Recombinant pro-CTSD (cathepsin D) enhances SNCA/α-Synuclein degradation in α-Synucleinopathy models-Reference-Cited by-同舟云学术

Recombinant pro-CTSD (cathepsin D) enhances SNCA/α-Synuclein degradation in α-Synucleinopathy models

Published:2022-04-28 Issue:5 Volume:18 Page:1127-1151
ISSN:1554-8627
Container-title:Autophagy
language:en
Short-container-title:Autophagy

Author:

Prieto Huarcaya Susy¹,Drobny Alice²^ORCID,Marques André R. A.³,Di Spiezio Alessandro¹^ORCID,Dobert Jan Philipp²,Balta Denise²,Werner Christian⁴,Rizo Tania⁵,Gallwitz Lisa¹,Bub Simon²,Stojkovska Iva⁶,Belur Nandkishore R.⁶,Fogh Jens⁷,Mazzulli Joseph R⁴,Xiang Wei²,Fulzele Amitkumar⁸,Dejung Mario⁸,Sauer Markus⁴,Winner Beate⁵,Rose-John Stefan¹,Arnold Philipp⁹,Saftig Paul¹^ORCID,Zunke Friederike²^ORCID

Affiliation:

1. Institute of Biochemistry, Christian-Albrechts-University Kiel, Kiel, Germany

2. Department of Molecular Neurology, University Hospital Erlangen, Friedrich-Alexander University Erlangen-Nürnberg (Fau), Erlangen, Germany

3. iNOVA4Health, Chronic Diseases Research Center (CEDOC), Nova Medical School, Nms, Nova University Lisbon, Lisboa, Portugal

4. Department of Biotechnology and Biophysics, University of Würzburg, Biocenter, Am Hubland, Würzburg, Germany

5. Department of Stem Cell Biology, University Hospital Erlangen, Friedrich-Alexander University Erlangen-Nürnberg, Erlangen, Germany

6. The Ken and Ruth Davee Department of Neurology, Northwestern University Feinberg School of Medicine, Chicago, Illinois USA

7. OrfoNeuro ApS, Lynge, Denmark

8. Institute of Molecular Biology (IMB), Ackermannweg 4, Mainz, Germany

9. Institute of Functional and Clinical Anatomy, Friedrich-Alexander-University Erlangen-Nürnberg (FAU), Erlangen, Germany

Funder

Deutsche Forschungsgemeinschaft

Bavarian Ministry of Science and the Arts

Interdisciplinary Center for Clinical Research (IZKF) at the University Hospital of the University of Erlangen-Nuremberg

Publisher

Informa UK Limited

Subject

Cell Biology,Molecular Biology

Link

https://www.tandfonline.com/doi/pdf/10.1080/15548627.2022.2045534

Reference126 articles.

1. Parkinson's disease

2. Parkinson's disease

3. Parkinson-associated risk variant in distal enhancer of α-synuclein modulates target gene expression

4. Large-scale meta-analysis of genome-wide association data identifies six new risk loci for Parkinson's disease

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