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by McRae, Jeremy F and Clayton, Stephen and Fitzgerald, Tomas W and Kaplanis, Joanna and Prigmore, Elena and Rajan, Diana and Sifrim, Alejandro and Aitken, Stuart and Akawi, Nadia and Alvi, Mohsan and Ambridge, Kirsty and Barrett, Daniel M and Bayzetinova, Tanya and Jones, Philip and Jones, Wendy D and King, Daniel and Krishnappa, Netravathi and Mason, Laura E and Singh, Tarjinder and Tivey, Adrian R and Ahmed, Munaza and Anjum, Uruj and Archer, Hayley and Armstrong, Ruth and Awada, Jana and Balasubramanian, Meena and Banka, Siddharth and Baralle, Diana and Barnicoat, Angela and Batstone, Paul and Baty, David and Bennett, Chris and Berg, Jonathan and Bernhard, Birgitta and Bevan, A. Paul and Bitner-Glindzicz, Maria and Blair, Edward and Blyth, Moira and Bohanna, David and Bourdon, Louise and Bourn, David and Bradley, Lisa and Brady, Angela and Brent, Simon and Brewer, Carole and Brunstrom, Kate and Bunyan, David J and Burn, John and Canham, Natalie and Castle, Bruce and Chandler, Kate and Chatzimichali, Elena and Cilliers, Deirdre and Clarke, Angus and Clasper, Susan and Clayton-Smith, Jill and Clowes, Virginia and Coates, Andrea and Cole, Trevor and Colgiu, Irina and Collins, Amanda and Collinson, Morag N and Connell, Fiona and Cooper, Nicola and Cox, Helen and Cresswell, Lara and Cross, Gareth and Crow, Yanick and D'Alessandro, Mariella and Dabir, Tabib and Davidson, Rosemarie and Davies, Sally and De Vries, Dylan and Dean, John and Deshpande, Charu and Devlin, Gemma and Dixit, Abhijit and Dobbie, Angus and Donaldson, Alan and Donnai, Dian and Donnelly, Deirdre and Donnelly, Carina and Douglas, Angela and Douzgou, Sofia and Duncan, Alexis and Eason, Jacqueline and Ellard, Sian and Ellis, Ian and Elmslie, Frances and Evans, Karenza and Everest, Sarah and Fendick, Tina and Fisher, Richard and Flinter, Frances and Foulds, Nicola and Fry, Andrew and Fryer, Alan and Gardiner, Carol and Gaunt, Lorraine and Ghali, Neeti and ... and Deciphering Developmental Disorders Study
Nature (London), ISSN 1476-4687, 2017, Volume 542, Issue 7642, pp. 433 - 438
The genomes of individuals with severe, undiagnosed developmental disorders are enriched in damaging de novo mutations (DNMs) in developmentally important... 
INTELLECTUAL DISABILITY | METAANALYSIS | VARIANTS | GENETICS | HEART-DEFECTS | MULTIDISCIPLINARY SCIENCES | GENES | SEQUENCE | FRAMEWORK | DISCOVERY | GENOME | Prevalence | Humans | Middle Aged | Parents | Male | Mi-2 Nucleosome Remodeling and Deacetylase Complex - genetics | Developmental Disabilities - genetics | Casein Kinase II - genetics | Autoantigens - genetics | Young Adult | ras GTPase-Activating Proteins - genetics | Adult | Female | Child | CDC2 Protein Kinase - genetics | Histone-Lysine N-Methyltransferase - genetics | Repressor Proteins - genetics | Sex Characteristics | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Mutation - genetics | Nerve Tissue Proteins - genetics | Sequence Analysis, DNA | Homeodomain Proteins - genetics | DEAD-box RNA Helicases - genetics | Exome - genetics | Phenotype | Myeloid-Lymphoid Leukemia Protein - genetics | Adolescent | Heredity - genetics | Protein Phosphatase 2C - genetics | Cohort Studies | Child development deviations | Genetic aspects | Genetic disorders | Developmental disabilities | Distribution | Genes | Families & family life | Births | Genomes | Mutation | Causality | Estimates | Age | TRIO | MYT1L | EHMT1 | HNRNPU | SUV420H1 | COL4A3BP | SYNGAP1 | PPP2R1A | POGZ | EP300 | KCNH1 | SCN1A | MEF2C | CDKL5 | CSNK2A1 | DYRK1A | CASK | ALG13 | FOXP1 | KAT6B | TBL1XR1 | KAT6A | SCN8A | KCNQ2 | EEF1A2 | KCNQ3 | ADNP | PhenIcons | SET | KMT2A | ANKRD11 | STXBP1 | FOXG1 | ZC4H2 | ITPR1 | De novo mutation | Seizures | ZBTB18 | CREBBP | SMAD4 | PDHA1 | IQSEC2 | AUTS2 | BCL11A | BRAF | SMARCA2 | GRIN2B | MED13L | GNAO1 | CNOT3 | TCF4 | SCN2A | CDK13 | GABRB3 | SETD5 | KDM5B | Developmental Disease | DDX3X | CHD8 | PTEN | CHD4 | TCF20 | CTCF | CHD2 | WDR45 | SLC6A1 | MECP2 | CHAMP1 | KIF1A | Average Faces | MSL3 | PPP2R5D | SMC1A | ARID1B | DNM1 | CNKSR2 | PACS1 | WAC | ZMYND11 | AHDC1 | NFIX | SATB2 | HDAC8 | PPM1D | GNAI1 | PURA | PUF60 | NSD1 | Intellectual Disability | SLC35A2 | DYNC1H1 | NAA10 | USP9X | PTPN11 | GATAD2B | ASXL1 | KANSL1 | ASXL3 | CTNNB1 | QRICH1
Journal Article
Nature genetics, ISSN 1546-1718, 2012, Volume 44, Issue 12, pp. 1310 - 1315
Journal Article
The Journal of Clinical Endocrinology & Metabolism, ISSN 1945-7197, 2017, Volume 102, Issue 8, pp. 3029 - 3039
Context: Only a few genetic causes for childhood obesity have been identified to date... 
ENDOCRINOLOGY & METABOLISM | FAT | LOCI | MUTATIONS | REARRANGEMENTS | ASSOCIATION | DELETIONS | TYPE-2 | CONTRIBUTES | INSIGHTS | Hydrolases - genetics | Humans | DNA Repair Enzymes - genetics | Transcriptome | Child, Preschool | Male | Chromosome Duplication - genetics | RNA, Messenger - metabolism | Autoantigens - genetics | Case-Control Studies | DNA Copy Number Variations | Intellectual Disability - genetics | Young Adult | Chromosomes, Human, Pair 22 - genetics | Subcutaneous Fat - metabolism | Cell Cycle Proteins - genetics | Adult | Female | Chromosomes, Human, Pair 1 - genetics | Nuclear Proteins - genetics | Child | Microfilament Proteins - genetics | Abnormalities, Multiple - genetics | DiGeorge Syndrome - genetics | Chromosomes, Human, Pair 16 - genetics | Siblings | Autistic Disorder - genetics | Chromosome Deletion | Megalencephaly - genetics | Extracellular Matrix Proteins - genetics | Pediatric Obesity - genetics | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Proteins - genetics | Comparative Genomic Hybridization | Adolescent | Ataxia Telangiectasia Mutated Proteins - genetics | Kruppel-Like Transcription Factors - genetics | Acid Phosphatase - genetics | Chromosome Disorders - genetics | Obesity | Adipose tissue | Prader-Willi syndrome | Copy number | Genes | mRNA | Hybridization | Gene expression | Ribonucleic acid--RNA | Body mass index | DNA microarrays | Pathways | Clonal deletion | Body mass | Body size | Children | Age | deletions | insights | bardet-biedl-syndrome | association | Klinisk medicin | contributes | population | type-2 | Clinical Medicine | mutations | rearrangements | Endocrinology & Metabolism | loci
Journal Article
The American Journal of Human Genetics, ISSN 0002-9297, 04/2012, Volume 90, Issue 4, pp. 648 - 660
Systemic lupus erythematosus (SLE) is a chronic heterogeneous autoimmune disorder characterized by the loss of tolerance to self-antigens and dysregulated... 
RHEUMATOID-ARTHRITIS | GENETIC SUSCEPTIBILITY | IMMUNE-RESPONSE | RISK LOCI | CROHNS-DISEASE | VARIANTS | PRIMARY BILIARY-CIRRHOSIS | GENETICS & HEREDITY | FOLLOW-UP | FAMILIAL AGGREGATION | GENOME-WIDE ASSOCIATION | European Continental Ancestry Group - genetics | Genetic Predisposition to Disease | Hispanic Americans - genetics | Membrane Proteins - genetics | Humans | Asian Continental Ancestry Group - genetics | Interferon Regulatory Factors - genetics | Male | Chromosome Mapping | Sequence Analysis, DNA | Ikaros Transcription Factor - genetics | Haplotypes - genetics | Lupus Erythematosus, Systemic - ethnology | Lupus Erythematosus, Systemic - genetics | Indians, North American - genetics | Polymorphism, Single Nucleotide - genetics | Female | African Continental Ancestry Group - genetics | Egg Proteins - genetics | Europeans | Lupus erythematosus | Genetic aspects | Research | Genetic transcription | Gene expression | Genetic regulation | Risk factors | Diseases | Lupus | Disease susceptibility | Systemic lupus erythematosus | Racially mixed people | Analysis | Haplotypes | Ikaros protein | Autoantigens | Environmental factors | Immunological tolerance | Zona pellucida | Membrane proteins | Etiology | Interleukin 1 | Replication | Zinc finger proteins | Autoimmune diseases | Gene mapping | Interferon regulatory factor
Journal Article
PLoS genetics, ISSN 1553-7390, 09/2012, Volume 8, Issue 9, p. e1002932
Journal Article
PloS one, ISSN 1932-6203, 2017, Volume 12, Issue 1, p. e0169648
The structural maintenance of chromosome 5/6 complex (Smc5/6) is a restriction factor that represses hepatitis B virus (HBV) transcription. HBV counters this... 
CELLS | NUCLEAR-BODIES | HEPATITIS-B-VIRUS | REPLICATION | DNA | MULTIDISCIPLINARY SCIENCES | GENE-EXPRESSION | EPIGENETIC REGULATION | COMPONENTS | BINDING | HUMANIZED MICE | Autoantigens - metabolism | Hepatitis B - metabolism | Antigens, Nuclear - metabolism | Humans | Hepatitis B - virology | Male | Hepatocytes - metabolism | Autoantigens - genetics | Hepatitis B - immunology | Hepatocytes - cytology | Trans-Activators - genetics | Cell Cycle Proteins - genetics | Promyelocytic Leukemia Protein - metabolism | Nuclear Proteins - genetics | Cytokines - genetics | Hepatitis B virus - immunology | Promyelocytic Leukemia Protein - genetics | Cytokines - metabolism | Cell Cycle Proteins - metabolism | Cells, Cultured | Chromosomal Proteins, Non-Histone | Nuclear Proteins - metabolism | Mice, SCID | Immunity, Innate - immunology | Animals | Antigens, Nuclear - genetics | Virus Replication | Trans-Activators - metabolism | Mice | Immune response | Analysis | Genetic aspects | Hepatitis B virus | Research | Genetic transcription | Hepatitis B | Cell culture | HBX protein | Pathogenesis | Viruses | Infections | Genomes | Degradation | Proteins | Hepatitis | Hepatology | Localization | Bioinformatics | Chromosomes | Deoxyribonucleic acid--DNA | Immune system | Antigens | Cytokines | Chromosome 5 | Gene expression | Ribonucleic acid--RNA | Hepatocytes | Interferon | Kinetics | X protein | RNA | Deoxyribonucleic acid | Ribonucleic acid
Journal Article
American journal of human genetics, ISSN 0002-9297, 10/2016, Volume 99, Issue 4, pp. 934 - 941
Journal Article