William P. Miller
Pennsylvania State University
16 Papers
1 Citations
William P. Miller is an academic researcher from Pennsylvania State University. The author has contributed to research in topics: Oxidative stress & Biology. The author has an hindex of 8, co-authored 11 publications.
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Papers
Role of Oxidative Stress in Ocular Diseases: A Balancing Act
Daisy Y. Shu,Suman Chaudhary,Kin-Sang Cho,Anton Lennikov,William P. Miller,David C. Thorn,Meng Yang,Tina B. McKay +7 more
TL;DR: In this article , the authors present the current evidence for oxidative stress and mitochondrial dysfunction in conditions affecting both the anterior segment (e.g., dry eye disease, keratoconus, cataract) and posterior segment (age-related macular degeneration, proliferative vitreoretinopathy, diabetic retinopathy and glaucoma) of the human eye.
Deletion of the Akt/mTORC1 Repressor REDD1 Prevents Visual Dysfunction in a Rodent Model of Type 1 Diabetes.
William P. Miller,Chen Yang,Maria L. Mihailescu,Joshua A. Moore,Weiwei Dai,Alistair J. Barber,Michael D. Dennis +6 more
TL;DR: A role for REDD1 in diabetes-induced retinal neurodegeneration is supported, and diabetic wild-type mice exhibited functional deficiencies in visual acuity and contrast sensitivity, whereas diabetic REDD 1-deficient mice had no visual dysfunction.
REDD1 Activates a ROS-Generating Feedback Loop in the Retina of Diabetic Mice.
TL;DR: In the retina of diabetic mice and cells exposed to hyperglycemic conditions, NAC normalized ROS and prevented an increase in REDD1 expression, providing new insight into the mechanism whereby diabetes-induced hyperglycemia causes oxidative stress and visual dysfunction.
O-GlcNAcylation alters the selection of mRNAs for translation and promotes 4E-BP1–dependent mitochondrial dysfunction in the retina
Sadie K. Dierschke,William P. Miller,John S. Favate,Premal Shah,Yuka Imamura Kawasawa,Anna C. Salzberg,Scot R. Kimball,Leonard S. Jefferson,Michael D. Dennis +8 more
TL;DR: Evidence is provided for a mechanism whereby diabetes-induced O-GlcNAcylation promotes oxidative stress in the retina by altering the selection of mRNAs for translation.
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The Translational Repressor 4E-BP1 Contributes to Diabetes-Induced Visual Dysfunction.
William P. Miller,Maria L. Mihailescu,Chen Yang,Alistair J. Barber,Scot R. Kimball,Leonard S. Jefferson,Michael D. Dennis +6 more
TL;DR: The findings support a model whereby elevated 4E-BP1 expression observed in the retina of diabetic rodents is the result of O-GlcNAcylation of 4E -BP1 within its PEST motif.