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Gut, ISSN 0017-5749, 01/2018, Volume 67, Issue 1, pp. 108 - 119
.... We composed genetic risk scores from 11 functional genetic variants proven to be associated with IBD... 
BACTERIA | CROHNS-DISEASE | VARIANTS | RARE | GENOTYPE | ULCERATIVE-COLITIS | RISK | LOCI | ASSOCIATION | BACTERIAL INTERACTIONS | INFLAMMATORY BOWEL DISEASE | GENETICS | INTESTINAL BACTERIA | CROHNS | GASTROENTEROLOGY & HEPATOLOGY | Severity of Illness Index | Crohn Disease - genetics | Risk Assessment - methods | Genetic Predisposition to Disease | Humans | Middle Aged | Colitis, Ulcerative - genetics | Male | Colitis, Ulcerative - pathology | Dysbiosis - complications | Dysbiosis - microbiology | Gastrointestinal Microbiome - genetics | Case-Control Studies | Feces - microbiology | Colitis, Ulcerative - microbiology | Dysbiosis - genetics | Host-Pathogen Interactions - genetics | Crohn Disease - pathology | Inflammatory Bowel Diseases - pathology | Inflammatory Bowel Diseases - genetics | Adult | Crohn Disease - microbiology | Female | Inflammatory Bowel Diseases - microbiology | Inflammatory bowel diseases | Care and treatment | Genetic aspects | Research | Microbiota (Symbiotic organisms) | Genetic variation | Phenotypes | Bacterial infections | Breastfeeding & lactation | rRNA 16S | Pathogenesis | Genomes | Inflammation | Crohn's disease | Family medical history | Crohns disease | Inflammatory bowel disease | Genetic variance | Microbiota | Antibiotics | Intestine | Gastroenterology | Peripheral blood | Genetics | Gene loci | Colon | Endoscopy | Acetic acid | NOD2 protein | Gut microbiota | Healthy controls | Host genetics
Journal Article
The New England journal of medicine, ISSN 1533-4406, 2008, Volume 359, Issue 26, pp. 2767 - 2777
Journal Article
Current Opinion in Pediatrics, ISSN 1040-8703, 12/2013, Volume 25, Issue 6, pp. 708 - 714
.... Recent progress includes the identification of gain-of-function mutations in STAT1 as a cause of an IPEX-like disease, emerging FOXP3genotype/phenotype relationships in IPEX, and the elucidation... 
ITCH | autoimmunity | STAT1 | T regulatory cells | STAT5 | CD25 | FOXP3 | tolerance | TGF-BETA | GROWTH-HORMONE INSENSITIVITY | STAT5B MUTATION | CHRONIC MUCOCUTANEOUS CANDIDIASIS | CUTTING EDGE | INTESTINAL INFLAMMATION | ALPHA-CHAIN | TRANSCRIPTION FACTOR FOXP3 | REGULATORY T-CELLS | PEDIATRICS | SCURFY MOUSE MUTANT | Forkhead Transcription Factors - immunology | Immunologic Deficiency Syndromes - pathology | Humans | STAT5 Transcription Factor - immunology | Autoimmunity - genetics | Diabetes Mellitus, Type 1 - congenital | Male | Intestinal Diseases - immunology | Diarrhea - pathology | T-Lymphocytes, Regulatory - immunology | STAT5 Transcription Factor - genetics | Ubiquitin-Protein Ligases - immunology | Interleukin-2 Receptor alpha Subunit - genetics | Autoimmunity - immunology | Diarrhea - immunology | Female | Genetic Diseases, X-Linked - genetics | Polyendocrinopathies, Autoimmune - genetics | Immunologic Deficiency Syndromes - immunology | Interleukin-2 Receptor alpha Subunit - immunology | Genetic Predisposition to Disease | Intestinal Diseases - genetics | Repressor Proteins - genetics | Polyendocrinopathies, Autoimmune - pathology | Forkhead Transcription Factors - genetics | Mutation - genetics | Polyendocrinopathies, Autoimmune - immunology | Genetic Diseases, X-Linked - immunology | Immune System Diseases - congenital | Autoantibodies - immunology | Diarrhea - genetics | Repressor Proteins - immunology | Genetic Diseases, X-Linked - pathology | Immunologic Deficiency Syndromes - genetics | Ubiquitin-Protein Ligases - genetics | Intestinal Diseases - pathology | Tolerance
Journal Article
Nature reviews. Molecular cell biology, ISSN 1471-0080, 2017, Volume 18, Issue 12, pp. 758 - 770
... (for example, inside of a tumour lump), is central to our understanding of physiology and disease pathogenesis... 
YES-ASSOCIATED PROTEIN | BREAST-CANCER | TRANSCRIPTION FACTORS | NUCLEAR-LOCALIZATION | F-ACTIN | BETA-CATENIN ACTIVATION | PULMONARY-HYPERTENSION | HIPPO SIGNALING PATHWAY | INTESTINAL REGENERATION | MESENCHYMAL STEM-CELLS | CELL BIOLOGY | Neoplasms - metabolism | Atherosclerosis - genetics | Humans | Extracellular Matrix - metabolism | Muscular Dystrophies - genetics | Phosphoproteins - metabolism | Extracellular Matrix - genetics | Neoplasms - genetics | Cell Shape | Transcription, Genetic | Atherosclerosis - pathology | Shear Strength | Muscular Dystrophies - metabolism | Hypertension, Pulmonary - genetics | Hypertension, Pulmonary - metabolism | Phosphoproteins - genetics | Transcription Factors - genetics | Muscular Dystrophies - pathology | Atherosclerosis - metabolism | Transcription Factors - metabolism | Mechanotransduction, Cellular | Animals | Adaptor Proteins, Signal Transducing - genetics | Fibrosis | Adaptor Proteins, Signal Transducing - metabolism | Extracellular Matrix - pathology | Hypertension, Pulmonary - pathology | Transcription factors | Genetic aspects | Disease susceptibility | Health aspects | Cellular control mechanisms | Regulators | Pathogenesis | Rigidity | Muscular dystrophy | Atherosclerosis | Extracellular matrix | Physiology | Gravity | Hypertension | Cues | Gravitation | Lung diseases | Muscles | Gene expression | Muscle contraction | Blood flow | Yes-associated protein | Regeneration | Arteriosclerosis | Stem cells | Shear stress | Mechanotransduction | Dystrophy | Mechanical stimuli | Cell size | Aberration | Cancer | Tumors
Journal Article
Gut, ISSN 0017-5749, 08/2005, Volume 54, Issue 8, pp. 1182 - 1193
.... Recent observations suggest new (patho-) physiological mechanisms of how functional versus dysfunctional TLRx/NOD2 pathways may oppose or favour inflammatory bowel disease (IBD... 
SIGNALING PATHWAYS | INFLAMMATORY-BOWEL-DISEASE | CROHNS-DISEASE | EPITHELIAL-CELLS | INNATE IMMUNE-RESPONSES | ULCERATIVE-COLITIS | PROINFLAMMATORY GENE-EXPRESSION | GASTROENTEROLOGY & HEPATOLOGY | NF-KAPPA-B | HELICOBACTER-PYLORI | CELIAC-DISEASE | Crohn Disease - genetics | Humans | Inflammatory Bowel Diseases - immunology | Immunity, Mucosal | Intracellular Signaling Peptides and Proteins - immunology | Signal Transduction - immunology | Toll-Like Receptors | Bacteria - immunology | Bacterial Infections - genetics | Bacterial Infections - immunology | Intestinal Mucosa - immunology | Inflammatory Bowel Diseases - genetics | Membrane Glycoproteins - immunology | Intracellular Signaling Peptides and Proteins - genetics | Genetic Predisposition to Disease - genetics | Polymorphism, Genetic - immunology | Homeostasis - immunology | Nod2 Signaling Adaptor Protein | Signal Transduction - genetics | Bacteria - genetics | Crohn Disease - immunology | Receptors, Cell Surface - immunology | Membrane Glycoproteins - genetics | Ligands | Polymorphism, Genetic - genetics | Homeostasis - genetics | Receptors, Cell Surface - genetics | Physiological aspects | Inflammatory bowel diseases | Ir genes | Immunity | Analysis | Gastric mucosa | Immunoglobulin M | Cell culture | Primary biliary cirrhosis | Chromatin | Mucosa | Immunoglobulin G | Frameshift mutation | Small intestine | Cofactors | Disease resistance | Microorganisms | Cell activation | Missense mutation | Intestine | Interleukin 1 | Bacteria | Immune system | NOD2 protein | CpG islands | Antigen-antibody complexes | Pathogens | Autoantibodies | Cytokines | Dendritic cells | Antimicrobial agents | Genetic diversity | Crohns disease | Inflammatory bowel disease | Celiac disease | Cirrhosis | Lymphocytes B | Rheumatoid arthritis | Autoimmune diseases | Chemokines | Apoptosis | Recent Advances in Basic Science | commensal bacteria | innate immunity | inflammatory bowel disease | host defence
Journal Article
The Journal of experimental medicine, ISSN 1540-9538, 2010, Volume 207, Issue 8, pp. 1625 - 1636
Signaling through the adaptor protein myeloid differentiation factor 88 (MyD88) promotes carcinogenesis in several cancer models. In contrast, MyD88 signaling... 
INTESTINAL INFLAMMATION | PATHOGENESIS | MEDICINE, RESEARCH & EXPERIMENTAL | CELLS | COLITIS | STAT3 | MICE | IMMUNOLOGY | BETA-CATENIN | CANCER | TUMORIGENESIS | INNATE IMMUNITY | Colonic Neoplasms - genetics | Intestinal Mucosa - metabolism | Adenocarcinoma - pathology | Azoxymethane - pharmacology | Epithelial Cells - metabolism | Gene Expression - drug effects | Apoptosis - drug effects | Gene Expression - genetics | Adenocarcinoma - chemically induced | Colonic Polyps - pathology | Epithelial Cells - drug effects | Colon - drug effects | DNA Repair Enzymes - genetics | Apoptosis - genetics | Colonic Neoplasms - chemically induced | Gene Expression Profiling | Inflammatory Bowel Diseases - metabolism | Colonic Neoplasms - metabolism | Intestinal Mucosa - drug effects | Adenocarcinoma - metabolism | Cyclooxygenase 2 - genetics | Inflammatory Bowel Diseases - pathology | Inflammatory Bowel Diseases - genetics | Interleukin-18 Receptor alpha Subunit - genetics | Inflammatory Bowel Diseases - chemically induced | Adenocarcinoma - genetics | Phosphorylation - drug effects | STAT3 Transcription Factor - genetics | Dextran Sulfate - pharmacology | Genetic Predisposition to Disease - genetics | Specific Pathogen-Free Organisms | Colon - pathology | Mice, Inbred C57BL | Epithelial Cells - pathology | Mutation - genetics | Colon - metabolism | beta Catenin - genetics | Mice, Knockout | Animals | Colonic Neoplasms - pathology | Receptors, Interleukin-1 Type I - genetics | Signal Transduction - physiology | Cell Proliferation - drug effects | Mice | Interleukin-18 - genetics | Myeloid Differentiation Factor 88 - metabolism | Interleukin-18 - metabolism | Intestinal Mucosa - pathology | Index Medicus
Journal Article
PloS one, ISSN 1932-6203, 2018, Volume 13, Issue 7, p. e0199664
Background Genetic risk factors, intestinal microbiota and a dysregulated immune system contribute to the pathogenesis of inflammatory bowel disease (IBD... 
PATHOGENESIS | CELLS | BACTERIA | INFLAMMATORY-BOWEL-DISEASE | IMMUNE-SYSTEM | CROHNS-DISEASE | PHOSPHATASE NONRECEPTOR TYPE-2 | MULTIDISCIPLINARY SCIENCES | ULCERATIVE-COLITIS | GUT MICROBIOTA | GENOME-WIDE ASSOCIATION | Humans | Middle Aged | Inflammatory Bowel Diseases - diagnosis | Male | Genetic Variation | Young Adult | Adult | Female | Inflammatory Bowel Diseases - etiology | Severity of Illness Index | Genetic Predisposition to Disease | Disease Susceptibility | Risk Assessment | Protein Tyrosine Phosphatase, Non-Receptor Type 22 - genetics | Risk Factors | Gastrointestinal Microbiome | Genotype | Protein Tyrosine Phosphatase, Non-Receptor Type 2 - genetics | Switzerland | Biopsy | Models, Biological | Alleles | RNA, Ribosomal, 16S - genetics | Polymorphism, Single Nucleotide | Cohort Studies | Inflammatory bowel diseases | Care and treatment | Microbiota (Symbiotic organisms) | Genetic variation | Development and progression | Esterases | Genetic aspects | Health aspects | rRNA 16S | Biomedical research | Laboratories | Pathogenesis | Mucosa | Genes | Phosphatase | Autophagy | Genera | Risk factors | Proteins | Genotype & phenotype | Microorganisms | Microbiota | Alterations | Intestine | Rodents | Hepatology | Surgery | Gastroenterology | Phylogenetics | Bacteria | Intestinal microflora | Genotypes | Deoxyribonucleic acid--DNA | Immune system | Tyrosine | Composition | Cytokines | Health risks | Abundance | Preventive medicine | Risk analysis | Patients | Crohns disease | Carriers | Inflammatory bowel disease | Disease prevention | Hospitals | Relative abundance | In vivo methods and tests |