Nature Communications (Jan 2018)
Oxidation of SQSTM1/p62 mediates the link between redox state and protein homeostasis
- Bernadette Carroll,
- Elsje G. Otten,
- Diego Manni,
- Rhoda Stefanatos,
- Fiona M. Menzies,
- Graham R. Smith,
- Diana Jurk,
- Niall Kenneth,
- Simon Wilkinson,
- Joao F. Passos,
- Johannes Attems,
- Elizabeth A. Veal,
- Elisa Teyssou,
- Danielle Seilhean,
- Stéphanie Millecamps,
- Eeva-Liisa Eskelinen,
- Agnieszka K. Bronowska,
- David C. Rubinsztein,
- Alberto Sanz,
- Viktor I. Korolchuk
Affiliations
- Bernadette Carroll
- Institute for Cell and Molecular Biosciences (ICaMB), Newcastle University Institute for Ageing (NUIA), Newcastle University
- Elsje G. Otten
- Institute for Cell and Molecular Biosciences (ICaMB), Newcastle University Institute for Ageing (NUIA), Newcastle University
- Diego Manni
- Institute for Cell and Molecular Biosciences (ICaMB), Newcastle University Institute for Ageing (NUIA), Newcastle University
- Rhoda Stefanatos
- Institute for Cell and Molecular Biosciences (ICaMB), Newcastle University Institute for Ageing (NUIA), Newcastle University
- Fiona M. Menzies
- Cambridge Institute for Medical Research, Wellcome Trust/MRC Building
- Graham R. Smith
- Institute for Cell and Molecular Biosciences (ICaMB), Newcastle University Institute for Ageing (NUIA), Newcastle University
- Diana Jurk
- Institute for Cell and Molecular Biosciences (ICaMB), Newcastle University Institute for Ageing (NUIA), Newcastle University
- Niall Kenneth
- Institute for Cell and Molecular Biosciences (ICaMB), Newcastle University Institute for Ageing (NUIA), Newcastle University
- Simon Wilkinson
- Edinburgh Cancer Research UK Centre, Institute of Genetics and Molecular Medicine, Western General Hospital, University of Edinburgh
- Joao F. Passos
- Institute for Cell and Molecular Biosciences (ICaMB), Newcastle University Institute for Ageing (NUIA), Newcastle University
- Johannes Attems
- Institute of Neuroscience (IoN); Newcastle University Institute for Ageing (NUIA), Newcastle University
- Elizabeth A. Veal
- Institute for Cell and Molecular Biosciences (ICaMB), Newcastle University Institute for Ageing (NUIA), Newcastle University
- Elisa Teyssou
- Institut du Cerveau et de la Moelle épinière (ICM), INSERM U1127, CNRS UMR7225, Sorbonne Universités, Université Pierre et Marie Curie, University of Paris 06, UPMC-P6 UMRS1127, Hôpital Pitié-Salpêtrière
- Danielle Seilhean
- Institut du Cerveau et de la Moelle épinière (ICM), INSERM U1127, CNRS UMR7225, Sorbonne Universités, Université Pierre et Marie Curie, University of Paris 06, UPMC-P6 UMRS1127, Hôpital Pitié-Salpêtrière
- Stéphanie Millecamps
- Institut du Cerveau et de la Moelle épinière (ICM), INSERM U1127, CNRS UMR7225, Sorbonne Universités, Université Pierre et Marie Curie, University of Paris 06, UPMC-P6 UMRS1127, Hôpital Pitié-Salpêtrière
- Eeva-Liisa Eskelinen
- Department of Biosciences, University of Helsinki
- Agnieszka K. Bronowska
- School of Chemistry, Newcastle University
- David C. Rubinsztein
- Cambridge Institute for Medical Research, Wellcome Trust/MRC Building
- Alberto Sanz
- Institute for Cell and Molecular Biosciences (ICaMB), Newcastle University Institute for Ageing (NUIA), Newcastle University
- Viktor I. Korolchuk
- Institute for Cell and Molecular Biosciences (ICaMB), Newcastle University Institute for Ageing (NUIA), Newcastle University
- DOI
- https://doi.org/10.1038/s41467-017-02746-z
- Journal volume & issue
-
Vol. 9,
no. 1
pp. 1 – 11
Abstract
The cellular mechanisms underlying autophagy are conserved; however it is unclear how they evolved in higher organisms. Here the authors identify two oxidation-sensitive cysteine residues in the autophagy receptor SQSTM1/p62 in vertebrates which allow activation of pro-survival autophagy in stress conditions.
