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Sam M. Greenwood
Researcher at University of Edinburgh
Publications - 2
Citations - 1146
Sam M. Greenwood is an academic researcher from University of Edinburgh. The author has contributed to research in topics: RNA editing & RNA silencing. The author has an hindex of 2, co-authored 2 publications receiving 890 citations.
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Journal ArticleDOI
Mutations in ADAR1 cause Aicardi-Goutières syndrome associated with a type I interferon signature
Gillian I. Rice,Paul R. Kasher,Gabriella Forte,Niamh M. Mannion,Sam M. Greenwood,Marcin Szynkiewicz,Jonathan E. Dickerson,Sanjeev S. Bhaskar,Massimiliano Zampini,Tracy A Briggs,Emma M. Jenkinson,Carlos A. Bacino,Roberta Battini,Enrico Bertini,Paul A. Brogan,Louise Brueton,Marialuisa Carpanelli,Corinne De Laet,Pascale de Lonlay,Mireia Del Toro,Isabelle Desguerre,Elisa Fazzi,Angels García-Cazorla,Arvid Heiberg,Masakazu Kawaguchi,Ram L. Kumar,Jean-Pierre Lin,Charles Marques Lourenço,Alison Male,Wilson Marques,Cyril Mignot,Ivana Olivieri,Simona Orcesi,Prab Prabhakar,Magnhild Rasmussen,Robert Robinson,Flore Rozenberg,Johanna L. Schmidt,Katharina Steindl,Tiong Yang Tan,William G. Van Der Merwe,Adeline Vanderver,Grace Vassallo,Emma Wakeling,Evangeline Wassmer,Elizabeth Whittaker,John H. Livingston,Pierre Lebon,Tamio Suzuki,Paul J. McLaughlin,Liam Keegan,Mary A O'Connell,Simon C. Lovell,Yanick J. Crow +53 more
TL;DR: It is shown that mutations in ADAR1 cause the autoimmune disorder Aicardi-Goutières syndrome (AGS), and it is speculated that ADar1 may limit the cytoplasmic accumulation of the dsRNA generated from genomic repetitive elements.
Journal ArticleDOI
The RNA-Editing Enzyme ADAR1 Controls Innate Immune Responses to RNA
Niamh M. Mannion,Sam M. Greenwood,Robert Young,Sarah L. Cox,James Brindle,David Read,Christoffer Nellåker,Cornelia Vesely,Chris P. Ponting,Paul J. McLaughlin,Michael F. Jantsch,Julia R. Dorin,Ian R. Adams,A. D. J. Scadden,Marie Öhman,Liam Keegan,Mary A O'Connell,Mary A O'Connell +17 more
TL;DR: In this article, inosine in cellular RNA inhibits antiviral inflammatory and interferon responses by altering RLR interactions and restoring the expression of editing-active cytoplasmic ADARs.