scispace - formally typeset
J

Julie D. Atkin

Researcher at Macquarie University

Publications -  93
Citations -  11681

Julie D. Atkin is an academic researcher from Macquarie University. The author has contributed to research in topics: Amyotrophic lateral sclerosis & Neurodegeneration. The author has an hindex of 39, co-authored 87 publications receiving 10470 citations. Previous affiliations of Julie D. Atkin include University of Sheffield & University of Melbourne.

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.

of amyotrophic lateral sclerosis

TL;DR: This Seminar summarises current concepts about the origin of the disease, what predisposes patients to develop the disorder, and why all cases of ALS are not the same.
Journal ArticleDOI

C9ORF72, implicated in amytrophic lateral sclerosis and frontotemporal dementia, regulates endosomal trafficking

TL;DR: It is demonstrated that C9ORF72 regulates endosomal trafficking and colocalized with Rab proteins implicated in autophagy and endocytic transport, and increased colocalization between C9orF72 and Rab7 and Rab11 compared with controls, suggesting possible dysregulation of trafficking in patients bearing the C9 ORF72 repeat expansion.
Journal ArticleDOI

Endoplasmic reticulum stress and induction of the unfolded protein response in human sporadic amyotrophic lateral sclerosis

TL;DR: This study shows that a full UPR, including induction of stress sensor kinases, chaperones and apoptotic mediators, is also present in spinal cords of human patients with sporadic disease and shows up-regulation of UPR prior to the onset of symptoms in SOD1 rodents, implying an active role in disease.
Journal ArticleDOI

Induction of the Unfolded Protein Response in Familial Amyotrophic Lateral Sclerosis and Association of Protein-disulfide Isomerase with Superoxide Dismutase 1

TL;DR: These findings implicate unfolded protein response and ER stress-induced apoptosis in the patho-physiology of familial ALS and the possibility that PDI may be a therapeutic target to prevent SOD1 aggregation is raised.