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1. Full Text NOD2-mediated dysbiosis predisposes mice to transmissible colitis and colorectal cancer
by Couturier-Maillard, Aurélie and Secher, Thomas and Rehman, Ateequr and Normand, Sylvain and De Arcangelis, Adèle and Haesler, Robert and Huot, Ludovic and Grandjean, Teddy and Bressenot, Aude and Delanoye-Crespin, Anne and Gaillot, Olivier and Schreiber, Stefan and Lemoine, Yves and Ryffel, Bernhard and Hot, David and Nùñez, Gabriel and Chen, Grace and Rosenstiel, Philip and Chamaillard, Mathias
Journal of Clinical Investigation, ISSN 0021-9738, 02/2013, Volume 123, Issue 2, pp. 700 - 711
Instability in the composition of gut bacterial communities (dysbiosis) has been linked to common human intestinal disorders, such as Crohn's disease and... 
MEDICINE, RESEARCH & EXPERIMENTAL | CARCINOGENESIS | CROHNS-DISEASE | FECAL MICROBIOTA | MOUSE MODEL | SUSCEPTIBILITY | RECEPTOR | NOD2 | INFLAMMATORY BOWEL DISEASES | INTESTINAL EPITHELIAL-CELLS | INNATE IMMUNITY | Nod2 Signaling Adaptor Protein - deficiency | Humans | Colitis - pathology | Male | Nod2 Signaling Adaptor Protein - genetics | Colorectal Neoplasms - etiology | Female | Colorectal Neoplasms - metabolism | Disease Models, Animal | Digestive System - metabolism | Risk Factors | Colorectal Neoplasms - microbiology | Mice, Knockout | Digestive System - pathology | Pregnancy | Colitis - etiology | Receptor-Interacting Protein Serine-Threonine Kinases - genetics | Animals | Colitis - microbiology | Colitis - metabolism | Mice | Receptor-Interacting Protein Serine-Threonine Kinases - deficiency | Colorectal Neoplasms - pathology | Metagenome | Digestive System - microbiology | Care and treatment | Microbiota (Symbiotic organisms) | Colorectal cancer | Physiological aspects | Genetic aspects | Research | Colitis | Risk factors | Index Medicus | Abridged Index Medicus | Receptor-Interacting Protein Serine-Threonine Kinases | Nod2 Signaling Adaptor Protein | Life Sciences | Immunology | Digestive System | Colorectal Neoplasms
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2. Full Text Induction and rescue of Nod2-dependent Th1-driven granulomatous inflammation of the ileum
by Amlan Biswas and Yuen-Joyce Liu and Liming Hao and Atsushi Mizoguchi and Nita H. Salzman and Charles L. Bevins and Koichi S. Kobayashi and Laurie H. Glimcher
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 8/2010, Volume 107, Issue 33, pp. 14739 - 14744
Mutations in the NOD2 gene are strong genetic risk factors for ileal Crohn's disease. However, the mechanism by which these mutations predispose to intestinal... 
T lymphocytes | Crohn disease | Peyers patches | Epithelial cells | Crypts | Inflammation | Bone marrow cells | Ileum | Genetic mutation | Lymph nodes | Helicobacter hepaticus | Granuloma | Innate immunity | Crohn's disease | Paneth cells | IMMUNITY | PEYERS-PATCHES | MULTIDISCIPLINARY SCIENCES | INNATE | ILEAL CROHNS-DISEASE | BOWEL-DISEASE | innate immunity | EPITHELIAL-CELLS | granuloma | FRAMESHIFT MUTATION | NOD2 MUTATION | DEFENSIN EXPRESSION | Crohn Disease - genetics | Nod2 Signaling Adaptor Protein - deficiency | Peyer's Patches - metabolism | Humans | Crohn Disease - metabolism | Ileum - metabolism | Male | Nod2 Signaling Adaptor Protein - genetics | Interleukin-1beta - genetics | Ileum - immunology | Th1 Cells - immunology | Host-Pathogen Interactions - immunology | Th1 Cells - metabolism | Flow Cytometry | Peyer's Patches - microbiology | Female | Interferon-gamma - genetics | Interleukin-6 - genetics | Helicobacter hepaticus - immunology | Mice, Inbred C57BL | Helicobacter hepaticus - physiology | Interleukin-1beta - immunology | Nod2 Signaling Adaptor Protein - immunology | Helicobacter Infections - immunology | Reverse Transcriptase Polymerase Chain Reaction | Crohn Disease - immunology | Mice, Knockout | Animals | Interferon-gamma - immunology | Interleukin-6 - immunology | Mice | Peyer's Patches - immunology | Ileum - microbiology | Helicobacter Infections - microbiology | Gene mutations | Genetic aspects | Research | Health aspects | Risk factors | Cytokines | Rodents | Bone marrow | Mutation | Gram-negative bacteria | Gene expression | Small intestine | Crohns disease | Index Medicus | Peyer's patches | Animal models | Inflammatory bowel diseases | CD8 antigen | Helper cells | Transgenic mice | Antimicrobial agents | Lymphocytes T | CD4 antigen | Intestine | gamma -Interferon | NOD2 protein | Biological Sciences | Crohn’s disease
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3. Full Text Activation of Pattern Recognition Receptors Up-Regulates Metallothioneins, Thereby Increasing Intracellular Accumulation of Zinc, Autophagy, and Bacterial Clearance by Macrophages
by Lahiri, Amit and Abraham, Clara
Gastroenterology, ISSN 0016-5085, 2014, Volume 147, Issue 4, pp. 835 - 846
Background & Aims Continuous stimulation of pattern recognition receptors (PRRs), including nucleotide-binding oligomerization domain-2 (NOD2) (variants in... 
Gastroenterology and Hepatology | Inflammatory Bowel Disease | Signal Transduction | Intestinal Inflammation | Innate Immunity | Disease | Bowel | Inflammation | Immunity | Intestinal | Signal | Inflammatory | Innate | Transduction | CYTOKINE SECRETION | STIMULATION | PROTEIN | TOLERANCE | INNATE | NOD2 | SUPPLEMENTATION | ATG16L1 | GASTROENTEROLOGY & HEPATOLOGY | Intestines - drug effects | Metallothionein - metabolism | Nod2 Signaling Adaptor Protein - deficiency | Zinc - metabolism | Humans | Caspase 1 - metabolism | NF-kappa B - metabolism | Nod2 Signaling Adaptor Protein - genetics | Intestines - metabolism | Autophagy - drug effects | DNA-Binding Proteins - metabolism | Transfection | RNA Interference | Time Factors | Nod2 Signaling Adaptor Protein - agonists | Toll-Like Receptors - metabolism | Macrophages - microbiology | Intestines - pathology | Macrophages - pathology | Mice, Inbred C57BL | Cells, Cultured | Gene Expression Regulation | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Mice, Knockout | Transcription Factors - metabolism | Macrophages - metabolism | Animals | Intestines - microbiology | Metallothionein - genetics | Nod2 Signaling Adaptor Protein - metabolism | Macrophages - drug effects | Anti-Bacterial Agents - pharmacology | Mice | Oligomers | Macrophages | Index Medicus | Abridged Index Medicus
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4. Full Text Deep resequencing of GWAS loci identifies independent rare variants associated with inflammatory bowel disease
by Rivas, Manuel A and Beaudoin, Mélissa and Gardet, Agnes and Stevens, Christine and Sharma, Yashoda and Zhang, Clarence K and Boucher, Gabrielle and Ripke, Stephan and Ellinghaus, David and Burtt, Noel and Fennell, Tim and Kirby, Anew and Latiano, Anna and Goyette, Philippe and Green, Todd and Halfvarson, Jonas and Haritunians, Talin and Korn, Joshua M and Kuruvilla, Finny and Lagacé, Caroline and Neale, Benjamin and Lo, Ken Sin and Schumm, Phil and Törkvist, Leif and Dubinsky, Marla C and Brant, Steven R and Silverberg, Mark S and Duerr, Richard H and Altshuler, David and Gabriel, Stacey and Lettre, Guillaume and Franke, Ane and D'Amato, Mauro and McGovern, Dermot P. B and Cho, Judy H and Rioux, John D and Xavier, Ramnik J and Daly, Mark J and Parkes, Miles and Lee, James and Zhang, Hu and Bredin, Francesca and Ahmad, Tariq and Satsangi, Jack and Nimmo, Elaine and mmond, Hazel and Lees, Charlie and Mansfield, John and Mathew, Christopher G and Prescott, Natalie and Harrison, Kristina and Sanderson, Jeremy and Newman, William and Phillips, Anne and Mowat, Craig and Edwards, Cathryn and Wilson, David C and Barrett, Jeffrey and Anderson, Carl and Gray, Emma and Edkins, Sarah and Russell, Richard K and Henderson, Paul and Anderson, Carl A and Annese, Vito and Baldassano, Robert N and Balschun, Tobias and Barclay, Murray and Barrett, Jeffrey C and Bayless, Theodore M and Bis, Joshua C and Brand, Stephan and Bumpstead, Suzanne and Buning, Carsten and Cohen, Albert and Colombel, Jean-Frederick and Cottone, Mario and D'Inca, Renata and Denson, Ted and Dubinsky, Marla and Florin, Tim and Franchimont, Denis and Gearry, Richard and Georges, Michel and Glas, Jurgen and van Gossum, Ane and Griffiths, Anne M and Guthery, Stephen L and Hakonarson, Hakon and Hugot, Jean-Pierre and de Jong, Dirk J and Jostins, Luke and Kugathasan, Subra and Kullack-Ublick, Gerd and Laukens, Debby and Lawrance, Ian and Lees, Charlie W and Lemann, Marc and Levine, Arie and Libioulle, Cecile and ... and United Kingdom Inflammatory Bowel and Natl Inst Diabet Digestive Kidney and Int Inflammatory Bowel Dis and United Kingdom Inflammatory Bowel Disease Genetics Consortium and National Institute of Diabetes and Digestive Kidney Diseases Inflammatory Bowel Disease Genetics Consortium (NIDDK IBDGC) and International Inflammatory Bowel Disease Genetics Consortium and Hälsoakademin and Örebro universitet
Nature genetics, ISSN 1061-4036, 2011, Volume 43, Issue 11, pp. 1066 - 1073
More than 1,000 susceptibility loci have been identified through genome-wide association studies (GWAS) of common variants; however, the specific genes and... 
RECRUITMENT | RISK LOCI | CROHNS-DISEASE | GENE | FREQUENCY | GENETICS & HEREDITY | MURAMYL DIPEPTIDE RECOGNITION | SUSCEPTIBILITY LOCI | CARD15 MUTATIONS | NOD2 | GENOME-WIDE ASSOCIATION | Cell Line | Genetic Predisposition to Disease | Genome-Wide Association Study | RNA Splicing | Humans | Inflammatory Bowel Diseases - genetics | Nod2 Signaling Adaptor Protein - genetics | Receptors, Interleukin - genetics | Sequence Analysis, DNA | Case-Control Studies | Inflammatory bowel disease | Studies | Design | Medical research | Genealogy | Genes | Genetics | Data processing | Genomes | Grants | Diabetes | Twins | Index Medicus | Medicin | Medicine | Medical and Health Sciences | Medicin och hälsovetenskap
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5. Full Text Increased NOD2-mediated recognition of N-glycolyl muramyl dipeptide
by Coulombe, François and Divangahi, Maziar and Veyrier, Frédéric and De Léséleuc, Louis and Gleason, James L and Yang, Yibin and Kelliher, Michelle A and Pandey, Amit K and Sassetti, Christopher M and Reed, Michael B and Behr, Marcel A
Journal of Experimental Medicine, ISSN 0022-1007, 08/2009, Volume 206, Issue 8, pp. 1709 - 1716
Peptidoglycan-derived muramyl dipeptide (MDP) activates innate immunity via the host sensor NOD2. Although MDP is N-acetylated in most bacteria, mycobacteria... 
MEDICINE, RESEARCH & EXPERIMENTAL | WALLS | ACTIVATION | PEPTIDOGLYCAN | ACID | MYCOBACTERIUM-TUBERCULOSIS INFECTION | ADJUVANT ACTIVITY | MICE | NOD2 | IMMUNOLOGY | POLYUBIQUITINATION | IDENTIFICATION | Nod2 Signaling Adaptor Protein - deficiency | Mycobacterium smegmatis - immunology | Acetylmuramyl-Alanyl-Isoglutamine - chemistry | Male | Mixed Function Oxygenases - metabolism | Nod2 Signaling Adaptor Protein - genetics | Actinobacteria - immunology | Base Sequence | Female | Macrophages - immunology | Macrophages - microbiology | Mycobacterium smegmatis - genetics | Acetylmuramyl-Alanyl-Isoglutamine - analogs & derivatives | Mice, Inbred C57BL | Nod2 Signaling Adaptor Protein - immunology | Immunity, Innate | Macrophage Activation | Mice, Knockout | Glycols - chemistry | Models, Immunological | Animals | DNA, Bacterial - genetics | Acetylmuramyl-Alanyl-Isoglutamine - immunology | Mice | Mutation | Mixed Function Oxygenases - genetics | Cytokines - biosynthesis | Index Medicus | Brief Definitive Report
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6. Full Text Nucleotide-Binding Oligomerization Domain-2 Inhibits Toll-Like Receptor-4 Signaling in the Intestinal Epithelium
by Richardson, Ward M and Sodhi, Chhinder P and Russo, Anthony and Siggers, Richard H and Afrazi, Amin and Gribar, Steven C and Neal, Matthew D and Dai, Shipan and Prindle, Thomas and Branca, Maria and Ma, Congrong and Ozolek, John and Hackam, David J
Gastroenterology, ISSN 0016-5085, 2010, Volume 139, Issue 3, pp. 904 - 917.e6
Background & Aims Factors that regulate enterocyte apoptosis in necrotizing enterocolitis (NEC) remain incompletely understood, although Toll-like receptor-4... 
Gastroenterology and Hepatology | TLR4 | NEC | NOD2 | TRANSLOCATION | ACTIVATION | NECROTIZING ENTEROCOLITIS | ENTEROCYTE MIGRATION | PATHOGENESIS | NOD-LIKE RECEPTORS | HOST-DEFENSE | RESTITUTION | GASTROENTEROLOGY & HEPATOLOGY | EXPRESSION | Intestinal Mucosa - metabolism | Nod2 Signaling Adaptor Protein - deficiency | Age Factors | Endotoxemia - genetics | Enterocytes - metabolism | Enterocolitis, Necrotizing - genetics | Enterocolitis, Necrotizing - metabolism | Humans | NF-kappa B - metabolism | Nod2 Signaling Adaptor Protein - genetics | Endotoxemia - pathology | Intestinal Mucosa - drug effects | Mitochondrial Proteins - metabolism | Nod2 Signaling Adaptor Protein - agonists | Enterocolitis, Necrotizing - pathology | Disease Models, Animal | Animals, Newborn | Severity of Illness Index | Cell Line | Transduction, Genetic | Enterocolitis, Necrotizing - prevention & control | Mice, Inbred C57BL | Rats | Toll-Like Receptor 4 - genetics | Toll-Like Receptor 4 - metabolism | Mice, Knockout | Acetylmuramyl-Alanyl-Isoglutamine - pharmacology | Animals | Carrier Proteins - metabolism | Nod2 Signaling Adaptor Protein - metabolism | Signal Transduction - drug effects | Protein Array Analysis | Mice | Endotoxemia - metabolism | Apoptosis | Cell Movement | Intestinal Mucosa - pathology | Oligomers | Fluorescence | Mitogens | Nitric oxide | Index Medicus | Abridged Index Medicus
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7. Full Text Enhancement of Muramyl Dipeptide‐Dependent NOD2 Activity by a Self‐Derived Peptide
by Mann, Jasdeep K and Shen, Jiaochen and Park, Sheldon
Journal of Cellular Biochemistry, ISSN 0730-2312, 05/2017, Volume 118, Issue 5, pp. 1227 - 1238
The Crohn's disease‐associated mutation, R702W, in NOD2 lowers the activity the molecule by an unknown mechanism. We show that a NOD2 derived peptide... 
MECHANISM OF ACTIVATION | AUTOINHIBITION | CROHN'S DISEASE | NOD2 | PEPTIDE LIGAND | DOMAIN | CROHNS-DISEASE | CRYSTAL-STRUCTURE | BIOCHEMISTRY & MOLECULAR BIOLOGY | LEUCINE-RICH REPEAT | CELL BIOLOGY | ADAPTIVE IMMUNITY | CAENORHABDITIS-ELEGANS | INFLAMMATION | PANETH CELLS | RECEPTORS | BINDING | Crohn Disease - genetics | Humans | Nod2 Signaling Adaptor Protein - chemistry | Models, Molecular | Nod2 Signaling Adaptor Protein - genetics | Acetylmuramyl-Alanyl-Isoglutamine - pharmacology | Peptides - metabolism | Nod2 Signaling Adaptor Protein - metabolism | HEK293 Cells | Protein Domains | Protein Conformation | Structural Homology, Protein | Mutation | Oligomers | Peptides | Analysis | Binding | Inflammatory bowel diseases | Oligomerization | Muramyl dipeptide | Immune response | Nlr protein | Homology | Activation | Gastrointestinal tract | Crohn's disease | Adaptive immunity | Pattern recognition | Leucine | Immunity | Immune systems | Proteins | Receptors | Cell activation | Gastrointestinal system | Ligands | NOD2 protein | Index Medicus
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8. Full Text CARD domain of rat RIP2 kinase: Refolding, solution structure, pH-dependent behavior and protein-protein interactions
by Goncharuk, Sergey A and Artemieva, Lilya E and Tabakmakher, Valentin M and Arseniev, Alexander S and Mineev, Konstantin S
PLoS ONE, ISSN 1932-6203, 10/2018, Volume 13, Issue 10, pp. e0206244 - e0206244
RIP2, one of the RIP kinases, interacts with p75 neurotrophin receptor, regulating the neuron survival, and with NOD1 and NOD2 proteins, causing the innate... 
MULTIDISCIPLINARY SCIENCES | DISEASE | N-15 | RELAXATION | COUPLINGS | NOD2 | CELL-DEATH | Amino Acid Sequence | Nod1 Signaling Adaptor Protein - chemistry | Magnetic Resonance Spectroscopy - methods | Nod2 Signaling Adaptor Protein - chemistry | Protein Multimerization | Protein Refolding | Models, Molecular | Nod2 Signaling Adaptor Protein - genetics | Receptor-Interacting Protein Serine-Threonine Kinase 2 - genetics | Static Electricity | Nod1 Signaling Adaptor Protein - metabolism | Receptor-Interacting Protein Serine-Threonine Kinase 2 - metabolism | Sequence Homology, Amino Acid | Nod2 Signaling Adaptor Protein - metabolism | Solutions | Receptor-Interacting Protein Serine-Threonine Kinase 2 - chemistry | Protein Binding | Caspase Activation and Recruitment Domain | Hydrogen-Ion Concentration | Nod1 Signaling Adaptor Protein - genetics | Physiological aspects | Genetic aspects | Research | Properties | Structure | Protein kinases | Protein-protein interactions | Gram-positive bacteria | Homology | Drug development | Kinases | pH effects | Neurogenesis | Inflammatory diseases | Magnetic resonance spectroscopy | Proteins | Oligomers | Protein folding | Neurodegeneration | pH | Nod1 protein | NOD2 protein | Cell survival | Oligomerization | Immune response | Caspase | Electrostatic properties | Physics | Domains | Immune systems | Chemistry | Protein expression | Protein interaction | NMR spectroscopy | Protein structure | Index Medicus
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9. Full Text Disease phenotype and genotype are associated with shifts in intestinal-associated microbiota in inflammatory bowel diseases
by Frank, Daniel N and Robertson, Charles E and Hamm, Christina M and Kpadeh, Zegbeh and Zhang, Tianyi and Chen, Hongyan and Zhu, Wei and Sartor, R. Balfour and Boedeker, Edgar C and Harpaz, Noam and Pace, Norman R and Li, Ellen
Inflammatory Bowel Diseases, ISSN 1078-0998, 01/2011, Volume 17, Issue 1, pp. 179 - 184
Background: Abnormal host-microbe interactions are implicated in the pathogenesis of inflammatory bowel diseases. Previous 16S rRNA sequence analysis of... 
microbiota | NOD2 | inflammatory bowel diseases | ATG16L1 | SUSCEPTIBILITY LOCI | IMBALANCES | MECHANISMS | COMMUNITIES | ILEAL CROHNS-DISEASE | PATHOGENESIS | PANETH CELLS | GASTROENTEROLOGY & HEPATOLOGY | EXPRESSION | GENOME-WIDE ASSOCIATION | Crohn Disease - genetics | Autophagy-Related Proteins | Intestines - pathology | Prognosis | Humans | Colitis, Ulcerative - genetics | Genotype | Nod2 Signaling Adaptor Protein - genetics | Colitis, Ulcerative - pathology | RNA, Ribosomal - genetics | Case-Control Studies | Carrier Proteins - genetics | Metagenome - genetics | Phenotype | Intestines - microbiology | Colitis, Ulcerative - microbiology | Crohn Disease - pathology | Polymorphism, Single Nucleotide - genetics | Crohn Disease - microbiology | Inflammatory bowel diseases | Statistical analysis | rRNA 16S | Data processing | Crohn's disease | Multivariate analysis | Intestine | Surgery | Mathematical models | Models | Age | Genotypes | NOD2 protein | Ulcerative colitis | Index Medicus
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10. Full Text Nucleotide-Binding Oligomerization Domain-Containing Protein 2 Variants in Patients with Spontaneous Bacterial Peritonitis
by Harputluoglu, Murat M. M and Dertli, Ramazan and Otlu, Baris and Demirel, Ulvi and Yener, Ozkan and Bilgic, Yilmaz and Erdogan, Mehmet Ali and Atayan, Yahya and Cagin, Yasir Furkan
Digestive Diseases and Sciences, ISSN 0163-2116, 6/2016, Volume 61, Issue 6, pp. 1545 - 1552
The occurrence of spontaneous bacterial peritonitis (SBP) is significantly increased in carriers of nucleotide-binding oligomerization domain-containing... 
Biochemistry, general | Cirrhosis | Spontaneous bacterial peritonitis | Medicine & Public Health | Hepatology | Gastroenterology | Oncology | NOD2 | Bacterial translocation | Transplant Surgery | NOD2/CARD15 | FACTOR-ALPHA | LIVER-CIRRHOSIS | TUMOR-NECROSIS-FACTOR | NOD2 GENE VARIANTS | SERUM-LEVELS | SEPTIC SHOCK | CIRRHOTIC-PATIENTS | GASTROENTEROLOGY & HEPATOLOGY | TURKISH PATIENTS | SEVERE SEPSIS | Genetic Predisposition to Disease | Gene Expression Regulation - immunology | Humans | Middle Aged | Male | Nod2 Signaling Adaptor Protein - genetics | Bacterial Translocation | Genetic Variation | Bacterial Infections - genetics | Peritonitis - microbiology | Nod2 Signaling Adaptor Protein - metabolism | Peritonitis - genetics | Adult | Female | Aged | Bacterial Infections - microbiology | Oligomers | Care and treatment | Interleukins | Microbiology | Liver | Liver cirrhosis | Mitogens | Peritonitis | Protein binding | Index Medicus | Abridged Index Medicus
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11. Full Text Genetic association and phenotypic correlation of TLR4 but not NOD2 variants with Tunisian inflammatory bowel disease
by Feki, Sawsan and Bouzid, Dorra and Abida, Olfa and Chtourou, Lassaad and Elloumi, Nesrine and Toumi, Amina and Hachicha, Hend and Amouri, Ali and Tahri, Nabil and Masmoudi, Hatem
Journal of Digestive Diseases, ISSN 1751-2972, 11/2017, Volume 18, Issue 11, pp. 625 - 633
OBJECTIVEThe common association between NOD2/CARD15 and TLR4 gene variants with inflammatory bowel disease (IBD) has not been replicated in all studies. We... 
Crohn disease | TLR4, ulcerative colitis | inflammatory bowel diseases | NOD2/CARD15, single nucleotide polymorphism | CROHNS-DISEASE | single nucleotide polymorphism | ULCERATIVE-COLITIS | SUSCEPTIBILITY | NOD2/CARD15 GENE | NOD2 | TOLL-LIKE RECEPTOR-4 | ASP299GLY POLYMORPHISM | CARD15/NOD2 | AUSTRALIAN POPULATION | CARD15 | ulcerative colitis | MUTATIONS | GASTROENTEROLOGY & HEPATOLOGY | TLR4 | THR399ILE POLYMORPHISMS | Colitis, Ulcerative - complications | Crohn Disease - genetics | Humans | Middle Aged | Colitis, Ulcerative - genetics | Toll-Like Receptor 4 - genetics | Genotype | Male | Nod2 Signaling Adaptor Protein - genetics | Arthritis - genetics | Case-Control Studies | Young Adult | Phenotype | Arthritis - complications | Alleles | Adult | Female | Heterozygote | Polymorphism, Single Nucleotide | Mutation | Tunisia | Inflammatory bowel diseases | Genes | Crohn's disease | Arthritis | TLR4 protein | Gene polymorphism | Population genetics | Inflammatory bowel disease | Polymerase chain reaction | Restriction fragment length polymorphism | Intestine | Toll-like receptors | NOD2 protein | Ulcerative colitis | Index Medicus
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12. Full Text Genetic basis for increased intestinal permeability in families with Crohn's disease: Role of CARD15 3020insC mutation?
by Buhner, S and Buning, C and Genschel, J and Kling, K and Herrmann, D and Dignass, A and Kuechler, I and Krueqer, S and Schmidt, H.H.-J and Lochs, H
Gut, ISSN 0017-5749, 03/2006, Volume 55, Issue 3, pp. 342 - 347
Background and aim: A genetically impaired intestinal barrier function has long been suspected to be a predisposing factor for Crohn's disease ( CD). Recently,... 
NOD2 GENE | INFLAMMATORY-BOWEL-DISEASE | PEPTIDOGLYCAN | EPITHELIAL-CELLS | VARIANTS | SUSCEPTIBILITY | HEALTHY RELATIVES | NOD2/CARD15 GENE | RISK | GASTROENTEROLOGY & HEPATOLOGY | ASSOCIATION | Crohn Disease - genetics | Genetic Predisposition to Disease | Humans | Middle Aged | Male | Nod2 Signaling Adaptor Protein | Permeability | Polymorphism, Genetic | Intestinal Absorption - genetics | Adolescent | Adult | Female | Aged | Crohn Disease - physiopathology | Mutation | Intracellular Signaling Peptides and Proteins - physiology | Intracellular Signaling Peptides and Proteins - genetics | Gene mutations | Physiological aspects | Development and progression | Crohn's disease | Genetic aspects | Research | Intestinal mucosa | Inflammatory bowel disease | Small intestine | Genes | Index Medicus | Abridged Index Medicus | intestinal permeability | CARD15 | Inflammatory Bowel Disease | intestinal barrier function | gene analysis | NOD2 mutation
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