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science & technology (769) 769
life sciences & biomedicine (717) 717
humans (678) 678
mucin-2 (424) 424
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mucin-2 - metabolism (355) 355
male (340) 340
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immunohistochemistry (264) 264
mucins - metabolism (250) 250
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biochemistry & molecular biology (130) 130
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intestinal mucosa - metabolism (121) 121
mucins - biosynthesis (120) 120
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gastroenterology. liver. pancreas. abdomen (111) 111
adenocarcinoma - metabolism (99) 99
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immunology (72) 72
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molecular sequence data (69) 69
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stomach. duodenum. small intestine. colon. rectum. anus (66) 66
research (65) 65
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stomach neoplasms - metabolism (64) 64
gene expression regulation, neoplastic (63) 63
mucin 5ac - metabolism (63) 63
glycosylation (62) 62
homeodomain proteins - metabolism (62) 62
mice, knockout (62) 62
proteins (62) 62
stomach neoplasms - pathology (62) 62
disease models, animal (59) 59
mucin-2 - biosynthesis (59) 59
mucins - analysis (59) 59
colorectal neoplasms - metabolism (57) 57
gene expression regulation (57) 57
intestinal mucosa - pathology (57) 57
reverse transcriptase polymerase chain reaction (56) 56
rna, messenger - genetics (56) 56
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bacteria (54) 54
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multidisciplinary sciences (52) 52
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surgery (52) 52
cell differentiation (51) 51
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colorectal neoplasms - pathology (50) 50
epithelial cells - metabolism (50) 50
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colonic neoplasms - metabolism (49) 49
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fundamental and applied biological sciences. psychology (48) 48
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microbiology (48) 48
pancreatic neoplasms - pathology (48) 48
physiology (48) 48
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1. 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 (New York, N.Y. 1943), ISSN 0016-5085, 2009, Volume 137, Issue 6, pp. 2052 - 2062
Gastroenterology and Hepatology | Gastroenterology & Hepatology | Life Sciences & Biomedicine | Science & Technology | 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 | Index Medicus | Abridged Index Medicus
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2. Full Text The protective effect of icariin and phosphorylated icariin against LPS-induced intestinal goblet cell dysfunction
by Xiong, Wen and Ma, Haoyue and Zhang, Zhu and Jin, Meilan and Wang, Jian and Xu, Yuwei and Wang, Zili
Innate immunity (London, England), ISSN 1753-4259, 2/2020, Volume 26, Issue 2, pp. 97 - 106
Biochemistry & Molecular Biology | Immunology | Life Sciences & Biomedicine | Microbiology | Medicine, Research & Experimental | Science & Technology | Research & Experimental Medicine | L-Lactate Dehydrogenase - metabolism | Tumor Necrosis Factor-alpha - metabolism | Transcription Factor CHOP - genetics | Phosphorylation | Reactive Oxygen Species - metabolism | Apoptosis - drug effects | Goblet Cells - enzymology | Humans | Caspase 3 - metabolism | Apoptosis - genetics | Goblet Cells - drug effects | Caspases, Initiator - genetics | Heat-Shock Proteins - genetics | Inflammation - metabolism | Caspases, Initiator - metabolism | Interleukin-1beta - metabolism | Superoxide Dismutase-1 - metabolism | Caspase 3 - genetics | Flavonoids - pharmacology | Interleukin-8 - metabolism | Interleukin-6 - metabolism | Malondialdehyde - metabolism | Mucin-2 - metabolism | Cell Survival - drug effects | Glutathione Peroxidase - metabolism | Heat-Shock Proteins - metabolism | Goblet Cells - metabolism | Hydrogen Peroxide - metabolism | Catalase - metabolism | X-Box Binding Protein 1 - metabolism | Flavonoids - metabolism | Lipopolysaccharides - pharmacology | Inflammation - genetics | Cell Proliferation - drug effects | Transcription Factor CHOP - metabolism | Mucin-2 - biosynthesis | X-Box Binding Protein 1 - genetics | Oxidative stress | Hydrogen peroxide | Cell viability | Tumor necrosis factor-α | Caspase-4 | IL-1β | Caspase-3 | L-Lactate dehydrogenase | Lipopolysaccharides | Interleukin 6 | Mucin | Enzymatic activity | Intestine | Lactic acid | Interleukin 8 | Apoptosis | Index Medicus | Icariin | phosphorylated icariin | mucus barrier | LS174T cells | Original | LPS
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3. 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
dextran sodium sulfate | estrogen receptor‐beta | colon cancer | azoxymethane | inflammatory bowel disease | estrogen receptor-beta | Gastroenterology. Liver. Pancreas. Abdomen | Stomach. Duodenum. Small intestine. Colon. Rectum. Anus | Biological and medical sciences | Medical sciences | Other diseases. Semiology | Tumors | 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 | Index Medicus | Estrogen receptor-beta
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4. 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
β-catenin | Gastric adenocarcinoma | Helicobacter pylori CagA | E-cadherin | Intestinal metaplasia | Biochemistry & Molecular Biology | Oncology | Genetics & Heredity | Life Sciences & Biomedicine | Science & Technology | Cell Biology | Biological and medical sciences | Cell physiology | Molecular and cellular biology | Medical sciences | Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes | Fundamental and applied biological sciences. Psychology | Gastroenterology. Liver. Pancreas. Abdomen | Stomach. Duodenum. Small intestine. Colon. Rectum. Anus | Bacterial diseases of the digestive system and abdomen | Infectious diseases | Bacterial diseases | Human bacterial diseases | Tumors | 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 | Index Medicus
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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 & microbe, ISSN 1931-3128, 07/2017, Volume 22, Issue 1, pp. 25 - 37.e6
indolepropionic acid | Muc2 | Peptostreptococcus | indoleacrylic acid | mucus | organoid | Parasitology | Life Sciences & Biomedicine | Microbiology | Science & Technology | Virology | 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 | Index Medicus
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6. 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
inflammatory bowel disease | colitis | extracellular vesicles | Gastroenterology & Hepatology | Life Sciences & Biomedicine | Science & Technology | 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 | Index Medicus
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7. 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 (American Association for the Advancement of Science), ISSN 0036-8075, 06/2016, Volume 352, Issue 6293, pp. 1535 - 1542
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 | Index Medicus | Tableware | Crypts | Guards | Mucus | Secretions | Epithelium | Protective | inflammasome activation | Clinical Medicine | Klinisk medicin | mucosa
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8. 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
Intestines | Transcription factors | Epithelial cells | Genes | Crypts | Cell lines | Stem cells | Epithelium | Cells | Intestinal mucosa | SOX9 | CDX2 | Differentiation | Intestinal epithelium | Wnt | Life Sciences & Biomedicine | Science & Technology | Cell Biology | 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 | Proteins | Signal transduction | Gene expression | Small intestine | Index Medicus | High Mobility Group Proteins | Cytoskeletal Proteins | Carcinoma | RNA | Stem Cells | Life Sciences | Genetics | Trans-Activators | Human health and pathology | Homeodomain Proteins | DNA | Mucins | Transcription Factors | Cell Nucleus | Colonic Neoplasms | Cancer | SOX9; Wnt; CDX2; intestinal epithelium; differentiation
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9. 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
World journal of gastroenterology : WJG, ISSN 1007-9327, 2014, Volume 20, Issue 42, pp. 15715 - 15726
Adenocarc | Metaplasia | pylori | Helicobacter | Esophagus | Adenocarcinoma | Animal model | Helicobacter pylori | Gastroenterology & Hepatology | Life Sciences & Biomedicine | Science & Technology | 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 | Index Medicus | Original
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