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Claire H. Mitchell

Researcher at University of Pennsylvania

Publications -  126
Citations -  9829

Claire H. Mitchell is an academic researcher from University of Pennsylvania. The author has contributed to research in topics: Retinal ganglion & Adenosine. The author has an hindex of 41, co-authored 123 publications receiving 8935 citations. Previous affiliations of Claire H. Mitchell include Government of the United States of America.

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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.
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Presenilin 1 Maintains Lysosomal Ca2+ Homeostasis via TRPML1 by Regulating vATPase-Mediated Lysosome Acidification

TL;DR: The results indicate that vATPase deficiency in PS1 loss-of-function states causes lysosomal/autophagy deficits and contributes to abnormal cellular Ca(2+) homeostasis, thus linking two AD-related pathogenic processes through a common molecular mechanism.
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A release mechanism for stored ATP in ocular ciliary epithelial cells

TL;DR: Both layers of the ciliary epithelium store and release ATP, and purines likely modulate aqueous humor flow by paracrine and/or autocrine mechanisms within the two cell layers of this epithelia.
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Lysosomal alkalization and dysfunction in human fibroblasts with the Alzheimer's disease-linked presenilin 1 A246E mutation can be reversed with cAMP

TL;DR: A small elevation in the lysosomal pH of human PS1-fAD fibroblasts is confirmed, and it is demonstrated that this lysOSomal alkalization is associated with chronic changes in autophagy and degradation, and suggested that treatment to reacidify the lYSosomes with cAMP can reverse these changes.
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CATSPER Channel-Mediated Ca2+ Entry into Mouse Sperm Triggers a Tail-to-Head Propagation

TL;DR: It is shown that a Ca2+ influx in the principal piece through CATSPER channels can not only initiate hyperactivated motility, but can also trigger a tail-to-head Ca2- propagation that leads to an increase in [NADH] and may regulate ATP homeostasis.