G
Guy A. Rouleau
Researcher at Montreal Neurological Institute and Hospital
Publications - 935
Citations - 75050
Guy A. Rouleau is an academic researcher from Montreal Neurological Institute and Hospital. The author has contributed to research in topics: Gene & Genome-wide association study. The author has an hindex of 129, co-authored 884 publications receiving 65892 citations. Previous affiliations of Guy A. Rouleau include Utrecht University & University of Helsinki.
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Journal ArticleDOI
TAR DNA-Binding Protein 43 (TDP-43) Regulates Stress Granule Dynamics via Differential Regulation of G3BP and TIA-1
Karli K. McDonald,Anaïs Aulas,Laurie Destroismaisons,Sarah Pickles,Evghenia Beleac,William Camu,Guy A. Rouleau,Christine Vande Velde +7 more
TL;DR: The results demonstrate that TDP-43 and hnRNP A2 are localized to stress granules (SGs), following oxidative stress, heat shock and exposure to thapsigargin, and the cellular function of T DP-43 extends beyond splicing and places it as a participant of the central cellular response to stress and an active player in RNA storage.
Journal ArticleDOI
Mutations in a Gene Encoding a Novel Protein Containing a Phosphotyrosine-Binding Domain Cause Type 2 Cerebral Cavernous Malformations
Christina L. Liquori,Michel J. Berg,Adrian M. Siegel,Elizabeth Huang,Jon S. Zawistowski,T’Prien Stoffer,Dominique J. Verlaan,Fiyinfolu Balogun,Lori Hughes,Tracey P. Leedom,Nicholas W. Plummer,Milena Cannella,Vittorio Maglione,Ferdinando Squitieri,Eric W. Johnson,Guy A. Rouleau,Louis J. Ptáček,Douglas A. Marchuk +17 more
TL;DR: A novel gene, MGC4607, exhibits eight different mutations in nine families with type 2 CCM (CCM2), similar to the KRIT1 binding partner ICAP1alpha, and may be part of the complex pathway of integrin signaling that causes abnormal vascular morphogenesis in the brain, leading to CCM formation.
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Genome-wide association study reveals two new risk loci for bipolar disorder
Thomas W. Mühleisen,Thomas W. Mühleisen,Markus Leber,Markus Leber,Thomas G. Schulze,Jana Strohmaier,Franziska Degenhardt,Jens Treutlein,Manuel Mattheisen,Manuel Mattheisen,Andreas J. Forstner,Johannes Schumacher,René Breuer,Sandra Meier,Stefan Herms,Stefan Herms,Per Hoffmann,André Lacour,Stephanie H. Witt,Andreas Reif,Bertram Müller-Myhsok,Bertram Müller-Myhsok,Susanne Lucae,Wolfgang Maier,M.P. Schwarz,Helmut Vedder,Jutta Kammerer-Ciernioch,Andrea Pfennig,Michael Bauer,Martin Hautzinger,Susanne Moebus,Lutz Priebe,Piotr M. Czerski,Joanna Hauser,Jolanta Lissowska,Neonila Szeszenia-Dabrowska,Paul Brennan,James McKay,Adam Wright,Adam Wright,Philip B. Mitchell,Philip B. Mitchell,Janice M. Fullerton,Janice M. Fullerton,Peter R. Schofield,Peter R. Schofield,Grant W. Montgomery,Sarah E. Medland,Scott D. Gordon,Nicholas G. Martin,Valery Krasnow,Alexander Chuchalin,Gulja Babadjanova,Galina Pantelejeva,Lilia I. Abramova,Alexander S. Tiganov,Alexey Polonikov,Elza Khusnutdinova,Martin Alda,Paul Grof,Guy A. Rouleau,Gustavo Turecki,Catherine Laprise,Fabio Rivas,Fermín Mayoral,Manolis Kogevinas,Maria Grigoroiu-Serbanescu,Peter Propping,Tim Becker,Tim Becker,Marcella Rietschel,Markus M. Nöthen,Sven Cichon +72 more
TL;DR: Results from the largest BD GWAS to date are presented by investigating 2.3 million single-nucleotide polymorphisms (SNPs) in a sample of 24,025 patients and controls and detecting 56 genome-wide significant SNPs in five chromosomal regions including previously reported risk loci ANK3, ODZ4 and TRANK1.
Journal ArticleDOI
Excess of De Novo Deleterious Mutations in Genes Associated with Glutamatergic Systems in Nonsyndromic Intellectual Disability
Fadi F. Hamdan,Julie Gauthier,Yoichi Araki,Da Ting Lin,Yuhki Yoshizawa,Kyohei Higashi,A-Reum Park,Dan Spiegelman,Sylvia Dobrzeniecka,Amélie Piton,Hideyuki Tomitori,Hussein Daoud,Christine Massicotte,Edouard Henrion,Ousmane Diallo,Masoud Shekarabi,Claude Marineau,Michael Shevell,Bruno Maranda,Grant A. Mitchell,Amélie Nadeau,Guy D'Anjou,Michel Vanasse,Myriam Srour,Ronald G. Lafrenière,Pierre Drapeau,Jean-Claude Lacaille,Eunjoon Kim,Jae-Ran Lee,Kazuei Igarashi,Richard L. Huganir,Guy A. Rouleau,Jacques L. Michaud +32 more
TL;DR: In this article, de novo mutations (DNMs) in synaptic genes explain an important fraction of sporadic nonsyndromic intellectual disability (NSID) cases, finding 11 DNMs, including ten potentially deleterious mutations (three nonsense, two splicing, one frameshift, four missense) and one neutral mutation (silent).
Journal ArticleDOI
Genetics of motor neuron disorders: new insights into pathogenic mechanisms
TL;DR: The functional classes of MND genes identified so far are likely to aid the selection of high-priority candidate genes for future investigation, including those for so-called sporadic cases.