D
Der-Fen Suen
Researcher at Academia Sinica
Publications - 24
Citations - 9680
Der-Fen Suen is an academic researcher from Academia Sinica. The author has contributed to research in topics: Mitochondrion & Parkin. The author has an hindex of 17, co-authored 22 publications receiving 8590 citations. Previous affiliations of Der-Fen Suen include University of California, Riverside & National Institutes of Health.
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Journal ArticleDOI
Parkin is recruited selectively to impaired mitochondria and promotes their autophagy
TL;DR: It is shown that Parkin is selectively recruited to dysfunctional mitochondria with low membrane potential in mammalian cells and this recruitment promotes autophagy of damaged mitochondria and implicate a failure to eliminate dysfunctional mitochondira in the pathogenesis of Parkinson's disease.
Journal ArticleDOI
PINK1 is selectively stabilized on impaired mitochondria to activate Parkin.
Derek P. Narendra,Seok Min Jin,Atsushi Tanaka,Der-Fen Suen,Clement A. Gautier,Jie Shen,Mark R. Cookson,Richard J. Youle +7 more
TL;DR: The authors suggest that PINK1 and Parkin form a pathway that senses damaged mitochondria and selectively targets them for degradation.
Journal ArticleDOI
Proteasome and p97 mediate mitophagy and degradation of mitofusins induced by Parkin
Atsushi Tanaka,Megan M. Cleland,Shan-Shan Xu,Derek P. Narendra,Der-Fen Suen,Mariusz Karbowski,Richard J. Youle +6 more
TL;DR: The Parkin ubiquitin ligase marks the mitofusins Mfn1 and Mfn2 for proteasome-dependent degradation, promoting disposal of damaged mitochondria by preventing their fusion with healthy organelles.
Journal ArticleDOI
Mitochondrial dynamics and apoptosis
TL;DR: This review will cover the recent advances and presents competing models on how the mitochondrial fission and fusion machinery may intersect apoptosis pathways.
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Parkin overexpression selects against a deleterious mtDNA mutation in heteroplasmic cybrid cells
TL;DR: Long-term overexpression of Parkin can eliminate mitochondria with deleterious COXI mutations in heteroplasmic cybrid cells, thereby enriching cells for wild-type mtDNA and restoring cytochrome c oxidase activity, and support the model that Parkin functions in a mitochondrial quality control pathway.