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George R. Jackson

Researcher at Baylor College of Medicine

Publications -  103
Citations -  12281

George R. Jackson is an academic researcher from Baylor College of Medicine. The author has contributed to research in topics: Neurodegeneration & Nerve growth factor. The author has an hindex of 43, co-authored 101 publications receiving 10598 citations. Previous affiliations of George R. Jackson include UCLA Medical Center & Veterans Health Administration.

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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.
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Histone deacetylase inhibitors arrest polyglutamine-dependent neurodegeneration in Drosophila

Joan S. Steffan, +14 more
- 18 Oct 2001 - 
TL;DR: It is shown that the polyglutamine-containing domain of Htt, Htt exon 1 protein (Httex1p), directly binds the acetyltransferase domains of two distinct proteins: CREB-binding protein (CBP) and p300/CBP-associated factor (P/CAF).
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Polyglutamine-Expanded Human Huntingtin Transgenes Induce Degeneration of Drosophila Photoreceptor Neurons

George R. Jackson, +7 more
- 01 Sep 1998 - 
TL;DR: A Drosophila model for Huntington's disease is described, and coexpression of the viral antiapoptotic protein, P35, did not rescue the cell death phenotype induced by polyglutamine-expanded huntingtin.
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Human Wild-Type Tau Interacts with wingless Pathway Components and Produces Neurofibrillary Pathology in Drosophila

George R. Jackson, +6 more
- 16 May 2002 - 
TL;DR: It is shown that tau overexpression, in combination with phosphorylation by the Drosophila glycogen synthase kinase-3 (GSK-3) homolog and wingless pathway component (Shaggy), exacerbated neurodegeneration induced by tauverexpression alone, leading to neurofibrillary pathology in the fly.
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Tau oligomers impair memory and induce synaptic and mitochondrial dysfunction in wild-type mice

Cristian A. Lasagna-Reeves, +5 more
- 06 Jun 2011 - 
TL;DR: It is reported that oligomers of recombinant full-length human tau protein are neurotoxic in vivo after subcortical stereotaxic injection into mice, and suggests that tau oligomers induce neurodegeneration by affecting mitochondrial and synaptic function, both of which are early hallmarks in AD and other tauopathies.