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by Tsoi, Lam C and Spain, Sarah L and Knight, Jo and Ellinghaus, Eva and Stuart, Philip E and Capon, Francesca and Ding, Jun and Li, Yanming and Tejasvi, Trilokraj and Gudjonsson, Johann E and Kang, Hyun M and Allen, Michael H and McManus, Ross and Novelli, Giuseppe and Samuelsson, Lena and Schalkwijk, Joost and Ståhle, Mona and Burden, A David and Smith, Catherine H and Cork, Michael J and Estivill, Xavier and Bowcock, Anne M and Krueger, Gerald G and Weger, Wolfgang and Worthington, Jane and Tazi-Ahnini, Rachid and Nestle, Frank O and Hayday, Adrian and Hoffmann, Per and Winkelmann, Juliane and Wijmenga, Cisca and Langford, Cordelia and Edkins, Sarah and Andrews, Robert and Blackburn, Hannah and Strange, Amy and Band, Gavin and Pearson, Richard D and Vukcevic, Damjan and Spencer, Chris C A and Deloukas, Panos and Mrowietz, Ulrich and Schreiber, Stefan and Weidinger, Stephan and Koks, Sulev and Kingo, Külli and Esko, Tonu and Metspalu, Andres and Lim, Henry W and Voorhees, John J and Weichenthal, Michael and Wichmann, H Erich and Chandran, Vinod and Rosen, Cheryl F and Rahman, Proton and Gladman, Dafna D and Griffiths, Christopher E M and Reis, Andre and Kere, Juha and Nair, Rajan P and Franke, Andre and Barker, Jonathan N W N and Abecasis, Goncalo R and Elder, James T and Trembath, Richard C and Psoriasis Association Genetics Extension and Genetic Analysis of Psoriasis Consortium and Collaborative Association Study of Psoriasis (CASP) and Wellcome Trust Case Control Consortium 2 and Collaborative Assoc Study Psoriasi and Psoriasis Assoc Genetics Extension and Genetic Anal Psoriasis Consortium and Wellcome Trust Case Control Consor and Sahlgrenska akademin and Institutionen för biomedicin, avdelningen för medicinsk genetik och klinisk genetik and Göteborgs universitet and Gothenburg University and Institute of Biomedicine, Department of Medical and Clinical Genetics and Sahlgrenska Academy
Nature genetics, ISSN 1546-1718, 2012, Volume 44, Issue 12, pp. 1341 - 1348
To gain further insight into the genetic architecture of psoriasis, we conducted a meta-analysis of 3 genome-wide association studies (GWAS) and 2 independent... 
COMMON VARIANTS | SIGNALING PATHWAYS | MULTIPLE COMMON | INTERFERON-GAMMA | TH17 DIFFERENTIATION | GENETICS & HEREDITY | GENE-EXPRESSION | T-CELL DEVELOPMENT | GENOME-WIDE ASSOCIATION | CELIAC-DISEASE | NEGATIVE REGULATOR | Oligonucleotide Array Sequence Analysis | Humans | Immunity, Innate - genetics | Genetic Loci | CARD Signaling Adaptor Proteins - genetics | Psoriasis - genetics | Core Binding Factor Alpha 3 Subunit - immunology | STAT3 Transcription Factor - genetics | Skin - immunology | Psoriasis - immunology | CARD Signaling Adaptor Proteins - immunology | DEAD Box Protein 58 | European Continental Ancestry Group - genetics | Genetic Predisposition to Disease | Genome-Wide Association Study | Guanylate Cyclase - immunology | Membrane Proteins - genetics | Membrane Proteins - immunology | GTPase-Activating Proteins - immunology | DEAD-box RNA Helicases - genetics | Core Binding Factor Alpha 3 Subunit - genetics | DEAD-box RNA Helicases - immunology | Guanylate Cyclase - genetics | T-Lymphocytes - immunology | Polymorphism, Single Nucleotide | GTPase-Activating Proteins - genetics | STAT3 Transcription Factor - immunology | Psoriasis | Physiological aspects | Disease susceptibility | Genetic aspects | Research | Autoimmune diseases | Gene expression | Chromosomes | Risk factors | genetic analysis | innate immunity | Dermatologi och venereologi | Dermatology and Venereal Diseases | psoriasis
Journal Article
Plant Physiology, ISSN 0032-0889, 9/2013, Volume 163, Issue 1, pp. 135 - 149
A previously uncharacterized lipid-binding protein is modified by the ubiquitin-like protein NEDD8 and by ubiquitin . NEDD8 (NEURAL PRECURSOR CELL-EXPRESSED,... 
Cell Biology
Journal Article
Journal of molecular and cellular cardiology, ISSN 0022-2828, 2018, Volume 123, pp. 59 - 63
.... Most patients are heterozygous and allelic expression differs between cells. We hypothesized that this would lead to cell-to-cell variation in cardiac myosin binding protein-C... 
hypertrophic cardiomyopathy | α-actin | variable expression | cardiac myosin binding protein-C | MYBPC3 mutation | PHENOTYPE DEVELOPMENT | CARDIAC & CARDIOVASCULAR SYSTEMS | TRIGGER | TISSUE | PATTERNS | HAPLOINSUFFICIENCY | CELL BIOLOGY | HEART | alpha-actin | DISEASE | GENE-EXPRESSION | MICE | Cardiomyopathy, Hypertrophic | Actin | Analysis | Myosin | Genetic research | Genetic aspects | Muscle proteins | Cardiology | Protein binding
Journal Article
Journal Article
Journal Article
The Journal of physiology, ISSN 0022-3751, 07/2017, Volume 595, Issue 14, pp. 4677 - 4693
Journal Article