Q
Qing Sheng
Researcher at Novartis
Publications - 16
Citations - 5792
Qing Sheng is an academic researcher from Novartis. The author has contributed to research in topics: Signal transduction & Cancer. The author has an hindex of 12, co-authored 16 publications receiving 4812 citations. Previous affiliations of Qing Sheng include Harvard University & Genomics Institute of the Novartis Research Foundation.
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Journal ArticleDOI
Systematic RNA interference reveals that oncogenic KRAS-driven cancers require TBK1
David A. Barbie,Pablo Tamayo,Jesse S. Boehm,So Young Kim,Susan Moody,Ian F. Dunn,Anna C. Schinzel,Peter Sandy,Etienne Meylan,Claudia Scholl,Stefan Fröhling,Edmond M. Chan,Martin L. Sos,Kathrin Michel,Craig H. Mermel,Serena J. Silver,Barbara A. Weir,Jan H. Reiling,Qing Sheng,Piyush Gupta,Raymond C. Wadlow,Raymond C. Wadlow,Hanh Le,Sebastian Hoersch,Ben S. Wittner,Ben S. Wittner,Sridhar Ramaswamy,Sridhar Ramaswamy,David M. Livingston,David M. Sabatini,Matthew Meyerson,Matthew Meyerson,Roman K. Thomas,Eric S. Lander,Jill P. Mesirov,David E. Root,D. Gary Gilliland,Tyler Jacks,William C. Hahn +38 more
TL;DR: Observations indicate that TBK1 and NF-κB signalling are essential in KRAS mutant tumours, and establish a general approach for the rational identification of co-dependent pathways in cancer.
Journal ArticleDOI
Control of BRCA2 Cellular and Clinical Functions by a Nuclear Partner, PALB2
Bing Xia,Qing Sheng,Koji Nakanishi,Akihiro Ohashi,Jianmin Wu,Nicole Christ,Xinggang Liu,Maria Jasin,Fergus J. Couch,David M. Livingston +9 more
TL;DR: PALB2 licenses key cellular biochemical properties of BRCA2 and ensures its tumor suppression function, as well as enabling homologous recombination (HR)-based, error-free DNA double-strand break repair (DSBR) and intra-S phase DNA damage checkpoint control.
Journal ArticleDOI
AKT-Independent Signaling Downstream of Oncogenic PIK3CA Mutations in Human Cancer
Krishna Murthi Vasudevan,David A. Barbie,David A. Barbie,Michael A. Davies,Rosalia Rabinovsky,Chontelle J. McNear,Jessica J. Kim,Bryan T. Hennessy,Hsiuyi Tseng,Panisa Pochanard,So Young Kim,So Young Kim,Ian F. Dunn,Anna C. Schinzel,Anna C. Schinzel,Peter Sandy,Sebastian Hoersch,Qing Sheng,Piyush Gupta,Jesse S. Boehm,Jan H. Reiling,Serena J. Silver,Yiling Lu,Katherine Stemke-Hale,Bhaskar Dutta,Corwin Joy,Aysegul A. Sahin,Ana M. Gonzalez-Angulo,Ana Lluch,Lucia E. Rameh,Tyler Jacks,David E. Root,Eric S. Lander,Gordon B. Mills,William C. Hahn,William R. Sellers,William R. Sellers,Levi A. Garraway +37 more
TL;DR: This paper showed that SGK3 undergoes PI3K-and PDK1-dependent activation in PIK3CA mutant cancer cells and showed that these cells retain robust PDK 1 activation and membrane localization and exhibit dependency on the SGK 1 substrate SGK 3.
Journal ArticleDOI
Fanconi anemia is associated with a defect in the BRCA2 partner PALB2.
Bing Xia,Josephine C. Dorsman,Najim Ameziane,Yne de Vries,Martin A. Rooimans,Qing Sheng,Gerard Pals,Abdellatif Errami,Eliane Gluckman,Julián Llera,Weidong Wang,David M. Livingston,Hans Joenje,Johan P. de Winter +13 more
TL;DR: PALB2-deficient cells showed hypersensitivity to cross-linking agents and lacked chromatin-bound BRCA2; these defects were corrected upon ectopic expression of PALB2 or by spontaneous reversion.
AKT-Independent Signaling Downstream of Oncogenic PIK3CA Mutations in Human Cancer
Krishna Murthi Vasudevan,David A. Barbie,David A. Barbie,Michael A. Davies,Rosalia Rabinovsky,Chontelle J. McNear,Jessica J. Kim,Bryan T. Hennessy,Hsiuyi Tseng,Panisa Pochanard,So Young Kim,So Young Kim,Ian F. Dunn,Anna C. Schinzel,Anna C. Schinzel,Peter Sandy,Sebastian Hoersch,Qing Sheng,Piyush Gupta,Jesse S. Boehm,Jan H. Reiling,Serena J. Silver,Yiling Lu,Katherine Stemke-Hale,Bhaskar Dutta,Corwin Joy,Aysegul A. Sahin,Ana M. Gonzalez-Angulo,Ana Lluch,Lucia E. Rameh,Tyler Jacks,David E. Root,Eric S. Lander,Gordon B. Mills,William C. Hahn,William R. Sellers,William R. Sellers,Levi A. Garraway +37 more
TL;DR: It is shown through phosphoprotein profiling and functional genomic studies that many PIK3CA mutant cancer cell lines and human breast tumors exhibit only minimal AKT activation and a diminished reliance on AKT for anchorage-independent growth.