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Vinod Sundaramoorthy

Researcher at Macquarie University

Publications -  25
Citations -  6700

Vinod Sundaramoorthy is an academic researcher from Macquarie University. The author has contributed to research in topics: Golgi apparatus & Autophagy. The author has an hindex of 16, co-authored 24 publications receiving 6011 citations. Previous affiliations of Vinod Sundaramoorthy include La Trobe University & Deakin University.

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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.
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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.
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CCNF mutations in amyotrophic lateral sclerosis and frontotemporal dementia

Kelly L. Williams, +81 more
TL;DR: In this article, the authors used genome-wide linkage analysis in a large ALS/FTD kindred to identify a novel disease locus on chromosome 16p13.3, which encodes cyclin F, a component of an E3 ubiquitin-protein ligase complex (SCFCyclin F).
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ALS-associated TDP-43 induces endoplasmic reticulum stress, which drives cytoplasmic TDP-43 accumulation and stress granule formation

TL;DR: It is demonstrated that pharmacological induction of ER stress causes TAR DNA binding protein 43 to accumulate in the cytoplasm, where TDP-43 also associates with stress granules (SGs) and forms large inclusions, providing evidence for ER stress as a pathogenic pathway in T DP-43-mediated disease.
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Ataxin-2 interacts with FUS and intermediate-length polyglutamine expansions enhance FUS-related pathology in Amyotrophic Lateral Sclerosis

TL;DR: New cellular mechanisms linking ALS with ataxin-2 intermediate length polyQ expansions are described and further evidence linking disruption to ER-Golgi compartments and FUS pathology in ALS is provided.