Abstract

How cells regulate their lysosomal proteolytic capacity is only partly understood. Here, the authors show that lysosomal protease deficiency or substrate overload induces lysosomal stress leading to activation of a STAT3-dependent, TFEB-independent pathway of lysosomal hydrolase expression.

Details

Title
Lysosomal protease deficiency or substrate overload induces an oxidative-stress mediated STAT3-dependent pathway of lysosomal homeostasis
Author
Martínez-Fábregas, Jonathan 1 ; Prescott, Alan 1 ; Sander van Kasteren 2   VIAFID ORCID Logo  ; Pedrioli, Deena Leslie 3 ; McLean, Irwin 4   VIAFID ORCID Logo  ; Moles, Anna 5 ; Reinheckel, Thomas 6 ; Poli, Valeria 7   VIAFID ORCID Logo  ; Watts, Colin 1   VIAFID ORCID Logo 

 Division of Cell Signalling and Immunology, School of Life Sciences, University of Dundee, Dundee, UK 
 Division of Bio-Organic Chemistry, Leiden Institute of Chemistry, Leiden, Netherlands 
 Division of Molecular Medicine, School of Life Sciences, University of Dundee, Dundee, UK; Department of Molecular Mechanisms of Disease, University of Zurich, Winterthurestrasse190, Switzerland 
 Division of Molecular Medicine, School of Life Sciences, University of Dundee, Dundee, UK 
 Fibrosis Research Group, Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, UK; Institute of Biomedical Research of Barcelona, Spanish Research Council, Barcelona, Spain 
 Institute of Molecular Medicine and Cell Research, Medical Faculty, Albert-Ludwigs-University, Freiburg, Germany 
 Department of Genetics, Biology and Biochemistry, University of Turin, Turin, Italy 
Pages
1-16
Publication year
2018
Publication date
Dec 2018
Publisher
Nature Publishing Group
e-ISSN
20411723
Source type
Scholarly Journal
Language of publication
English
ProQuest document ID
2157865900
Copyright
© 2018. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.