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Matthew E. Gegg

Researcher at UCL Institute of Neurology

Publications -  52
Citations -  9299

Matthew E. Gegg is an academic researcher from UCL Institute of Neurology. The author has contributed to research in topics: Glucocerebrosidase & PINK1. The author has an hindex of 30, co-authored 45 publications receiving 7695 citations. Previous affiliations of Matthew E. Gegg include University of Texas Medical Branch & University College London.

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Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy

Daniel J. Klionsky, +1287 more
- 01 Apr 2012 - 
TL;DR: These guidelines are presented for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy 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

Mitofusin 1 and mitofusin 2 are ubiquitinated in a PINK1/parkin-dependent manner upon induction of mitophagy

Matthew E. Gegg, +5 more
- 15 Dec 2010 - 
TL;DR: Overexpression and RNAi studies indicated that PINK1 and parkin were required for mitophagy following CCCP-induced mitochondrial damage, and inhibition of this pathway may lead to the accumulation of defective mitochondria which may contribute to PD pathogenesis.

Mitofusin 1 and mitofusin 2 are ubiquitinated in a PINK1/parkin-dependent manner upon induction of mitophagy (vol 19, pg 4861, 2010)

Matthew E. Gegg, +5 more
Journal ArticleDOI

Glucocerebrosidase deficiency in substantia nigra of parkinson disease brains

Matthew E. Gegg, +8 more
- 01 Sep 2012 - 
TL;DR: This work investigated the enzymatic activity of glucocerebrosidase (GCase) in PD brains carrying heterozygote GBA mutations (PD+GBA) and sporadic PD brains.
Journal ArticleDOI

Mitochondria and quality control defects in a mouse model of Gaucher disease--links to Parkinson's disease.

Laura D. Osellame, +11 more
- 04 Jun 2013 - 
TL;DR: Using a mouse model of neuronopathic GD, it is shown that autophagic machinery and proteasomal machinery are defective in neurons and astrocytes lacking gba, and markers of neurodegeneration—p62/SQSTM1, ubiquitinated proteins, and insoluble α-synuclein—accumulate.