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Robert A. Screaton

Researcher at University of Toronto

Publications -  57
Citations -  10935

Robert A. Screaton is an academic researcher from University of Toronto. The author has contributed to research in topics: CREB & CRTC2. The author has an hindex of 31, co-authored 53 publications receiving 9968 citations. Previous affiliations of Robert A. Screaton include Sunnybrook Research Institute & Salk Institute for Biological Studies.

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Journal ArticleDOI

Genome-wide RNAi screen identifies ATPase inhibitory factor 1 (ATPIF1) as essential for PARK2 recruitment and mitophagy

Valerie Lefebvre, +7 more
- 07 Aug 2013 - 
TL;DR: A genome-wide RNAi screen searching for genes that are required for PARK2 translocation to the mitochondria identified ATPIF1 and the ATP synthase as novel components of the PINK1-PARK2 mitophagy pathway and provide genetic evidence that loss of ΔΨ is an essential trigger forMitophagy.
Journal Article

Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2459 more
- 01 Jan 2016 - 
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Role of the SIK2–p35–PJA2 complex in pancreatic β-cell functional compensation

Jun-Ichi Sakamaki, +11 more
- 01 Mar 2014 - 
TL;DR: It is demonstrated that the SIK2–p35–PJA2 complex is essential for glucose homeostasis and provides a link between p35–CDK5 and the AMPK family in excitable cells.
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The coactivator CRTC1 promotes cell proliferation and transformation via AP-1

Gianluca Canettieri, +9 more
- 03 Feb 2009 - 
TL;DR: It is demonstrated that CRTC1-Maml2 oncoprotein, which causes mucoepidermoid carcinomas, binds and activates both c-Jun and c-Fos, and ablation of AP-1 function disrupts the cellular transformation and proliferation mediated by this oncogene.
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Homozygous mutations in MFN2 cause multiple symmetric lipomatosis associated with neuropathy

Sarah L. Sawyer, +9 more
- 15 Sep 2015 - 
TL;DR: Findings show that homozygous mutations at p.R707W in MFN2 are a novel cause of multiple symmetrical lipomatosis, a mitochondrial disorder with impaired brown fat metabolism that has been associated with MERRF mutations in some, but not all, patients.