P
Peter W. Lewis
Researcher at University of Wisconsin-Madison
Publications - 54
Citations - 8010
Peter W. Lewis is an academic researcher from University of Wisconsin-Madison. The author has contributed to research in topics: Histone H3 & Histone. The author has an hindex of 30, co-authored 49 publications receiving 6652 citations. Previous affiliations of Peter W. Lewis include Rockefeller University & University of Southern California.
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Journal ArticleDOI
Distinct Factors Control Histone Variant H3.3 Localization at Specific Genomic Regions
Aaron D Goldberg,Laura A. Banaszynski,Kyung-Min Noh,Peter W. Lewis,Simon J. Elsaesser,Sonja C. Stadler,Scott Dewell,Martin J. Law,Xingyi Guo,Xuan Li,Duancheng Wen,Duancheng Wen,Ariane Chapgier,Russell Dekelver,Jeffrey C. Miller,Ya Li Lee,Elizabeth A. Boydston,Michael C. Holmes,Philip D. Gregory,John M. Greally,Shahin Rafii,Shahin Rafii,Chingwen Yang,Peter J. Scambler,David Garrick,Richard J. Gibbons,Douglas R. Higgs,Ileana M. Cristea,Fyodor D. Urnov,Deyou Zheng,C. David Allis +30 more
TL;DR: It is demonstrated that multiple and distinct factors are responsible for H3.3 localization at specific genomic locations in mammalian cells.
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Inhibition of PRC2 Activity by a Gain-of-Function H3 Mutation Found in Pediatric Glioblastoma
Peter W. Lewis,Manuel M. Müller,Matthew S. Koletsky,Francisco Cordero,Shu Lin,Laura A. Banaszynski,Benjamin A. Garcia,Tom W. Muir,Oren J. Becher,C. David Allis +9 more
TL;DR: It is proposed that K-to-M substitutions may represent a mechanism to alter epigenetic states in a variety of pathologies and be sufficient to cause specific reduction in methylation through inhibition of SET-domain enzymes.
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Daxx is an H3.3-specific histone chaperone and cooperates with ATRX in replication-independent chromatin assembly at telomeres
TL;DR: It is found that the ATRX–Daxx complex is bound to telomeric chromatin, and that both components of this complex are required for H3.3 deposition at telomeres in murine embryonic stem cells (ESCs).
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Isolation of the Cdc45/Mcm2–7/GINS (CMG) complex, a candidate for the eukaryotic DNA replication fork helicase
TL;DR: RNA interference knock-down experiments targeting the GINS and Cdc45 components establish that the proteins are required for the S phase transition in Drosophila cells, and suggest that this complex forms the core helicase machinery for eukaryotic DNA replication.
Journal ArticleDOI
Genomic analysis of diffuse intrinsic pontine gliomas identifies three molecular subgroups and recurrent activating ACVR1 mutations
Pawel Buczkowicz,Christine M. Hoeman,Patricia Rakopoulos,Sanja Pajovic,Louis Letourneau,Misko Dzamba,Andrew Morrison,Peter W. Lewis,Eric Bouffet,Ute Bartels,Jennifer Zuccaro,Sameer Agnihotri,Scott Ryall,Mark Barszczyk,Yevgen Chornenkyy,Mathieu Bourgey,Guillaume Bourque,Alexandre Montpetit,Francisco Cordero,Pedro Castelo-Branco,Joshua Mangerel,Uri Tabori,King Ching Ho,Annie Huang,Kathryn R. Taylor,Alan Mackay,Anne Bendel,Javad Nazarian,Jason Fangusaro,Matthias A. Karajannis,David Zagzag,Nicholas K. Foreman,Andrew M. Donson,Julia V Hegert,Amy Smith,Jennifer A. Chan,Lucy Lafay-Cousin,Sandra E. Dunn,Juliette Hukin,Chris Dunham,Katrin Scheinemann,Jean Michaud,Shayna Zelcer,David A. Ramsay,Jason E. Cain,Cameron Brennan,Mark M. Souweidane,Chris Jones,C. David Allis,Michael Brudno,Michael Brudno,Oren J. Becher,Cynthia Hawkins +52 more
TL;DR: This work integrated whole-genome sequencing with methylation, expression and copy number profiling, discovering that DIPGs comprise three molecularly distinct subgroups (H3-K27M, silent and MYCN) and uncovering a new recurrent activating mutation affecting the activin receptor gene ACVR1 in 20% of DIPG.