Y
Yves Pommier
Researcher at National Institutes of Health
Publications - 847
Citations - 65543
Yves Pommier is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Topoisomerase & DNA. The author has an hindex of 123, co-authored 789 publications receiving 58898 citations. Previous affiliations of Yves Pommier include Purdue University & Kyushu University.
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Erratum: Interfacial inhibitors: targeting macromolecular complexes
Yves Pommier,Christophe Marchand +1 more
TL;DR: In Table 1, the information listed in the 'Substrates' column for 'Etoposide and teniposide' and 'Mitoxantrone' is incorrect; 'TOP1– DNA complex' should be 'TOP2–DNA complex' in both instances.
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Resistance to Integrase Inhibitors
TL;DR: This review focuses on IN resistance based on structural and biochemical data, and on the role of the IN flexible loop i.e., between residues G140-G149 in drug action and resistance.
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Nonclassic Functions of Human Topoisomerase I: Genome-Wide and Pharmacologic Analyses
Ze-Hong Miao,Audrey Player,Uma Shankavaram,Yong Hong Wang,Drazen B. Zimonjic,Philip L. Lorenzi,Zhi Yong Liao,Hong Liu,Tsutomu Shimura,Hongliang Zhang,Linghua Meng,Yong-Wei Zhang,Ernest S. Kawasaki,Nicholas C. Popescu,Mirit I. Aladjem,David J. Goldstein,John N. Weinstein,Yves Pommier +17 more
TL;DR: It is shown that Top1, in addition to being the target of camptothecins, also regulates DNA replication, rDNA stability, and apoptosis, and the pleiotropic nature of human Top1 activities is shown.
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Camptothecins and topoisomerase I: a foot in the door. Targeting the genome beyond topoisomerase I with camptothecins and novel anticancer drugs: importance of DNA replication, repair and cell cycle checkpoints.
TL;DR: Camptothecins selectively target topoisomerase I (Top1) by trapping the catalytic intermediate of the Top1-DNA reaction, the cleavage complex, and represent a paradigm for targeting macromolecular interactions.
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Targeting chk2 kinase: molecular interaction maps and therapeutic rationale.
TL;DR: Chk2 inhibitors might be used to enhance the tumor selectivity of DNA targeted agents in p53-deficient tumors, and for the treatment of tumors whose growth depends on enhanced Chk2 activity.