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Yaoyan Qiu
Researcher at University of Michigan
Publications - 4
Citations - 106
Yaoyan Qiu is an academic researcher from University of Michigan. The author has contributed to research in topics: Autophagy & Photoreceptor cell. The author has an hindex of 3, co-authored 3 publications receiving 58 citations. Previous affiliations of Yaoyan Qiu include Central South University.
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Journal ArticleDOI
Inhibiting autophagy reduces retinal degeneration caused by protein misfolding.
Jingyu Yao,Yaoyan Qiu,Eric Frontera,Lin Jia,Naheed W. Khan,Daniel J. Klionsky,Thomas A. Ferguson,Debra A. Thompson,David N. Zacks +8 more
TL;DR: It is proposed that modulating the flux of misfolded proteins from autophagy to the proteasome may represent an important therapeutic strategy for reducing proteotoxicity in adRP and other diseases caused by protein folding defects.
Journal ArticleDOI
Shifting the balance of autophagy and proteasome activation reduces proteotoxic cell death: a novel therapeutic approach for restoring photoreceptor homeostasis.
TL;DR: The conclusion that normalizing the A:P ratio, either by reducing the ERS-induced activation of autophagy, or by increasing proteasome activity, improves photoreceptor survival, is supported and a potential new therapeutic strategy for the treatment of adRP caused by protein folding defects is suggested.
Journal ArticleDOI
Autophagosome immunoisolation from GFP-LC3B mouse tissue
TL;DR: A protocol for rapid and efficient enrichment of autophagosomes from various tissues of the GFP-LC3 mouse with a single intraperitoneal injection of leupeptin before tissue harvesting is described.
Journal ArticleDOI
Loss of Fas Receptor Function Preserves Photoreceptor Structure and Function in Two Mouse Models of Inherited Retinal Degeneration
TL;DR: The protective effect of a nonfunctional Fas receptor in two different mouse models of retinal degeneration suggests that whereas the individual IRD mutation may be specific, the retina's response to the different stressors appears to be shared and driven by Fas.