scispace - formally typeset
S

Shusaku Shibutani

Researcher at Yamaguchi University

Publications -  30
Citations -  6800

Shusaku Shibutani is an academic researcher from Yamaguchi University. The author has contributed to research in topics: Autophagy & Medicine. The author has an hindex of 11, co-authored 23 publications receiving 6127 citations. Previous affiliations of Shusaku Shibutani include University of North Carolina at Chapel Hill & Osaka 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

Autophagy and autophagy-related proteins in the immune system

Shusaku Shibutani, +4 more
- 01 Oct 2015 - 
TL;DR: Advances in the knowledge of the roles of autophagy and its components in immunity, including innate immunity, inflammatory responses and adaptive immunity are introduced.
Journal ArticleDOI

A current perspective of autophagosome biogenesis

Shusaku Shibutani, +1 more
- 01 Jan 2014 - 
TL;DR: Each Atg functional unit is briefly introduced and the origin of the autophagosomal membrane is discussed with an introduction to selected recent studies addressing this problem.
Journal ArticleDOI

Membrane molecules mobile even after chemical fixation

Kenji A K Tanaka, +10 more
- 01 Nov 2010 - 
TL;DR: Results indicate that, in interpreting immunolocalization data, antibody-induced clustering Membrane molecules mobile even after chemical fixation is indicated.
Journal ArticleDOI

Control of Drosophila endocycles by E2F and CRL4 CDT2

Norman Zielke, +15 more
- 01 Dec 2011 - 
TL;DR: It is proposed that it is the transient loss of E2F1 during S phases that creates the window of low Cdk activity required for preRC formation, and it is found that altering cell growth by changing nutrition or target of rapamycin (TOR) signalling impacts E 2F1 translation, thereby making endocycle progression growth-dependent.