R
Ryan M. Cinalli
Researcher at New York University
Publications - 16
Citations - 4949
Ryan M. Cinalli is an academic researcher from New York University. The author has contributed to research in topics: Phosphorylation & Kinase. The author has an hindex of 15, co-authored 16 publications receiving 4658 citations. Previous affiliations of Ryan M. Cinalli include Icahn School of Medicine at Mount Sinai & University of Pennsylvania.
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Journal ArticleDOI
Akt stimulates aerobic glycolysis in cancer cells
Rebecca Elstrom,Daniel E. Bauer,Monica Buzzai,Robyn Karnauskas,Marian H. Harris,David R. Plas,Hongming Zhuang,Ryan M. Cinalli,Abass Alavi,Charles M. Rudin,Craig B. Thompson +10 more
TL;DR: It is suggested that activation of the Akt oncogene is sufficient to stimulate the switch to aerobic glycolysis characteristic of cancer cells and that Akt activity renders cancer cells dependent on aerobic glyCOlysis for continued growth and survival.
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MicroRNAs Regulate Brain Morphogenesis in Zebrafish
Antonio J. Giraldez,Ryan M. Cinalli,Margaret E. Glasner,Anton J. Enright,J. Michael Thomson,Scott Baskerville,Scott M. Hammond,David P. Bartel,Alexander F. Schier +8 more
TL;DR: Injection of miR-430 miRNAs rescues the brain defects in MZdicer mutants, revealing essential roles for miRNas during morphogenesis.
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Akt-Directed Glucose Metabolism Can Prevent Bax Conformation Change and Promote Growth Factor-Independent Survival
Jeffrey C. Rathmell,Casey J. Fox,David R. Plas,Peter S. Hammerman,Ryan M. Cinalli,Craig B. Thompson +5 more
TL;DR: Data indicate that Bax conformation is sensitive to glucose metabolism and that maintaining glucose uptake and phosphorylation can promote cell survival in the absence of growth factor.
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The serine/threonine kinase Pim-2 is a transcriptionally regulated apoptotic inhibitor
Casey J. Fox,Peter S. Hammerman,Ryan M. Cinalli,Stephen R. Master,Lewis A. Chodosh,Craig B. Thompson +5 more
TL;DR: The results establish Pim-2 as a direct link between growth factor-induced transcription and a novel, kinase-dependent pathway that promotes cell-autonomous survival.
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Deficiency in Bak and Bax perturbs thymic selection and lymphoid homeostasis.
TL;DR: The data indicate that Bak and Bax are required for thymic selection and peripheral lymphoid homeostasis and suggest that thymopoiesis can be negatively regulated by the accumulation of cells that would normally be eliminated by pro-apoptotic Bcl-2–related genes.