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1. Full Text Helicobacter pylori CagA interacts with E-cadherin and deregulates the β-catenin signal that promotes intestinal transdifferentiation in gastric epithelial cells
by Murata-Kamiya, N and Kurashima, Y and Teishikata, Y and Yamahashi, Y and Saito, Y and Higashi, H and Aburatani, H and Akiyama, T and Peek Jr, R.M and Azuma, T and Hatakeyama, M
Oncogene, ISSN 0950-9232, 07/2007, Volume 26, Issue 32, pp. 4617 - 4626
Infection with Helicobacter pylori cagA-positive strains is associated with gastric adenocarcinoma. Intestinal metaplasia is a precancerous lesion of the... 
β-catenin | Gastric adenocarcinoma | Helicobacter pylori CagA | E-cadherin | Intestinal metaplasia | beta-catenin | TARGET | ACTIVATION | PROTEIN | CDX1 | BIOCHEMISTRY & MOLECULAR BIOLOGY | CANCER | CELL BIOLOGY | gastric adenocarcinoma | GENE | ONCOLOGY | intestinal metaplasia | WNT PATHWAY | ATROPHIC GASTRITIS | GENETICS & HEREDITY | INFECTION | EXPRESSION | Intestinal Mucosa - metabolism | Phosphorylation | Adenocarcinoma - pathology | Cadherins - metabolism | beta Catenin - analysis | Adenocarcinoma - etiology | Homeodomain Proteins - metabolism | Humans | Transcriptional Activation | Gene Expression Regulation, Neoplastic | Stomach Neoplasms - metabolism | Cytoplasm - metabolism | Gastric Mucosa - pathology | Precancerous Conditions - metabolism | Stomach Neoplasms - pathology | Bacterial Proteins - analysis | Gastric Mucosa - metabolism | Adenocarcinoma - metabolism | Cell Nucleus - metabolism | Cyclin-Dependent Kinase Inhibitor p21 - genetics | Cell Transformation, Neoplastic - genetics | Mucins - metabolism | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Precancerous Conditions - pathology | Stomach Neoplasms - etiology | Cytoplasm - chemistry | Cell Line | Cadherins - analysis | Cell Transformation, Neoplastic - metabolism | Precancerous Conditions - genetics | beta Catenin - metabolism | Homeodomain Proteins - genetics | Mucin-2 | Tyrosine - metabolism | Antigens, Bacterial - analysis | Bacterial Proteins - metabolism | Cell Nucleus - chemistry | Cell Transformation, Neoplastic - pathology | Antigens, Bacterial - metabolism | Intestinal Mucosa - pathology
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2. Full Text Estrogen receptor‐β protects against colitis‐associated neoplasia in mice
by Saleiro, Diana and Murillo, Genoveva and Benya, Richard V and Bissonnette, Marc and Hart, John and Mehta, Rajendra G
International Journal of Cancer, ISSN 0020-7136, 12/2012, Volume 131, Issue 11, pp. 2553 - 2561
Estrogen receptor‐beta (ERβ) has been suggested to exert anti‐inflammatory and anti‐tumorigenic effects in the colon, providing a translational potential to... 
dextran sodium sulfate | estrogen receptor‐beta | colon cancer | azoxymethane | inflammatory bowel disease | estrogen receptor-beta | Estradiol - blood | Mucin-2 - genetics | Neoplasms - metabolism | Tumor Necrosis Factor-alpha - metabolism | Inflammation - pathology | Colitis - genetics | Colorectal Neoplasms - genetics | Tumor Necrosis Factor-alpha - genetics | Colitis - pathology | NF-kappa B - metabolism | Interferon-gamma - metabolism | Inflammatory Bowel Diseases - metabolism | Estrogen Receptor beta - metabolism | Cell Differentiation - genetics | Inflammation - metabolism | Estrogen Receptor beta - genetics | Proliferating Cell Nuclear Antigen - genetics | Neoplasms - genetics | Inflammatory Bowel Diseases - pathology | Inflammatory Bowel Diseases - genetics | Female | Interferon-gamma - genetics | Interleukin-6 - metabolism | Colorectal Neoplasms - metabolism | Mucin-2 - metabolism | Mucin-1 - metabolism | Interleukin-6 - genetics | Colon - pathology | Mice, Inbred C57BL | Caveolin 1 - genetics | Interleukin-17 - genetics | beta Catenin - metabolism | Colon - metabolism | beta Catenin - genetics | Mice, Knockout | Caveolin 1 - metabolism | Interleukin-17 - metabolism | Animals | NF-kappa B - genetics | Nitric Oxide Synthase Type II - genetics | Colitis - metabolism | Inflammation - genetics | Mice | Colorectal Neoplasms - pathology | Neoplasms - pathology | Proliferating Cell Nuclear Antigen - metabolism | Mucin-1 - genetics | Nitric Oxide Synthase Type II - metabolism | Estrogen receptor-beta
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3. Full Text Foxa1 and Foxa2 Control the Differentiation of Goblet and Enteroendocrine L- and D-Cells in Mice
by Ye, Diana Z and Kaestner, Klaus H
Gastroenterology, ISSN 0016-5085, 2009, Volume 137, Issue 6, pp. 2052 - 2062
Background & Aims The winged helix transcription factors Foxa1 and Foxa2 are expressed in all epithelia of the gastrointestinal tract from its embryonic origin... 
Gastroenterology and Hepatology | RESPONSE ELEMENT | GLUCOSE-HOMEOSTASIS | GLUCAGON-LIKE PEPTIDE-1 | PROGLUCAGON GENE-TRANSCRIPTION | IN-VIVO | INSULIN-SECRETION | PANCREATIC BETA-CELLS | GASTROENTEROLOGY & HEPATOLOGY | ISLET CELLS | EXPRESSION | ENDOCRINE-CELLS | Immunohistochemistry | Hepatocyte Nuclear Factor 3-beta - genetics | Intestine, Small - pathology | Peptide YY - metabolism | Homeodomain Proteins - metabolism | Male | RNA, Messenger - metabolism | Cell Differentiation | Enteroendocrine Cells - metabolism | Proglucagon - metabolism | Somatostatin - metabolism | Repressor Proteins - metabolism | Hepatocyte Nuclear Factor 3-beta - metabolism | Mucin-2 - metabolism | Enteroendocrine Cells - pathology | Somatostatin-Secreting Cells - pathology | Glucagon-Like Peptide 1 - metabolism | Glucagon-Like Peptide 2 - metabolism | Hepatocyte Nuclear Factor 3-alpha - deficiency | Hepatocyte Nuclear Factor 3-alpha - genetics | PAX6 Transcription Factor | Goblet Cells - metabolism | Hepatocyte Nuclear Factor 3-alpha - metabolism | Mice, Knockout | Mucin-5B - metabolism | Animals | Eye Proteins - metabolism | Mucin 5AC - metabolism | LIM-Homeodomain Proteins | Mice | Transcription Factors | Goblet Cells - pathology | Intestine, Small - metabolism | Somatostatin-Secreting Cells - metabolism | Hepatocyte Nuclear Factor 3-beta - deficiency | Paired Box Transcription Factors - metabolism | Chromatin | Messenger RNA | DNA binding proteins | Cholecystokinin | Peptides | Mucins
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4. Full Text The Protein Disulfide Isomerase AGR2 Is Essential for Production of Intestinal Mucus
by Sung-Woo Park and Guohua Zhen and Catherine Verhaeghe and Yasuhiro Nakagami and Louis T. Nguyenvu and Andrea J. Barczak and Nigel Killeen and David J. Erle and Armando J. Parodi
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 4/2009, Volume 106, Issue 17, pp. 6950 - 6955
Protein disulfide isomerases (PDIs) aid protein folding and assembly by catalyzing formation and shuffling of cysteine disulfide bonds in the endoplasmic... 
Intestines | Messenger RNA | Epithelial cells | Disulfides | Mucins | Cell lines | Goblets | Mucus | Colitis | Animal social behavior | Goblet cell | Protein processing | Mucin | Endoplasmic reticulum | colitis | METASTASIS | protein processing | MULTIDISCIPLINARY SCIENCES | goblet cell | ULCERATIVE-COLITIS | CANCER-CELL-LINES | FAMILY | mucin | INFLAMMATION | GENE-EXPRESSION | ENDOPLASMIC-RETICULUM | MICE | endoplasmic reticulum | HUMAN HOMOLOG | Disulfides - metabolism | Epithelial Cells - metabolism | Protein Disulfide-Isomerases - metabolism | Colitis - genetics | Endoplasmic Reticulum - metabolism | Colitis - pathology | Intestines - metabolism | Rectal Prolapse - metabolism | Rectal Prolapse - pathology | Epithelial Cells - secretion | Colitis - chemically induced | Mucus - metabolism | Thioredoxins - metabolism | Rectal Prolapse - genetics | Epithelial Cells - cytology | Mucoproteins - genetics | Mucin-2 - metabolism | Acute Disease | Genetic Predisposition to Disease | Mice, Knockout | Cell Lineage | Animals | Colitis - metabolism | Mucoproteins - deficiency | Mice | Mucoproteins - metabolism | Development and progression | Isomerases | Properties | Intestinal mucosa | Index Medicus | Biological Sciences
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5. Full Text Indoleacrylic Acid Produced by Commensal Peptostreptococcus Species Suppresses Inflammation
by Wlodarska, Marta and Luo, Chengwei and Kolde, Raivo and d'Hennezel, Eva and Annand, John W and Heim, Cortney E and Krastel, Philipp and Schmitt, Esther K and Omar, Abdifatah S and Creasey, Elizabeth A and Garner, Ashley L and Mohammadi, Sina and O'Connell, Daniel J and Abubucker, Sahar and Arthur, Timothy D and Franzosa, Eric A and Huttenhower, Curtis and Murphy, Leon O and Haiser, Henry J and Vlamakis, Hera and Porter, Jeffrey A and Xavier, Ramnik J
Cell Host and Microbe, ISSN 1931-3128, 07/2017, Volume 22, Issue 1, pp. 25 - 37.e6
Host factors in the intestine help select for bacteria that promote health. Certain commensals can utilize mucins as an energy source, thus promoting their... 
indolepropionic acid | Muc2 | Peptostreptococcus | indoleacrylic acid | mucus | organoid | CELLS | BACTERIAL SYMBIONT | CROHNS-DISEASE | MUCIN | ULCERATIVE-COLITIS | MICROBIOLOGY | BOWEL-DISEASE | VIROLOGY | ARYL-HYDROCARBON RECEPTOR | GUT MICROBIOME | HEME OXYGENASE-1 | MUCUS | PARASITOLOGY | Mucin-2 - genetics | Humans | Intestinal Mucosa - secretion | Indoles - metabolism | Inflammation - metabolism | Organoids | Mucins - metabolism | Bacteria - classification | Clostridiales - genetics | Indoles - pharmacology | Mucin-2 - metabolism | Symbiosis | Bacteria - metabolism | Cytokines - metabolism | Anti-Inflammatory Agents - pharmacology | Colon - pathology | Inflammatory Bowel Diseases | Cytokines - secretion | Intestinal Mucosa - microbiology | Bacteria - genetics | Mucins - secretion | Clostridiales - metabolism | Peptostreptococcus - metabolism | Dysbiosis - metabolism | Bacteroides - genetics | Bacteroides - metabolism | Animals | Intestines - microbiology | Colon - microbiology | Intestinal Mucosa - injuries | Mice | Mucins - genetics | Metabolites | Analysis | Gastrointestinal diseases | Mucins | Tryptophan | Inflammation | Sugars | Monosaccharides
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6. Full Text Commensal Akkermansia muciniphila Exacerbates Gut Inflammation in Salmonella Typhimurium-Infected Gnotobiotic Mice
by Ganesh, Bhanu Priya and Klopfleisch, Robert and Loh, Gunnar and Blaut, Michael
PLoS ONE, ISSN 1932-6203, 09/2013, Volume 8, Issue 9, p. e74963
Excessive mucin degradation by intestinal bacteria may contribute to inflammatory bowel diseases because access of luminal antigens to the intestinal immune... 
VIRULENCE FACTORS | INTERFERON-GAMMA | MACROPHAGES | MULTIDISCIPLINARY SCIENCES | ULCERATIVE-COLITIS | GASTROINTESTINAL-TRACT | MOUSE MODEL | MICROBIOTA | PERSISTENT INFECTION | INTESTINAL EPITHELIAL-CELLS | BOWEL-DISEASE | Mucin-2 - metabolism | Symbiosis | Tumor Necrosis Factor-alpha - metabolism | Interleukin-1 - metabolism | Inflammation - microbiology | Salmonella Infections - complications | Salmonella typhimurium - pathogenicity | Lymph Nodes - metabolism | Interleukin-12 - metabolism | Interferon-gamma - metabolism | RNA, Messenger - metabolism | Mice, Inbred C3H | Verrucomicrobia - physiology | Macrophages - metabolism | Animals | Intestines - microbiology | Germ-Free Life | Salmonella Infections - microbiology | Mice | Chemokine CXCL10 - metabolism | Interleukin-6 - metabolism | Salmonella | Microbiota (Symbiotic organisms) | RNA | Gastrointestinal diseases | Bacteria | Inflammation | Histochemistry | Inflammatory bowel diseases | Homeostasis | Mucus | mRNA | Infections | Lymph nodes | Degradation | Interleukin 6 | Microbiota | Histopathology | E coli | Intestine | IP-10 protein | Digestive tract | Immune system | Biodegradation | Antigens | Goblet cells | Nutrition | Cytokines | Digestive system | Cecum | Interleukin 12 | Tumor necrosis factor-α | Interleukin 17 | Sulfation | Studies | Inflammatory bowel disease | Mucin | γ-Interferon | Interferon
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7. Full Text Studies of mucus in mouse stomach, small intestine, and colon. III. Gastrointestinal Muc5ac and Muc2 mucin O-glycan patterns reveal a regiospecific distribution
by Larsson, Jessica M. Holmén and Thomsson, Kristina A and Rodríguez-Piñeiro, Ana M and Karlsson, Hasse and Hansson, Gunnar C and Sahlgrenska akademin and Göteborgs universitet and Gothenburg University and Institutionen för biomedicin, avdelningen för medicinsk kemi och cellbiologi and Institute of Biomedicine, Department of Medical Biochemistry and Cell Biology and Sahlgrenska Academy
American Journal of Physiology - Gastrointestinal and Liver Physiology, ISSN 0193-1857, 09/2013, Volume 305, Issue 5, pp. G357 - G363
The mouse intestinal mucus is mainly made up by the gel-forming Muc2 mucin and the stomach surface mucus Muc5ac, both extensively O-glycosylated. The... 
Muc2 | Mucin | Glycomics | Oligosaccharide | Mass spectrometry | Glycan | Muc5ac | PHYSIOLOGY | GUT MICROBIOTA | GLYCOSYLATION | LINKED OLIGOSACCHARIDES | IDENTIFICATION | BLOOD-GROUP-A | LAYERS | oligosaccharide | glycan | glycomics | BIOSYNTHESIS | mass spectrometry | MICE | DIVERSITY | GASTROENTEROLOGY & HEPATOLOGY | EXPRESSION | Mucin-2 - metabolism | Intestinal Mucosa - metabolism | Sulfates - metabolism | Electrophoresis, Polyacrylamide Gel | Fucose - metabolism | Mice, Inbred C57BL | Male | Glycosylation | Gastric Mucosa - metabolism | N-Acetylneuraminic Acid - metabolism | Colon - metabolism | Animals | Mass Spectrometry | Chromatography, Liquid | Mucin 5AC - metabolism | Female | Mucus - metabolism | Mice | Intestine, Small - metabolism | Proteomics - methods | Physiological aspects | Mucus | Health aspects | Gastrointestinal system | Mucins | Mucosal Biology | methods | Hälsovetenskaper | ATES OF AMERICA | Klinisk medicin | NIPPOSTRONGYLUS-BRASILIENSIS | Sulfates | Gastric Mucosa | Polyacrylamide Gel | Intestine | Electrophoresis | Colon | HELICOBACTER-PYLORI | Health Sciences | Intestinal Mucosa | BACTERIA | Small | Mucin 5AC | GLYCOSYLTRANSFERASE | N-Acetylneuraminic Acid | Chromatography | Inbred C57BL | Mucin-2 | Clinical Medicine | Liquid | Proteomics | metabolism | Fucose
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8. Full Text Luminal Extracellular Vesicles (EVs) in Inflammatory Bowel Disease (IBD) Exhibit Proinflammatory Effects on Epithelial Cells and Macrophages
by Mitsuhashi, Shuji and Feldbrügge, Linda and Csizmadia, Eva and Mitsuhashi, Masato and Robson, Simon C and Moss, Alan C
Inflammatory Bowel Diseases, ISSN 1078-0998, 06/2016, Volume 22, Issue 7, pp. 1587 - 1595
Background:Extracellular vesicles (EVs) are membrane-enclosed particles released by cells as a means of intercellular communication. They are potential novel... 
inflammatory bowel disease | colitis | extracellular vesicles | OUTER-MEMBRANE VESICLES | MESSENGER-RNAS | IMMUNE CELLS | CROHNS-DISEASE | FLUID | EXOSOMES | GASTROENTEROLOGY & HEPATOLOGY | Mucin-2 - genetics | Tumor Necrosis Factor-alpha - metabolism | Interleukin-8 - genetics | Epithelial Cells - metabolism | Extracellular Vesicles - ultrastructure | Leukocyte Common Antigens - metabolism | Humans | RNA, Messenger - metabolism | Inflammatory Bowel Diseases - metabolism | Extracellular Vesicles - metabolism | Interleukins - metabolism | Antigens, CD - metabolism | Lipopolysaccharide Receptors - metabolism | alpha-Defensins - genetics | Epithelial Cells - physiology | Interleukins - genetics | Flow Cytometry | Inflammatory Bowel Diseases - genetics | Calgranulin B - genetics | Colon | Interleukin-8 - metabolism | Macrophages - physiology | Cell Line | Microscopy, Electron, Transmission | Mucin-1 - metabolism | Cell Adhesion Molecules - metabolism | GPI-Linked Proteins - metabolism | Particle Size | Animals | Transforming Growth Factor beta - genetics | Mice | Cell Movement
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9. Full Text SOX9 Is an Intestine Crypt Transcription Factor, Is Regulated by the Wnt Pathway, and Represses the CDX2 and MUC2 Genes
by Philippe Blache and Marc van de Wetering and Isabelle Duluc and Claire Domon and Philippe Berta and Jean-Noël Freund and Hans Clevers and Philippe Jay
The Journal of Cell Biology, ISSN 0021-9525, 7/2004, Volume 166, Issue 1, pp. 37 - 47
TCF and SOX proteins belong to the high mobility group box transcription factor family. Whereas TCFs, the transcriptional effectors of the Wnt pathway, have... 
Intestines | Transcription factors | Epithelial cells | Genes | Crypts | Cell lines | Stem cells | Epithelium | Cells | Intestinal mucosa | SOX9 | CDX2 | Differentiation | Intestinal epithelium | Wnt | differentiation | AUTOSOMAL SEX REVERSAL | CAMPOMELIC DYSPLASIA | II COLLAGEN GENE | EMBRYONIC INTESTINE | BETA-CATENIN | CELL BIOLOGY | SRY-RELATED GENE | NEURAL CREST DEVELOPMENT | CHONDROCYTE-SPECIFIC ENHANCER | COLORECTAL-CANCER | intestinal epithelium | HOMEOBOX GENE | Immunohistochemistry | Neoplasm Transplantation | Homeodomain Proteins - metabolism | Humans | Gene Expression Regulation, Neoplastic | Intestines - metabolism | Stem Cells - metabolism | Colonic Neoplasms - metabolism | Cell Nucleus - metabolism | Transfection | Mucins - metabolism | Cytoskeletal Proteins - metabolism | Transcription, Genetic | Cell Differentiation | RNA - metabolism | Epithelium - metabolism | High Mobility Group Proteins - metabolism | Signal Transduction | beta Catenin | DNA - metabolism | Reverse Transcriptase Polymerase Chain Reaction | Blotting, Western | Mucin-2 | Transcription Factors - metabolism | Blotting, Northern | Phenotype | Animals | Image Processing, Computer-Assisted | Cell Line, Tumor | Trans-Activators - metabolism | Mice | Carcinoma - metabolism | CDX2 Transcription Factor | SOX9 Transcription Factor | Microscopy, Fluorescence | Genetic transcription | Research | SOX9; Wnt; CDX2; intestinal epithelium; differentiation
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10. Full Text Bifidobacterium bifidum improves intestinal integrity in a rat model of necrotizing enterocolitis
by Khailova, Ludmila and Dvorak, Katerina and Arganbright, Kelly M and Halpern, Melissa D and Kinouchi, Toshi and Yajima, Masako and Dvorak, Bohuslav
American Journal of Physiology - Gastrointestinal and Liver Physiology, ISSN 0193-1857, 11/2009, Volume 297, Issue 5, pp. G940 - G949
Khailova L, Dvorak K, Arganbright KM, Halpern MD, Kinouchi T, Yajima M, Dvorak B. Bifidobacterium bifidum improves intestinal integrity in a rat model of... 
Adherens junctions | Tight junctions | Intestinal barrier function | Mucins | PHYSIOLOGY | intestinal barrier function | TREFOIL FACTORS | PROBIOTICS | PRETERM INFANTS | mucins | PARACELLULAR PERMEABILITY | adherens junctions | IN-VITRO | INFLAMMATORY-BOWEL-DISEASE | tight junctions | TNF-ALPHA | BACTERIAL-INFECTION | GASTROENTEROLOGY & HEPATOLOGY | COLONIC EPITHELIAL-CELLS | Mucin-2 - genetics | Ileum - pathology | Cadherins - metabolism | Enterocolitis, Necrotizing - therapy | Enterocytes - metabolism | Gene Expression - genetics | Enterocolitis, Necrotizing - metabolism | Tumor Necrosis Factor-alpha - genetics | Stress, Physiological | Ileum - metabolism | Enterocolitis, Necrotizing - microbiology | Intestines - metabolism | Adherens Junctions - metabolism | Incidence | Occludin | Catenins - metabolism | Interleukins - genetics | Trefoil Factor-3 | Asphyxia - complications | Membrane Proteins - metabolism | Neuropeptides - genetics | Enterocolitis, Necrotizing - pathology | Mucin-3 - genetics | Disease Models, Animal | Animals, Newborn | Mucin-2 - metabolism | Tight Junctions - metabolism | Cold Temperature | Bifidobacterium | Intestines - pathology | Rats | Neuropeptides - metabolism | Rats, Sprague-Dawley | Claudin-3 | Animals | Intestines - microbiology | Probiotics - therapeutic use | Junctional complexes (Epithelium) | Enterocolitis, Pseudomembranous | Enterocolitis, Neonatal necrotizing | Physiological aspects | Cell junctions | Development and progression | Models | Properties | Mediators | Inflammation | Immunity
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11. Full Text Esophageal Helicobacter pylori colonization aggravates esophageal injury caused by reflux
by Yun-Xiang Chu Wei-Hong Wang Yun Dai Gui-Gen Teng Shu-Jun Wang
世界胃肠病学杂志：英文版（电子版）, ISSN 1007-9327, 2014, Volume 20, Issue 42, pp. 15715 - 15726
AIM: To investigate esophageal Helicobacter pylori(H. pylori) colonization on esophageal injury caused by reflux and the related mechanisms. METHODS: An... 
Adenocarc | Metaplasia | pylori | Helicobacter | Esophagus | Adenocarcinoma | Animal model | Helicobacter pylori | INTESTINAL METAPLASIA | CDX2 | BARRETTS-ESOPHAGUS | ESOPHAGOGASTRODUODENAL ANASTOMOSIS | RAT MODEL | GASTROESOPHAGEAL-REFLUX | GASTRIC EPITHELIAL-CELLS | INFECTION | GASTROENTEROLOGY & HEPATOLOGY | EXPRESSION | Adenocarcinoma - pathology | Cell Proliferation | Homeodomain Proteins - metabolism | Ki-67 Antigen - metabolism | Male | RNA, Messenger - metabolism | Helicobacter Infections - pathology | Esophageal Neoplasms - pathology | Esophagus - microbiology | Adenocarcinoma - metabolism | Barrett Esophagus - pathology | Helicobacter Infections - metabolism | Disease Models, Animal | Barrett Esophagus - metabolism | bcl-2-Associated X Protein - metabolism | Esophagus - metabolism | Helicobacter Infections - genetics | Rats, Sprague-Dawley | Cyclin D1 - genetics | Proto-Oncogene Proteins c-myc - genetics | Helicobacter Infections - microbiology | Mucin-2 - genetics | Cyclin D1 - metabolism | Esophageal Neoplasms - microbiology | Helicobacter pylori - pathogenicity | Helicobacter Infections - complications | Proto-Oncogene Proteins c-bcl-2 - metabolism | Esophagitis, Peptic - pathology | Esophageal Neoplasms - metabolism | Adenocarcinoma - genetics | Barrett Esophagus - microbiology | Barrett Esophagus - genetics | bcl-2-Associated X Protein - genetics | Mucin-2 - metabolism | Severity of Illness Index | Adenocarcinoma - microbiology | Gene Expression Regulation | Esophagitis, Peptic - microbiology | Esophagitis, Peptic - metabolism | Transcription Factors - genetics | Proto-Oncogene Proteins c-myc - metabolism | Homeodomain Proteins - genetics | Transcription Factors - metabolism | Esophagus - pathology | Animals | Gastroesophageal Reflux - complications | Esophageal Neoplasms - genetics | Esophagitis, Peptic - genetics | CDX2 Transcription Factor | Proto-Oncogene Proteins c-bcl-2 - genetics | Apoptosis | Original
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12. Full Text A sentinel goblet cell guards the colonic crypt by triggering Nlrp6-dependent Muc2 secretion
by Birchenough, George M.H and Nystrom, Elisabeth E.L and Johansson, Malin E.V and Hansson, Gunnar C and Sahlgrenska akademin and Göteborgs universitet and Gothenburg University and Institutionen för biomedicin, avdelningen för medicinsk kemi och cellbiologi and Institute of Biomedicine, Department of Medical Biochemistry and Cell Biology and Sahlgrenska Academy
Science, ISSN 0036-8075, 06/2016, Volume 352, Issue 6293, pp. 1535 - 1542
Innate immune signaling pathways contribute to the protection of host tissue when bacterially challenged. Colonic goblet cells are responsible for generating... 
Mucin-2 - metabolism | Toll-Like Receptor 5 - metabolism | Reactive Oxygen Species - metabolism | Signal Transduction | Calcium - metabolism | Mice, Inbred C57BL | Receptors, Cell Surface - metabolism | Colon - immunology | Intestinal Mucosa - microbiology | Toll-Like Receptor 2 - metabolism | Immunity, Innate | Toll-Like Receptor 4 - metabolism | Goblet Cells - immunology | Bacteria - immunology | Animals | Intestinal Mucosa - immunology | Inflammasomes - immunology | Ligands | Colon - microbiology | Mice | Gastrointestinal Microbiome - immunology | Myeloid Differentiation Factor 88 - metabolism | Endocytosis - immunology | Receptors, Cell Surface - genetics | Bacteria | Microbiology | Digestive system | Immune system | Tableware | Crypts | Guards | Mucus | Secretions | Epithelium | Protective | inflammasome activation | Clinical Medicine | Klinisk medicin | mucosa
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13. Full Text Neurenteric cyst or neuroendodermal cyst? Immunohistochemical study and pathogenesis
by Chen, Chun-Ting and Lai, Hung-Yi and Jung, Shih-Ming and Lee, Ching-Yi and Wu, Chieh-Tsai and Lee, Shih-Tseng
World Neurosurgery, ISSN 1878-8750, 2016, Volume 96, pp. 85 - 90
Abstract Background Neurenteric cysts are rare central nervous system lesions derived from an endodermal origin. There is no consensus concerning pathogenesis... 
Neurosurgery | Neuroendodermal cysts | Immunohistochemical | Endodermal cysts | Neurenteric cysts | Pathogenesis | OVARY | SURGERY | MANAGEMENT | CDX2 | CEREBELLOPONTINE ANGLE | PATHOLOGY | CLINICAL NEUROLOGY | ENTITY | MUC2 | CK20 | RESPIRATORY EPITHELIAL CYST | EXPRESSION | Immunohistochemistry | Central Nervous System Diseases - pathology | Recurrence | Thyroid Nuclear Factor 1 | Neural Tube Defects - diagnostic imaging | Cysts - surgery | Humans | Middle Aged | Alkaline Phosphatase - metabolism | Neural Tube Defects - pathology | Infant | Male | Neural Tube Defects - metabolism | Central Nervous System Diseases - metabolism | Young Adult | Cysts - metabolism | Isoenzymes - metabolism | Platelet Endothelial Cell Adhesion Molecule-1 - metabolism | Adult | Female | Retrospective Studies | Child | Endoderm | Mucin-2 - metabolism | Diagnosis, Differential | Central Nervous System Diseases - diagnostic imaging | Nuclear Proteins - metabolism | Neural Tube Defects - surgery | Cysts - pathology | Chorionic Gonadotropin - metabolism | GPI-Linked Proteins - metabolism | Transcription Factors - metabolism | CDX2 Transcription Factor - metabolism | Cysts - diagnostic imaging | Keratin-7 - metabolism | Central Nervous System Diseases - surgery | Mucin 5AC - metabolism | Aged | Keratin-20 - metabolism | Keratin | Medical research | Phosphatases | Chorionic gonadotropin | Mucins | Medicine, Experimental | Cell differentiation | Index Medicus
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14. Full Text Human Clostridium difficile infection: Altered mucus production and composition
by Engevik, Melinda A and Yacyshyn, Mary Beth and Engevik, Kristen A and Wang, Jiang and