Brendan D. Manning
Harvard University
133 Papers
1.5K Citations
Brendan D. Manning is an academic researcher from Harvard University. The author has contributed to research in topics: mTORC1 & PI3K/AKT/mTOR pathway. The author has an hindex of 66, co-authored 126 publications. Previous affiliations of Brendan D. Manning include Yale University & University of Massachusetts Amherst.
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Papers
AKT/PKB signaling: navigating downstream.
TL;DR: Those Akt substrates that are most likely to contribute to the diverse cellular roles of Akt, which include cell survival, growth, proliferation, angiogenesis, metabolism, and migration are discussed.
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AKT/PKB Signaling: Navigating the Network
Brendan D. Manning,Alex Toker +1 more
TL;DR: Improved understanding of the molecular wiring of the AKT signaling network continues to make an impact that cuts across most disciplines of the biomedical sciences.
3K
Activation of a Metabolic Gene Regulatory Network Downstream of mTOR Complex 1
Katrin Düvel,Jessica L. Yecies,Suchithra Menon,Pichai Raman,Alex Lipovsky,Amanda Souza,Ellen Triantafellow,Qicheng Ma,Regina Gorski,Stephen Cleaver,Matthew G. Vander Heiden,Jeffrey P. MacKeigan,Peter Finan,Clary B. Clish,Leon Murphy,Brendan D. Manning +15 more
TL;DR: It is demonstrated that mTORC1 activation is sufficient to stimulate specific metabolic pathways, including glycolysis, the oxidative arm of the pentose phosphate pathway, and de novo lipid biosynthesis, through the activation of a transcriptional program affecting metabolic gene targets of hypoxia-inducible factor and sterol regulatory element-binding protein.
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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.
Brendan D. Manning,Brendan D. Manning,Andrew R. Tee,M. Nicole Logsdon,John Blenis,Lewis C. Cantley,Lewis C. Cantley +6 more
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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The PI3K–AKT network at the interface of oncogenic signalling and cancer metabolism
Gerta Hoxhaj,Brendan D. Manning +1 more
TL;DR: The PI3K–AKT signalling network is discussed and its control of cancer cell metabolism through both direct and indirect regulation of nutrient transport and metabolic enzymes, thereby connecting oncogenic signalling and metabolic reprogramming to support cancer cell survival and proliferation.
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