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Reuben J. Shaw

Researcher at Salk Institute for Biological Studies

Publications -  132
Citations -  41110

Reuben J. Shaw is an academic researcher from Salk Institute for Biological Studies. The author has contributed to research in topics: AMPK & Kinase. The author has an hindex of 54, co-authored 123 publications receiving 34683 citations. Previous affiliations of Reuben J. Shaw include Howard Hughes Medical Institute & Massachusetts Institute of Technology.

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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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Resveratrol improves health and survival of mice on a high-calorie diet

Joseph A. Baur, +26 more
- 16 Nov 2006 - 
TL;DR: It is shown that resveratrol shifts the physiology of middle-aged mice on a high-calorie diet towards that of mice onA standard diet and significantly increases their survival and point to new approaches for treating obesity-related disorders and diseases of ageing.
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AMPK phosphorylation of raptor mediates a metabolic checkpoint.

Dana M. Gwinn, +7 more
- 25 Apr 2008 - 
TL;DR: AMPK directly phosphorylates the mTOR binding partner raptor on two well-conserved serine residues, and this phosphorylation induces 14-3-3 binding to raptor, uncovering a conserved effector of AMPK that mediates its role as a metabolic checkpoint coordinating cell growth with energy status.
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The AMPK signalling pathway coordinates cell growth, autophagy and metabolism

Maria M. Mihaylova, +1 more
- 01 Sep 2011 - 
TL;DR: A number of recent breakthroughs in the mechanistic understanding of AMPK function are reviewed, focusing on a number of newly identified downstream effectors of AM PK.
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Phosphorylation of ULK1 (hATG1) by AMP-Activated Protein Kinase Connects Energy Sensing to Mitophagy

Daniel F. Egan, +16 more
- 28 Jan 2011 - 
TL;DR: Reconstitution of ULK1-deficient cells with a mutant ULK2 that cannot be phosphorylated by AMPK revealed that such phosphorylation is required for mitochondrial homeostasis and cell survival during starvation.