scispace - formally typeset
H

Hua She

Researcher at Emory University

Publications -  23
Citations -  6675

Hua She is an academic researcher from Emory University. The author has contributed to research in topics: Autophagy & Transcription factor. The author has an hindex of 17, co-authored 22 publications receiving 6029 citations. Previous affiliations of Hua She include Central South University.

Papers
More filters
Journal ArticleDOI

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

Regulation of Neuronal Survival Factor MEF2D by Chaperone-Mediated Autophagy

TL;DR: It is found that chaperone-mediated autophagy regulated the activity of myocyte enhancer factor 2D (MEF2D), a transcription factor required for neuronal survival, and dysregulation of this pathway is associated with Parkinson's disease.
Journal ArticleDOI

Alternative Mitochondrial Electron Transfer as a Novel Strategy for Neuroprotection

TL;DR: Methylene blue functions as an alternative electron carrier, which accepts electrons from NADH and transfers them to cytochrome c and bypasses complex I/III blockage, and indicates that rerouting mitochondrial electron transfer by MB or similar molecules provides a novel strategy for neuroprotection against both chronic and acute neurological diseases involving mitochondrial dysfunction.
Journal ArticleDOI

p38 MAPK inhibits autophagy and promotes microglial inflammatory responses by phosphorylating ULK1.

TL;DR: A molecular mechanism that enables the initial TLR4-triggered signaling pathway to inhibit autophagy and optimize inflammatory responses is revealed, providing new understanding into the mechanistic basis of the neuroinflammatory process.
Journal ArticleDOI

Direct regulation of complex I by mitochondrial MEF2D is disrupted in a mouse model of Parkinson disease and in human patients

TL;DR: Direct regulation of complex I by mitochondrial MEF2D underlies its neuroprotective effects, and dysregulation of this pathway may contribute to PD.