Abstract
Mitochondrial dysfunction causes cellular damage and is linked to numerous pathological conditions. The prominent role of mitochondria in energy supply and cellular homeostasis highlights the importance of mitochondrial quality control mechanisms to preserve organelle function under stress and to eliminate irreversibly damaged mitochondria. Recent research revealed that two genes associated with familial Parkinson’s disease, Parkin and PINK1, function in mitochondrial quality control pathways.
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Cathrin Schnack 1999–2005 Biochemie- und Molekularbiologiestudium, Universität Kiel. 2005–2008 Promotion am Lehrstuhl für Molekulare Biologie, Universität Tübingen. 2009–2014 Postdoc, Experimentelle Neurologie, Universitätsklinikum Ulm. Seit 2014 Postdoc am Lehrstuhl für Molekulare Zellbiologie, Universität Bochum.
Lena Berlemann 2007–2012 Biologiestudium, Universität Bochum. Seit 2013 Promotion am Lehrstuhl für Molekulare Zellbiologie, Universität Bochum.
Konstanze F. Winklhofer 1985–1990 Pharmaziestudium, Universität Regensburg. 1990–1997 Humanmedizinstudium, LMU München. 1994–1998 Promotion am Max-Planck-Institut für Biochemie, Martinsried, dort 1998–2005 Postdoc und Habilitation an der Fakultät für Chemie und Pharmazie der LMU München. 2005–2013 Gruppenleiterin am Adolf-Butenandt-Institut der LMU München. Seit 2013 Leitung des Lehrstuhls Molekulare Zellbiologie, Universität Bochum.
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Schnack, C., Berlemann, L. & Winklhofer, K.F. Parkin — eine neuroprotektive E3-Ubiquitin-Ligase. Biospektrum 20, 724–728 (2014). https://doi.org/10.1007/s12268-014-0507-1
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DOI: https://doi.org/10.1007/s12268-014-0507-1