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Wolfdieter Springer

Researcher at Mayo Clinic

Publications -  60
Citations -  15336

Wolfdieter Springer is an academic researcher from Mayo Clinic. The author has contributed to research in topics: PINK1 & Parkin. The author has an hindex of 31, co-authored 52 publications receiving 13003 citations. Previous affiliations of Wolfdieter Springer include German Center for Neurodegenerative Diseases & University of Tübingen.

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Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy

Daniel J. Klionsky, +1287 more
- 01 Apr 2012 - 
TL;DR: These guidelines are presented for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
Journal ArticleDOI

PINK1/Parkin-mediated mitophagy is dependent on VDAC1 and p62/SQSTM1

Sven Geisler, +6 more
- 24 Jan 2010 - 
TL;DR: Functional links between PINK1, Parkin and the selective autophagy of mitochondria, which is implicated in the pathogenesis of Parkinson's disease, are provided.
Journal ArticleDOI

The PINK1/Parkin-mediated mitophagy is compromised by PD-associated mutations.

Sven Geisler, +7 more
- 01 Oct 2010 - 
TL;DR: It is shown that whole mitochondria are turned over via macroautophagy, and PD-associated PINK1 mutations abrogate autophagy of impaired mitochondria upstream of Parkin, which may contribute to disease pathogenesis.
Journal ArticleDOI

Knockdown of transactive response DNA-binding protein (TDP-43) downregulates histone deacetylase 6

Fabienne C. Fiesel, +18 more
- 06 Jan 2010 - 
TL;DR: Loss of functional TDP‐43 causes HDAC6 downregulation and might thereby contribute to pathogenesis, andHDAC6‐dependent reduction of cellular aggregate formation and increased cytotoxicity of polyQ‐expanded ataxin‐3 were found in T DP‐43 silenced cells.