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Loss of FBXO7 (PARK15) results in reduced proteasome activity and models a parkinsonism-like phenotype in mice

MPS-Authors
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Vingill,  Siv
Cellular molecular neurobiology, Max Planck Institute of Experimental Medicine, Max Planck Society;

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Brockelt,  David
Cellular molecular neurobiology, Max Planck Institute of Experimental Medicine, Max Planck Society;

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Dontcheva,  Guergana
Cellular molecular neurobiology, Max Planck Institute of Experimental Medicine, Max Planck Society;

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Schwedhelm-Domeyer,  Nicola
Cellular molecular neurobiology, Max Planck Institute of Experimental Medicine, Max Planck Society;

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Joseph,  Sabitha
Cellular molecular neurobiology, Max Planck Institute of Experimental Medicine, Max Planck Society;

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Mitkovski,  Miso
Light microscopy facility, Wiss. Servicegruppen, Max Planck Institute of Experimental Medicine, Max Planck Society;

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Goebbels,  Sandra
Developmental neurobiology, Neurogenetics, Max Planck Institute of Experimental Medicine, Max Planck Society;

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Nave,  Klaus-Armin
Neurogenetics, Max Planck Institute of Experimental Medicine, Max Planck Society;

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Stegmüller,  Judith
Cellular molecular neurobiology, Max Planck Institute of Experimental Medicine, Max Planck Society;

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Vingill_16.pdf
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Citation

Vingill, S., Brockelt, D., Lancelin, C., Tatenhorst, L., Dontcheva, G., Preisinger, C., et al. (2016). Loss of FBXO7 (PARK15) results in reduced proteasome activity and models a parkinsonism-like phenotype in mice. EMBO Journal, 35, 2008-2025. doi:10.15252/embj.201593585.


Cite as: https://hdl.handle.net/11858/00-001M-0000-002C-0F1C-B
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