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Cancer Research, ISSN 0008-5472, 10/2009, Volume 69, Issue 20, pp. 8208 - 8215
Journal Article
Nature, ISSN 0028-0836, 09/2011, Volume 477, Issue 7364, pp. 330 - 334
Intestinal immune homeostasis depends on a tightly regulated cross talk between commensal bacteria, mucosal immune cells and intestinal epithelial cells... 
APOPTOSIS | REGULATOR | DEATH PATHWAY | NECROPTOSIS | B-CELL | MULTIDISCIPLINARY SCIENCES | NETWORKS | TNF-ALPHA | DEFICIENT MICE | BOWEL-DISEASE | NEMO/IKK-GAMMA | Receptor-Interacting Protein Serine-Threonine Kinases - metabolism | Colon - enzymology | Epithelial Cells - metabolism | Paneth Cells - pathology | Colitis - pathology | Intracellular Signaling Peptides and Proteins - metabolism | Inflammatory Bowel Diseases - metabolism | Metagenome - physiology | Necrosis | Intracellular Signaling Peptides and Proteins - deficiency | Cysteine Endopeptidases - metabolism | Inflammatory Bowel Diseases - enzymology | Inflammatory Bowel Diseases - pathology | Enteritis - metabolism | Signal Transduction | Colon - pathology | Fas-Associated Death Domain Protein - metabolism | Fas-Associated Death Domain Protein - deficiency | Epithelial Cells - pathology | Enteritis - pathology | Tumor Necrosis Factors - deficiency | Colon - metabolism | Animals | Colitis - enzymology | Myeloid Differentiation Factor 88 - deficiency | Enteritis - enzymology | Colitis - metabolism | Epithelial Cells - enzymology | Mice | Receptor-Interacting Protein Serine-Threonine Kinases - antagonists & inhibitors | Chronic Disease | Myeloid Differentiation Factor 88 - metabolism | Apoptosis | Proteins | Inflammatory bowel disease | Pathogenesis | Colleges & universities | Homeostasis | Colon
Journal Article
Gastroenterology, ISSN 0016-5085, 2010, Volume 139, Issue 3, pp. 869 - 881.e9
Background & Aims Mechanisms responsible for crypt architectural distortion in chronic ulcerative colitis (CUC) are not well understood. Data indicate that... 
Gastroenterology and Hepatology | Intestinal Progenitor Cells | PI3K | Pik3r1 | Intestinal Stem Cells | ULCERATIVE-COLITIS | SELF-RENEWAL | COLORECTAL-CARCINOMA | IDENTIFICATION | INTERLEUKIN-10-DEFICIENT MICE | CANCER | INFLAMMATORY-BOWEL-DISEASE | PATHWAY | GENE-EXPRESSION | WNT | GASTROENTEROLOGY & HEPATOLOGY | Stem Cells - immunology | Colon - enzymology | Phosphorylation | Cell Proliferation | T-Lymphocytes - enzymology | Colitis - genetics | Humans | Colitis - complications | Colon - drug effects | Colitis - pathology | Colon - immunology | Phosphatidylinositol 3-Kinases - metabolism | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Wnt Proteins - metabolism | Intestinal Mucosa - drug effects | Phosphatidylinositol 3-Kinases - deficiency | Stem Cells - enzymology | Time Factors | Intestinal Mucosa - immunology | Colonoscopy | Intestinal Mucosa - enzymology | Colitis - immunology | Proto-Oncogene Proteins c-akt - metabolism | Disease Models, Animal | Interleukin-10 - deficiency | Colon - pathology | Mice, Inbred C57BL | beta Catenin - metabolism | Mice, Knockout | Phosphatidylinositol 3-Kinases - genetics | Animals | Colitis - enzymology | Signal Transduction - drug effects | Biopsy | Colonic Neoplasms - pathology | Interleukin-10 - genetics | Stem Cells - drug effects | Stem Cells - pathology | T-Lymphocytes - immunology | Colonic Neoplasms - enzymology | Mice | Protein Kinase Inhibitors - pharmacology | Intestinal Mucosa - pathology
Journal Article
Oncogene, ISSN 0950-9232, 08/2012, Volume 31, Issue 32, pp. 3679 - 3695
Colitis-associated colorectal cancers are an etiologically distinct subgroup of colon cancers that occur in individuals suffering from inflammatory bowel... 
intestinal barrier | inflammatory bowel disease | colon carcinogenesis | BIOCHEMISTRY & MOLECULAR BIOLOGY | HEPATOCYTE GROWTH-FACTOR | ULCERATIVE-COLITIS | BARRIER FUNCTION | INTESTINAL HOMEOSTASIS | PLASMINOGEN ACTIVATION | CELL BIOLOGY | MATRIX METALLOPROTEINASES | INFLAMMATORY-BOWEL-DISEASE | ONCOLOGY | COLORECTAL-CANCER | MOUSE MODEL | GENETICS & HEREDITY | SERINE-PROTEASE MATRIPTASE | Adenocarcinoma - pathology | Cell Proliferation | Epithelium - enzymology | Humans | Gene Expression Regulation, Neoplastic | Colitis - pathology | Mice, 129 Strain | Intestinal Absorption | Adenoma - enzymology | Inflammatory Bowel Diseases - enzymology | Inflammatory Bowel Diseases - pathology | Serine Endopeptidases - genetics | Basement Membrane - enzymology | Genes, Tumor Suppressor | Metagenome - drug effects | Epithelium - metabolism | Signal Transduction | Colon - pathology | Neoplasm Invasiveness | Mice, Inbred C57BL | Adenocarcinoma - enzymology | Basement Membrane - metabolism | Cell Transformation, Neoplastic - metabolism | beta Catenin - metabolism | Mice, Knockout | Gene Expression Regulation, Enzymologic | Membrane Proteins | Animals | Colitis - enzymology | Colitis - microbiology | Colonic Neoplasms - pathology | Inflammatory Bowel Diseases - microbiology | Anti-Bacterial Agents - pharmacology | Colonic Neoplasms - enzymology | Mice | Serine Endopeptidases - metabolism | Precancerous Conditions | Colon cancer | Immune response | Research | Carcinogenesis | Analysis | Stem cells | Inflammatory bowel disease | Proteins | Gene expression | Pathogenesis | Colorectal cancer | Index Medicus
Journal Article
PLoS ONE, ISSN 1932-6203, 01/2014, Volume 9, Issue 1, p. e85254
A functional mucus layer is a key requirement for gastrointestinal health as it serves as a barrier against bacterial invasion and subsequent inflammation.... 
CELLS | EXTRACTION | BACTERIA | MUCIN | DNA | INFLAMMATION | MULTIDISCIPLINARY SCIENCES | GUT MICROBIOTA | GERM-FREE | EXPRESSION | IRRITABLE-BOWEL-SYNDROME | Dextran Sulfate | Mucus - enzymology | Male | Intestines - immunology | Galactosemias - genetics | Intestinal Mucosa - immunology | Colitis - chemically induced | Intestinal Mucosa - enzymology | Bacteria - classification | Female | Colitis - immunology | Galactosemias - enzymology | Intestines - pathology | Microbiota - immunology | Galactosemias - immunology | Organ Size | Glycosylation | Intestinal Mucosa - microbiology | Mice, Knockout | Mucus - microbiology | Polysaccharides - metabolism | Galactosemias - microbiology | Animals | Colitis - enzymology | Colitis - microbiology | Intestines - microbiology | Mice | Mucus - immunology | Intestinal Mucosa - pathology | Intestines - enzymology | Physiological aspects | Polysaccharides | Inflammation | Colitis | Microbiota (Symbiotic organisms) | Gastrointestinal system | Disease | Laboratories | Core loss | Epithelial cells | Homeostasis | Mucus | Biochemistry | Biology | Sodium sulfates | Small intestine | Microbiota | Microorganisms | Intestine | Rodents | Gastroenterology | Bacteria | Colon | Digestive tract | Elongation | Antigens | Architecture | Digestive system | Muscles | Gastrointestinal tract | Metabolism | Ileum | Glycan | Inflammatory bowel disease | Dextran | Sodium | Crypts | Morphology | Irritable bowel syndrome | Clinical medicine | Other Basic Medicine | pathology | genetics | immunology | Intestinal Mucosa | Intestines | chemically induced | Galactosemias | microbiology | classification | enzymology | Knockout | Annan medicinsk grundvetenskap | metabolism
Journal Article
PLoS ONE, ISSN 1932-6203, 12/2014, Volume 9, Issue 12, p. e115175
We performed an analysis to determine the importance of bile acid modification genes in the gut microbiome of inflammatory bowel disease and type 2 diabetic... 
HUMAN GUT MICROBIOME | ACID RECEPTOR | ARTICLE | INFLAMMATORY-BOWEL-DISEASE | LIPID-METABOLISM | DYSBIOSIS | GLUCOSE | MULTIDISCIPLINARY SCIENCES | DIVERSITY | HEALTH | ASSOCIATION | Crohn Disease - genetics | Metagenomics | Colitis, Ulcerative - enzymology | Diabetes Mellitus, Type 2 - microbiology | Genes, Bacterial - genetics | Diabetes Mellitus, Type 2 - genetics | Humans | Colitis, Ulcerative - genetics | Phylogeny | Feces - microbiology | Microbiota | Crohn Disease - microbiology | Databases, Factual | Crohn Disease - enzymology | Amidohydrolases - genetics | Feces - enzymology | Diabetes Mellitus, Type 2 - enzymology | Gastrointestinal Tract - microbiology | Bile Acids and Salts - metabolism | Hydroxysteroid Dehydrogenases - genetics | Animals | Colitis, Ulcerative - microbiology | Bacteria - enzymology | Gastrointestinal Tract - enzymology | Mice | Metagenome | Type 2 diabetes | Enzymes | Diabetics | Analysis | Gastrointestinal diseases | Genes | Hydrolases | Colitis | Bacterial genetics | Vasopressin | Deoxycholic acid | Salts | Inflammatory bowel diseases | Populations | Hydrolase | Diabetes mellitus | Abundance | Crohn's disease | Disease control | Patients | Consortia | Datasets | Inflammatory bowel disease | Proteins | Reduction | Acids | Intestine | Bacteria | Strains (organisms) | Ulcerative colitis | Bile
Journal Article
FASEB Journal, ISSN 0892-6638, 05/2018, Volume 32, Issue 5, pp. 2339 - 2353
Journal Article
Journal of Pediatric Hematology/Oncology, ISSN 1077-4114, 11/2015, Volume 37, Issue 8, pp. 616 - 622
Glucose-6-phosphatase catalytic subunit 3 (G6PC3) deficiency was recently defined as a new severe congenital neutropenia subgroup remarkable with congenital... 
Inflammatory bowel disease | Severe congenital neutropenia | Combined immune deficiency | Intravenous γ-globulin | TYPE-4 | DEFECT | PHENOTYPE | combined immune deficiency | G-CSF THERAPY | intravenous gamma-globulin | inflammatory bowel disease | OSTEOPOROSIS | ONCOLOGY | SYNDROMIC NEUTROPENIA | PEDIATRICS | MUTATIONS | LEUKEMIA | SPECTRUM | HEMATOLOGY | severe congenital neutropenia | Glucose-6-Phosphatase - genetics | Frameshift Mutation | Colitis - genetics | Diarrhea - enzymology | Humans | Male | Failure to Thrive - enzymology | Lymphopenia - enzymology | Thrombocytopenia - genetics | Female | Respiratory Tract Infections - complications | Neutropenia - genetics | Child | Lymphocyte Subsets - pathology | Abnormalities, Multiple - genetics | Immunologic Deficiency Syndromes - enzymology | Catalytic Domain | Failure to Thrive - genetics | RNA Splice Sites - genetics | Thrombocytopenia - congenital | Exons - genetics | Codon, Nonsense | Glycogen Storage Disease Type I - immunology | Lymphopenia - congenital | Neutropenia - enzymology | Cell Lineage | Thrombocytopenia - enzymology | Phenotype | Colitis - enzymology | Glycogen Storage Disease Type I - genetics | Turkey | Diarrhea - genetics | Pedigree | Adolescent | Abnormalities, Multiple - enzymology | Immunologic Deficiency Syndromes - genetics | Consanguinity | Mutagenesis, Insertional | Lymphopenia - genetics | Bronchiectasis - etiology
Journal Article
Nature Communications, ISSN 2041-1723, 2014, Volume 5, Issue 1, p. 5103
Journal Article
Gastroenterology, ISSN 0016-5085, 12/2017, Volume 153, Issue 6, pp. 1607 - 1620
Polycomb group proteins are epigenetic factors that silence gene expression; they are dysregulated in cancer cells and contribute to carcinogenesis by unclear... 
PcG | Colon Cancer | Ulcerative Colitis | PAP | PANCREATIC DUCTAL ADENOCARCINOMA | INTESTINAL STEM-CELLS | SELF-RENEWAL | GENE | LIVER-REGENERATION | INFLAMMATION | MOUSE MODEL | IN-VIVO | MYC TRANSGENIC MICE | GASTROENTEROLOGY & HEPATOLOGY | TUMORIGENESIS | Colon - enzymology | Colonic Neoplasms - genetics | Phosphorylation | Cell Proliferation | Adenomatous Polyps - genetics | Polycomb Repressive Complex 1 - metabolism | Adenomatous Polyps - pathology | Colitis - genetics | Colonic Polyps - pathology | Humans | Colitis - complications | Colitis - pathology | Polycomb Repressive Complex 1 - deficiency | Adenomatous Polyps - enzymology | Polycomb Repressive Complex 1 - genetics | Colonic Polyps - genetics | Time Factors | Cell Transformation, Neoplastic - genetics | Colonic Polyps - enzymology | Intestinal Mucosa - enzymology | HEK293 Cells | Adenomatous Polyps - etiology | Colonic Neoplasms - etiology | STAT3 Transcription Factor - metabolism | Disease Models, Animal | Proto-Oncogene Proteins - metabolism | Genetic Predisposition to Disease | Signal Transduction | Colon - pathology | Mice, Inbred C57BL | Colonic Polyps - etiology | Proto-Oncogene Proteins - genetics | Blood Coagulation Factors - genetics | Proto-Oncogene Proteins - deficiency | Blood Coagulation Factors - metabolism | Cell Transformation, Neoplastic - metabolism | Disease Progression | Mice, Knockout | Phenotype | Animals | Colitis - enzymology | Colonic Neoplasms - pathology | Colonic Neoplasms - enzymology | Cell Transformation, Neoplastic - pathology | Apoptosis | Intestinal Mucosa - pathology | Pancreatitis-Associated Proteins - metabolism | Proteins | Dextran | Epigenetic inheritance | Colon cancer | DNA microarrays | Analysis | T cells | Gene expression | Cancer | Ulcerative colitis | Index Medicus | Abridged Index Medicus
Journal Article