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Chi C. Wong
Researcher at Wellcome Trust Sanger Institute
Publications - 6
Citations - 621
Chi C. Wong is an academic researcher from Wellcome Trust Sanger Institute. The author has contributed to research in topics: EIF6 & SBDS. The author has an hindex of 3, co-authored 5 publications receiving 561 citations. Previous affiliations of Chi C. Wong include Laboratory of Molecular Biology & University of Cambridge.
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Journal ArticleDOI
The Shwachman-Bodian-Diamond syndrome protein mediates translational activation of ribosomes in yeast.
Tobias F. Menne,Beatriz Goyenechea,Beatriz Goyenechea,Nuria Sánchez-Puig,Nuria Sánchez-Puig,Chi C. Wong,Chi C. Wong,Louise M. Tonkin,Louise M. Tonkin,Philip J Ancliff,Renee L. Brost,Michael Costanzo,Charles Boone,Alan J. Warren,Alan J. Warren +14 more
TL;DR: The function of the yeast SBDS ortholog Sdo1 is identified, showing that it is critical for the release and recycling of the nucleolar shuttling factor Tif6 from pre-60S ribosome, a key step in 60S maturation and translational activation of ribosomes.
Journal ArticleDOI
Mechanism of eIF6 release from the nascent 60S ribosomal subunit
Felix Weis,Emmanuel Giudice,Mark J. Churcher,Li Jin,Christine Hilcenko,Christine Hilcenko,Chi C. Wong,David Traynor,Robert R. Kay,Alan J. Warren,Alan J. Warren +10 more
TL;DR: Cryo-EM structures of human SBDS and SBDS–EFL1 bound to Dictyostelium discoideum 60S ribosomal subunits with and without endogenous eIF 6 reveal the conserved mechanism of eIF6 release, which is corrupted in both inherited and sporadic leukemias.
Journal ArticleDOI
Defective ribosome assembly in Shwachman-Diamond syndrome
Chi C. Wong,David Traynor,Nicolas Basse,Nicolas Basse,Robert R. Kay,Alan J. Warren,Alan J. Warren +6 more
TL;DR: Findings in Dictyostelium and SDS patient cells provide compelling support for the hypothesis that SDS is a ribosomopathy caused by corruption of an essential cytoplasmic step in 60S subunit maturation.
Posted ContentDOI
A screen for combination therapies inBRAF/NRASwild type melanoma identifies nilotinib plus MEK inhibitor as a synergistic combination
Marco Ranzani,Kristel Kemper,Magali Michaut,Oscar Krijgsman,Nanne Aben,Iyer,Kim Wong,Theodoros I. Roumeliotis,Velasco-Herrera Mdc,Jérémie Nsengimana,Gemma Turner,Nicola A. Thompson,Aida Shahrabi,Marcela Sjoberg,Mamunur Rashid,Anneliese O. Speak,Grinkevich,Fiona M. Behan,David Tamborero,Francesco Iorio,van Dongen S,Graham R. Bignell,Clara Alsinet,Sofia Y. Chen,Emmanuelle Supper,Ken Dutton-Regester,Antonia L. Pritchard,Chi C. Wong,Anton J. Enright,Julia Newton-Bishop,Ultan McDermott,Nicholas K. Hayward,Jyoti S. Choudhary,Kosuke Yusa,L. Wessels,Mathew J. Garnett,Daniel S. Peeper,David J. Adams +37 more
TL;DR: The results indicate that a nilotinib/MEK inhibitor combination may represent an effective therapy in BRAF/NRAS wild type melanoma patients.
Journal ArticleDOI
Population-based analysis of POT1 variants in a cutaneous melanoma case–control cohort
Irving Simonin-Wilmer,Raul Ossio,Emmett M Leddin,Mark Harland,Karen A. Pooley,Mauricio Gerardo Martil de la Garza,Sofia Obolenski,James Hewinson,Chi C. Wong,Vivek Iyer,John Taylor,Julia Newton-Bishop,D. Timothy Bishop,G. Andrés Cisneros,Mark M. Iles,David J. Adams,Carla Daniela Robles-Espinoza +16 more
TL;DR: POT1 variants are a minor contributor to melanoma burden in the general population, but should be screened in individuals with a strong family history of melanoma and/or multiple malignancies, and the role of variants in the regulation of telomere length and complex formation is defined through molecular dynamics simulations.