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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

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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The CREB coactivator TORC2 is a key regulator of fasting glucose metabolism

Seung Hoi Koo, +11 more
- 20 Oct 2005 - 
TL;DR: It is shown that hormonal and energy-sensing pathways converge on the coactivator TORC2 (transducer of regulated CREB activity 2) to modulate glucose output and compounds that enhanceTORC2 phosphorylation may offer therapeutic benefits in this setting.
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The CREB coactivator TORC2 functions as a calcium- and cAMP-sensitive coincidence detector.

Robert A. Screaton, +11 more
- 01 Oct 2004 - 
TL;DR: A signaling module that mediates the synergistic effects of these pathways on cellular gene expression by stimulating the dephosphorylation and nuclear entry of TORC2, a CREB coactivator, consists of the calcium-regulated phosphatase calcineurin and the Ser/Thr kinase SIK2, both of which associate withTORC2.
Journal ArticleDOI

TORCs: transducers of regulated CREB activity.

Michael D. Conkright, +6 more
- 01 Aug 2003 - 
TL;DR: A conserved family of coactivators, designated TORCs, for Transducers of Regulated CREB activity, that enhances CRE-dependent transcription via a phosphorylation-independent interaction with the bZIP DNA binding/dimerization domain of CREB is characterized.
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cAMP promotes pancreatic β-cell survival via CREB-mediated induction of IRS2

Ulupi S. Jhala, +9 more
- 01 Jul 2003 - 
TL;DR: It is shown that mice deficient in the activity of CREB, caused by expression of a dominant-negative A-CREB transgene in pancreatic β-cells, develop diabetes secondary to β-cell apoptosis, a novel mechanism by which opposing pathways cooperate in promoting cell survival.