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Robert T. Abraham

Researcher at Pfizer

Publications -  228
Citations -  37466

Robert T. Abraham is an academic researcher from Pfizer. The author has contributed to research in topics: Phosphorylation & PI3K/AKT/mTOR pathway. The author has an hindex of 88, co-authored 228 publications receiving 34712 citations. Previous affiliations of Robert T. Abraham include Sanford-Burnham Institute for Medical Research & Eli Lilly and Company.

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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.
Journal ArticleDOI

Cell cycle checkpoint signaling through the ATM and ATR kinases

Robert T. Abraham
- 01 Sep 2001 - 
TL;DR: These checkpoints contain, as their most proximal signaling elements, sensor proteins that scan chromatin for partially replicated DNA, DNA strand breaks, or other abnormalities, and translate these DNA-derived stimuli into biochemical signals that modulate the functions of specific downstream target proteins.
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The PI3K pathway in human disease

David A. Fruman, +5 more
- 10 Aug 2017 - 
TL;DR: A perspective on the roles of class I PI3Ks in the regulation of cellular metabolism and in immune system functions is provided, two topics closely intertwined with cancer biology.
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Regulation of 4E-BP1 phosphorylation: a novel two-step mechanism

Anne-Claude Gingras, +7 more
- 01 Jun 1999 - 
TL;DR: 4E-BP1 phosphorylation by FRAP/mTOR on Thr-37 and Thr-46 is a priming event for subsequent phosphorylated of the carboxy-terminal serum-sensitive sites, including those that interact with eIF4E.
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Regulation of Hypoxia-Inducible Factor 1α Expression and Function by the Mammalian Target of Rapamycin

Christine C. Hudson, +7 more
- 15 Oct 2002 - 
TL;DR: These studies position mTOR as an upstream activator of HIF-1 function in cancer cells and suggest that the antitumor activity of rapamycin is mediated, in part, through the inhibition of cellular responses to hypoxic stress.