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Andrew R. Tee

Researcher at Cardiff University

Publications -  81
Citations -  17174

Andrew R. Tee is an academic researcher from Cardiff University. The author has contributed to research in topics: PI3K/AKT/mTOR pathway & mTORC1. The author has an hindex of 42, co-authored 76 publications receiving 15045 citations. Previous affiliations of Andrew R. Tee include University of Dundee & Harvard University.

Papers
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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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Identification of the tuberous sclerosis complex-2 tumor suppressor gene product tuberin as a target of the phosphoinositide 3-kinase/akt pathway.

TL;DR: This approach identifies the tuberous sclerosis complex-2 gene product, tuberin, as a potential target of Akt/PKB, and demonstrates that, upon activation of PI3K, tuber in is phosphorylated on consensus recognition sites forPI3K-dependent S/T kinases.
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Tuberous sclerosis complex gene products, Tuberin and Hamartin, control mTOR signaling by acting as a GTPase-activating protein complex toward Rheb.

TL;DR: It is shown that Rheb acts as a novel mediator of the nutrient signaling input to mTOR and is the molecular target of TSC1 and TSC2 within mammalian cells.
Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)

Daniel J. Klionsky, +2983 more
- 08 Feb 2021 - 
TL;DR: In this article, the authors present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes.
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mTOR controls cell cycle progression through its cell growth effectors S6K1 and 4E-BP1/eukaryotic translation initiation factor 4E.

TL;DR: It is demonstrated that, as for the regulation of cell growth and cell size, the S6K1 and 4E-BP1/eIF4E pathways each represent critical mediators of mTOR-dependent cell cycle control.