Regulation of endoplasmic reticulum turnover by selective autophagy

Aliaksandr Khaminets, Theresa Heinrich, Muriel Mari, Paolo Grumati, Antje K. Huebner, Masato Akutsu, Lutz Liebmann, Alexandra Stolz, Sandor Nietzsche, Nicole Koch, Mario Mauthe, Istvan Katona, Britta Qualmann, Joachim Weis, Fulvio Reggiori, Ingo Kurth (), Christian A. Hübner () and Ivan Dikic ()
Additional contact information
Aliaksandr Khaminets: Institute of Biochemistry II, Goethe University School of Medicine
Theresa Heinrich: Institute of Human Genetics, Jena University Hospital, Friedrich-Schiller-University Jena
Muriel Mari: Center for Molecular Medicine, University Medical Center Utrecht
Paolo Grumati: Institute of Biochemistry II, Goethe University School of Medicine
Antje K. Huebner: Institute of Human Genetics, Jena University Hospital, Friedrich-Schiller-University Jena
Masato Akutsu: Buchmann Institute for Molecular Life Sciences, Goethe University Frankfurt, Riedberg Campus
Lutz Liebmann: Institute of Human Genetics, Jena University Hospital, Friedrich-Schiller-University Jena
Alexandra Stolz: Institute of Biochemistry II, Goethe University School of Medicine
Sandor Nietzsche: Electron Microscopy Center, Jena University Hospital, Friedrich-Schiller-University Jena
Nicole Koch: Institute for Biochemistry I, Jena University Hospital, Friedrich-Schiller-University Jena
Mario Mauthe: Center for Molecular Medicine, University Medical Center Utrecht
Istvan Katona: Institute of Neuropathology, RWTH Aachen University Hospital
Britta Qualmann: Institute for Biochemistry I, Jena University Hospital, Friedrich-Schiller-University Jena
Joachim Weis: Institute of Neuropathology, RWTH Aachen University Hospital
Fulvio Reggiori: Center for Molecular Medicine, University Medical Center Utrecht
Ingo Kurth: Institute of Human Genetics, Jena University Hospital, Friedrich-Schiller-University Jena
Christian A. Hübner: Institute of Human Genetics, Jena University Hospital, Friedrich-Schiller-University Jena
Ivan Dikic: Institute of Biochemistry II, Goethe University School of Medicine

Nature, 2015, vol. 522, issue 7556, 354-358

Abstract: The protein FAM134B is an endoplasmic reticulum (ER)-resident receptor that facilitates ER autophagy, and downregulation of this protein (mutations of which are also known to cause sensory neuropathy in humans) results in expanded ER structures and degeneration of mouse sensory neurons.

Date: 2015
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DOI: 10.1038/nature14498

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