36, 2009. Martinelli P, La Mattina V, Bernacchia A, Magnoni R, Cerri F, Cox G, Quattrini A, Casari G, Rugarli EI. Genetic interaction between the m-AAA protease isoenzymes reveals novel roles in cerebellar degeneration. Hum. Mol. Genet. 18, 2001-2013, 2009 Pirozzi M., Quattrini A., Andolfi G., Dina G., Malaguti M.C., Auricchio A., Rugarli E.I. Intramuscular viral delivery of paraplegin rescues peripheral axonopathy in a model of hereditary spastic paraplegia. J. Clin. Invest., 116, 202-208, 2006. Ferreirinha F., Quattrini A., Pirozzi M., Valsecchi V., Dina G., Broccoli V., Auricchio A., Piemonte F., Tozzi G., Gaeta L., Casari G., Ballabio A., Rugarli E.I. Axonal degeneration in paraplegin-deficient mice is associated with abnormal mitochondria and impairment of axonal transport, J. Clin. Invest., 113, 231-42, 2004.
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