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Dangerous duet: LRRK2 and α-synuclein jam at CMA

Nature Neuroscience volume 16, pages 375–377 (2013)Cite this article

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A report suggests that leucine-rich repeat kinase 2 (LRRK2) can be degraded through chaperone-mediated autophagy (CMA) in the lysosome, and several Parkinson's disease–causing LRRK2 mutants impair CMA-mediated selective degradation of cytosolic substrates.

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Figure 1: The interaction between LRRK2 and α-synuclein in chaperone-mediated autophagy in Parkinson's disease cells.

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Authors and Affiliations

  1. Zhenyu Yue is in the Departments of Neurology and Neuroscience, Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, New York, USA,

    Zhenyu Yue

  2. Department of Psychiatry and Biobehavioral Sciences, X. William Yang is at the Center for Neurobehavioral Genetics, Semel Institute for Neuroscience and Human Behavior, David Geffen School of Medicine, University of California, Los Angeles, California, USA.,

    X William Yang

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  1. Zhenyu Yue
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Correspondence to Zhenyu Yue or X William Yang.

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Yue, Z., Yang, X. Dangerous duet: LRRK2 and α-synuclein jam at CMA. Nat Neurosci 16, 375–377 (2013). https://doi.org/10.1038/nn.3361

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