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Debora Bonenfant
Researcher at Novartis
Publications - 29
Citations - 3192
Debora Bonenfant is an academic researcher from Novartis. The author has contributed to research in topics: Phosphorylation & Cancer research. The author has an hindex of 15, co-authored 23 publications receiving 2821 citations. Previous affiliations of Debora Bonenfant include University of Basel.
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Two TOR complexes, only one of which is rapamycin sensitive, have distinct roles in cell growth control
Robbie Loewith,Estela Jacinto,Stephan Wullschleger,Anja Lorberg,José L. Crespo,Debora Bonenfant,Wolfgang Oppliger,Paul Jenoe,Michael N. Hall +8 more
TL;DR: Two functionally distinct TOR complexes account for the diversity, specificity, and selective rapamycin inhibition of TOR signaling.
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Targeting fibroblast growth factor receptors blocks PI3K/AKT signaling, induces apoptosis, and impairs mammary tumor outgrowth and metastasis
Julien H. Dey,Fabrizio Bianchi,Johannes Voshol,Debora Bonenfant,Edward J. Oakeley,Nancy E. Hynes +5 more
TL;DR: An in vitro and in vivo analysis ofFGFRs in the breast cancer model cell lines 67NR and 4T1 shows that both tumor cell lines coexpress FGFRs and ligands and display autocrine FGFR signaling activity.
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Characterization of Histone H2A and H2B Variants and Their Post-translational Modifications by Mass Spectrometry
TL;DR: The first global mass spectrometric analysis of histone H2A and H2B variants derived from Jurkat cells provides a first step toward an understanding of the functional significance of the diversity of hist one structures.
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Analysis of Dynamic Changes in Post-translational Modifications of Human Histones during Cell Cycle by Mass Spectrometry
Debora Bonenfant,Harry Towbin,Michele Coulot,Patrick Schindler,Dieter Mueller,Jan van Oostrum +5 more
TL;DR: The results show that mitosis was the period of the cell cycle during which many modifications exhibit dynamic changes, and the pattern of cycle-dependent methylation was more complex: during G2/M, H3 Lys27 and Lys36 were decreased, whereas H4 Lys20 was increased.
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CLK2 inhibition ameliorates autistic features associated with SHANK3 deficiency
Michael Bidinosti,Paolo Botta,Sebastian Krüttner,Catia C. Proenca,Natacha Stoehr,Mario Bernhard,Isabelle Fruh,Matthias Mueller,Debora Bonenfant,Hans Voshol,Walter Carbone,Sarah J. Neal,Stephanie M. McTighe,Guglielmo Roma,Ricardo E. Dolmetsch,Jeffrey A. Porter,Pico Caroni,Tewis Bouwmeester,Andreas Lüthi,Ivan Galimberti +19 more
TL;DR: This study provides a novel mechanistic and potentially therapeutic understanding of deregulated signaling downstream of Shank3 deficiency, and uses unbiased, quantitative proteomics to identify changes in the phosphoproteome of Shank2-deficient neurons.