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Francois Natt

Researcher at Novartis

Publications -  87
Citations -  5784

Francois Natt is an academic researcher from Novartis. The author has contributed to research in topics: Oligonucleotide & RNA interference. The author has an hindex of 31, co-authored 87 publications receiving 5612 citations. Previous affiliations of Francois Natt include Friedrich Miescher Institute for Biomedical Research & Northwestern University.

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Amino acids mediate mTOR/raptor signaling through activation of class 3 phosphatidylinositol 3OH-kinase

TL;DR: A major pathway by which amino acids control mTOR signaling is distinct from that of insulin and that, instead of signaling through components of the insulin/class 1PI3K pathway, amino acids mediate mTOR activation by signaling through class 3 PI3K, hVps34.
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The mTOR Inhibitor RAD001 Sensitizes Tumor Cells to DNA-Damaged Induced Apoptosis through Inhibition of p21 Translation

TL;DR: It is shown that RAD001 (everolimus), a rapamycin derivative, dramatically enhances cisplatin-induced apoptosis in wild-type p53, but not mutant p53 tumor cells, showing that a general effect on a major anabolic process may dramatically enhance the efficacy of an established drug protocol in the treatment of cancer patients with solid tumors.
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siRNA relieves chronic neuropathic pain

TL;DR: It is shown that RNAi can block a pathophysiological pain response and provide relief from neuropathic pain in a rat disease model by down regulating an endogenous, neuronally expressed gene.
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Design of a genome-wide siRNA library using an artificial neural network.

TL;DR: The Stuttgart Neural Net Simulator was used to train algorithms on a data set of 2,182 randomly selected siRNAs targeted to 34 mRNA species, assayed through a high-throughput fluorescent reporter gene system and BIOPREDsi was used in the design of a genome-wide siRNA collection with two potent si RNAs per gene.
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Amino Acids Activate mTOR Complex 1 via Ca2+/CaM Signaling to hVps34

TL;DR: It is shown that AAs induce a rise in intracellular Ca(2+) ([Ca(2+)](i), which triggers mTOR Complex 1 and hVps34 activation, which increases the direct binding of Ca( 2+)/calmodulin (CaM) to an evolutionarily conserved motif in hVPS34 that is required for lipid kinase activity and increased mTOR complex 1 signaling.