T
Thomas F. Franke
Researcher at New York University
Publications - 51
Citations - 24067
Thomas F. Franke is an academic researcher from New York University. The author has contributed to research in topics: Protein kinase B & PI3K/AKT/mTOR pathway. The author has an hindex of 42, co-authored 51 publications receiving 23393 citations. Previous affiliations of Thomas F. Franke include Montreal Neurological Institute and Hospital & Massachusetts Institute of Technology.
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Journal ArticleDOI
Regulation of Cell Death Protease Caspase-9 by Phosphorylation
Michael H. Cardone,Natalie Roy,Henning R. Stennicke,Guy S. Salvesen,Thomas F. Franke,Eric J. Stanbridge,Steven M. Frisch,John C. Reed +7 more
TL;DR: In this paper, the kinase Akt and p21-Ras, an Akt activator, induced phosphorylation of pro-caspase-9 (pro-Casp9) in cells.
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Regulation of endothelium-derived nitric oxide production by the protein kinase Akt.
David Fulton,Jean-Philippe Gratton,Timothy J. McCabe,Jason Fontana,Yasushl Fujio,Kenneth Walsh,Thomas F. Franke,Andreas Papapetropoulos,William C. Sessa +8 more
TL;DR: It is shown that the serine/threonine protein kinase Akt (protein kinase B) can directly phosphorylate eNOS on serine 1179 and activate the enzyme, leading to NO production, whereas mutant eN OS (S1179A) is resistant to phosphorylation and activation by Akt.
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Regulation of Neuronal Survival by the Serine-Threonine Protein Kinase Akt
Henryk Dudek,Sandeep Robert Datta,Thomas F. Franke,Morris J. Birnbaum,Ryoji Yao,Geoffrey M. Cooper,Rosalind A. Segal,David R. Kaplan,Michael E. Greenberg +8 more
TL;DR: Findings suggest that in the developing nervous system, Akt is a critical mediator of growth factor-induced neuronal survival.
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The protein kinase encoded by the Akt proto-oncogene is a target of the PDGF-activated phosphatidylinositol 3-kinase
Thomas F. Franke,Sung-Il Yang,Tung O. Chan,Ketaki Datta,Andrius Kazlauskas,Deborah K. Morrison,David R. Kaplan,Philip N. Tsichlis +7 more
TL;DR: It is shown that Akt and the Akt-related kinase AKT2 are activated by PDGF, and it is suggested that the AkT PH domain may be a mediator of PI 3-kinase signaling.
Journal ArticleDOI
PI3K: Downstream AKTion Blocks Apoptosis
TL;DR: Results from Evan and colleagues demonstrated that mutants of V12 Ras that selectively stimulate PI3K and Akt/PKB but not the Raf/MEK/MAPK pathway are able to prevent c-myc-induced cell death in Rat-1 cells and granule neurons.