G
Gijs van Haaften
Researcher at Utrecht University
Publications - 87
Citations - 4699
Gijs van Haaften is an academic researcher from Utrecht University. The author has contributed to research in topics: Gene & Mutation. The author has an hindex of 32, co-authored 78 publications receiving 3823 citations. Previous affiliations of Gijs van Haaften include University Medical Center Utrecht & Netherlands Cancer Institute.
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Journal ArticleDOI
Somatic mutations of the histone H3K27 demethylase gene UTX in human cancer
Gijs van Haaften,Gillian L. Dalgliesh,Helen Davies,Lina Chen,Graham R. Bignell,Christopher Greenman,Sarah Edkins,Claire Hardy,Sarah O’Meara,Jon W. Teague,Adam Butler,Jonathan Hinton,Calli Latimer,Jenny Andrews,Syd Barthorpe,Dave Beare,Gemma Buck,Peter J. Campbell,Jennifer Cole,Simon A. Forbes,Mingming Jia,David T. Jones,Chai Yin Kok,Catherine Leroy,Meng-Lay Lin,David J. McBride,Mark Maddison,Simon Maquire,Kirsten McLay,Andrew Menzies,Tatiana Mironenko,Lee Mulderrig,Laura Mudie,Erin Pleasance,Rebecca Shepherd,Raffaella Smith,Lucy Stebbings,Philip J. Stephens,Gurpreet Tang,Patrick S. Tarpey,Rachel Turner,Kelly Turrell,Jennifer Varian,Sofie West,Sara Widaa,Paul Wray,V. Peter Collins,Koichi Ichimura,Simon Law,John Wong,Siu Tsan Yuen,Suet Yi Leung,Giovanni Tonon,Giovanni Tonon,Ronald A. DePinho,Yu-Tzu Tai,Kenneth C. Anderson,Richard J. Kahnoski,Aaron Massie,Sok Kean Khoo,Bin Tean Teh,Michael R. Stratton,Michael R. Stratton,P. Andrew Futreal +63 more
TL;DR: UTX reintroduction into cancer cells with inactivating UTX mutations resulted in slowing of proliferation and marked transcriptional changes, identifying UTX as a new human cancer gene.
Journal ArticleDOI
Genome-wide RNA interference screen identifies previously undescribed regulators of polyglutamine aggregation
Ellen A. A. Nollen,Susana M. D. A. Garcia,Gijs van Haaften,Soojin Kim,Alejandro Chavez,Richard I. Morimoto,Ronald H.A. Plasterk +6 more
TL;DR: A screen identified 186 genes corresponding to five principal classes of polyglutamine regulators: genes involved in RNA metabolism, protein synthesis, protein folding, and protein degradation; and those involved in protein trafficking, proposing that each represents a molecular machine collectively comprising the protein homeostatic buffer that responds to the expression of damaged proteins to prevent their misfolding and aggregation.
Journal ArticleDOI
The poly(A)-binding protein nuclear 1 suppresses alternative cleavage and polyadenylation sites
Mathias Jenal,Ran Elkon,Fabricio Loayza-Puch,Gijs van Haaften,Uwe Kühn,Fiona M. Menzies,Joachim A.F. Oude Vrielink,Arnold J. Bos,Jarno Drost,Koos Rooijers,David C. Rubinsztein,Reuven Agami +11 more
TL;DR: A reporter-based RNAi screen for APA was developed and a novel function for PABPN1 was elucidated as a suppressor of APA, which causes autosomal-dominant oculopharyngeal muscular dystrophy and its sequestration in nuclear aggregates.
Journal ArticleDOI
Identification of genes that protect the C. elegans genome against mutations by genome-wide RNAi
Joris Pothof,Gijs van Haaften,Karen L. Thijssen,Ravi S. Kamath,Andrew G. Fraser,Julie Ahringer,Ronald H.A. Plasterk,Marcel Tijsterman +7 more
TL;DR: An RNA interference-based genome-wide screen was performed to detect genes that contribute to genome stability in somatic cells of Caenorhabditis elegans, and 61 genes were identified; these also affect spontaneous mutagenesis in the germ line.
Journal ArticleDOI
Dominant missense mutations in ABCC9 cause Cantú syndrome
Magdalena Harakalova,Jeske J.T. van Harssel,Paulien A Terhal,Stef van Lieshout,Karen Duran,Ivo Renkens,David J. Amor,David J. Amor,Louise C. Wilson,Edwin P. Kirk,Claire L. S. Turner,Debbie Shears,Sixto García-Miñaur,Melissa Lees,Alison Ross,Hanka Venselaar,Gert Vriend,Hiroki Takanari,Martin B. Rook,Marcel A.G. van der Heyden,Folkert W. Asselbergs,Hans M P J Breur,Marielle E M Swinkels,Ingrid Scurr,Sarah F. Smithson,Nine V A M Knoers,Jasper J. van der Smagt,Isaac J. Nijman,Wigard P. Kloosterman,Mieke M. van Haelst,Mieke M. van Haelst,Gijs van Haaften,Edwin Cuppen,Edwin Cuppen +33 more
TL;DR: Using electrophysiological measurements, it is shown that mutations in ABCC9 reduce the ATP-mediated potassium channel inhibition, resulting in channel opening, and similarities between the phenotype of individuals with Cantú syndrome and side effects from the KATP channel agonist minoxidil indicate that the mutations inABCC9 result in channelOpening.