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Publication DateFASEB Journal, ISSN 0892-6638, 04/2017, Volume 31, Issue 4, pp. 1516 - 1530
Chronic inflammation is known to be a key causative factor in tumor progression, but we do not yet fully understand the molecular mechanism through which...
IL-1β | Colon cancer | FOXO3a | PHOSPHORYLATION | colon cancer | CYTOKINE REGULATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | IL-1 beta | PROLIFERATION | CELL BIOLOGY | INTESTINAL INFLAMMATION | CARCINOGENESIS | COLITIS | COLORECTAL-CANCER | CELL-MIGRATION | BIOLOGY | STRESS | PROMOTES | Colon - cytology | Syndecan-2 - metabolism | Cell Line | Intestinal Mucosa - metabolism | Colitis, Ulcerative - metabolism | Humans | Mice, Inbred C57BL | Male | NF-kappa B - metabolism | Colon - metabolism | Forkhead Box Protein O3 - metabolism | Oxygen - metabolism | Cell Hypoxia | HT29 Cells | Animals | Interleukin-1beta - metabolism | Syndecan-2 - genetics | Mice | p38 Mitogen-Activated Protein Kinases - metabolism | Transcription | Moon | Epithelial cells | Colorectal cancer | Activation | Sulfates | Cell surface | Azoxymethane | Rodents | Dextran sulfate | Colon | Localization | FOXO3 protein | Heparan sulfate | NF-κB protein | MAP kinase | Inflammation | Inflammatory bowel disease | Dextran | Sodium | Cell lines | Hypoxia | Sulfate | Colitis | Syndecan | Tumors | Cancer
IL-1β | Colon cancer | FOXO3a | PHOSPHORYLATION | colon cancer | CYTOKINE REGULATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | IL-1 beta | PROLIFERATION | CELL BIOLOGY | INTESTINAL INFLAMMATION | CARCINOGENESIS | COLITIS | COLORECTAL-CANCER | CELL-MIGRATION | BIOLOGY | STRESS | PROMOTES | Colon - cytology | Syndecan-2 - metabolism | Cell Line | Intestinal Mucosa - metabolism | Colitis, Ulcerative - metabolism | Humans | Mice, Inbred C57BL | Male | NF-kappa B - metabolism | Colon - metabolism | Forkhead Box Protein O3 - metabolism | Oxygen - metabolism | Cell Hypoxia | HT29 Cells | Animals | Interleukin-1beta - metabolism | Syndecan-2 - genetics | Mice | p38 Mitogen-Activated Protein Kinases - metabolism | Transcription | Moon | Epithelial cells | Colorectal cancer | Activation | Sulfates | Cell surface | Azoxymethane | Rodents | Dextran sulfate | Colon | Localization | FOXO3 protein | Heparan sulfate | NF-κB protein | MAP kinase | Inflammation | Inflammatory bowel disease | Dextran | Sodium | Cell lines | Hypoxia | Sulfate | Colitis | Syndecan | Tumors | Cancer
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A cell-intrinsic role for TLR2–MYD88 in intestinal and breast epithelia and oncogenesis
Nature Cell Biology, ISSN 1465-7392, 11/2014, Volume 16, Issue 12, pp. 1238 - 1248
It has been postulated that there is a link between inflammation and cancer. Here we describe a role for cell-intrinsic toll-like receptor-2 (TLR2; which is...
ADAPTIVE IMMUNITY | FUNCTIONAL MAMMARY-GLAND | RECOGNITION | INFLAMMATION | TOLL-LIKE RECEPTORS | TUMOR-SUPPRESSOR | IDENTIFICATION | GROUP BOX-1 PROTEIN | DUCTAL MORPHOGENESIS | CANCER STEM-CELLS | CELL BIOLOGY | Dextran Sulfate | Neoplasm Transplantation | Colonic Neoplasms - genetics | Intestinal Mucosa - metabolism | Interleukin-1 Receptor-Associated Kinases - genetics | Toll-Like Receptor 2 - antagonists & inhibitors | Toll-Like Receptor 2 - genetics | Receptors, G-Protein-Coupled - metabolism | Humans | Colitis - pathology | Breast - metabolism | Carcinogenesis - metabolism | Epithelial Cell Adhesion Molecule | Lipopolysaccharide Receptors - metabolism | RNA Interference | Regeneration - genetics | Colitis - chemically induced | Myeloid Differentiation Factor 88 - antagonists & inhibitors | HEK293 Cells | Antigens, Neoplasm - metabolism | Female | Tumor Cells, Cultured | Breast - pathology | Epithelium - pathology | Signal Transduction | Mice, Inbred C57BL | Carcinogenesis - genetics | Myeloid Differentiation Factor 88 - genetics | Toll-Like Receptor 2 - metabolism | Cell Adhesion Molecules - metabolism | Mice, Knockout | Animals | Breast Neoplasms - genetics | Breast Neoplasms - pathology | Colonic Neoplasms - pathology | Interleukin-1 Receptor-Associated Kinases - antagonists & inhibitors | Leukocyte Common Antigens - genetics | Mice | RNA, Small Interfering | Myeloid Differentiation Factor 88 - metabolism | Intestinal Mucosa - pathology | Toll-like receptors | Development and progression | Genetic aspects | Breast cancer | Properties | Gastrointestinal cancer
ADAPTIVE IMMUNITY | FUNCTIONAL MAMMARY-GLAND | RECOGNITION | INFLAMMATION | TOLL-LIKE RECEPTORS | TUMOR-SUPPRESSOR | IDENTIFICATION | GROUP BOX-1 PROTEIN | DUCTAL MORPHOGENESIS | CANCER STEM-CELLS | CELL BIOLOGY | Dextran Sulfate | Neoplasm Transplantation | Colonic Neoplasms - genetics | Intestinal Mucosa - metabolism | Interleukin-1 Receptor-Associated Kinases - genetics | Toll-Like Receptor 2 - antagonists & inhibitors | Toll-Like Receptor 2 - genetics | Receptors, G-Protein-Coupled - metabolism | Humans | Colitis - pathology | Breast - metabolism | Carcinogenesis - metabolism | Epithelial Cell Adhesion Molecule | Lipopolysaccharide Receptors - metabolism | RNA Interference | Regeneration - genetics | Colitis - chemically induced | Myeloid Differentiation Factor 88 - antagonists & inhibitors | HEK293 Cells | Antigens, Neoplasm - metabolism | Female | Tumor Cells, Cultured | Breast - pathology | Epithelium - pathology | Signal Transduction | Mice, Inbred C57BL | Carcinogenesis - genetics | Myeloid Differentiation Factor 88 - genetics | Toll-Like Receptor 2 - metabolism | Cell Adhesion Molecules - metabolism | Mice, Knockout | Animals | Breast Neoplasms - genetics | Breast Neoplasms - pathology | Colonic Neoplasms - pathology | Interleukin-1 Receptor-Associated Kinases - antagonists & inhibitors | Leukocyte Common Antigens - genetics | Mice | RNA, Small Interfering | Myeloid Differentiation Factor 88 - metabolism | Intestinal Mucosa - pathology | Toll-like receptors | Development and progression | Genetic aspects | Breast cancer | Properties | Gastrointestinal cancer
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Loading RightsClinical & Experimental Immunology, ISSN 0009-9104, 03/2017, Volume 187, Issue 3, pp. 428 - 440
Summary Intestinal epithelial cells (IECs), an important barrier to gut microbiota, are subject to low oxygen tension, particularly during intestinal...
HIF‐1α | IL‐33 | inflammatory bowel disease | IL-33 | HIF-1α | CELLS | IL-33 PROMOTES | ACTIVATION | HIF-1 alpha | IMMUNE HOMEOSTASIS | IFN-GAMMA | MICROBIOTA | FACTOR-I | KAPPA-B | IMMUNOLOGY | TUMOR-NECROSIS-FACTOR | TNF-ALPHA | Tumor Necrosis Factor-alpha - metabolism | Intestinal Mucosa - metabolism | Humans | Mice, Inbred C57BL | Male | Intestines - metabolism | Inflammatory Bowel Diseases - metabolism | Colon - metabolism | Hypoxia - metabolism | Inflammation - metabolism | Animals | Hypoxia-Inducible Factor 1, alpha Subunit - metabolism | Homeostasis - physiology | Colitis - metabolism | Interleukin-33 - metabolism | Adult | Female | Mice | Original
HIF‐1α | IL‐33 | inflammatory bowel disease | IL-33 | HIF-1α | CELLS | IL-33 PROMOTES | ACTIVATION | HIF-1 alpha | IMMUNE HOMEOSTASIS | IFN-GAMMA | MICROBIOTA | FACTOR-I | KAPPA-B | IMMUNOLOGY | TUMOR-NECROSIS-FACTOR | TNF-ALPHA | Tumor Necrosis Factor-alpha - metabolism | Intestinal Mucosa - metabolism | Humans | Mice, Inbred C57BL | Male | Intestines - metabolism | Inflammatory Bowel Diseases - metabolism | Colon - metabolism | Hypoxia - metabolism | Inflammation - metabolism | Animals | Hypoxia-Inducible Factor 1, alpha Subunit - metabolism | Homeostasis - physiology | Colitis - metabolism | Interleukin-33 - metabolism | Adult | Female | Mice | Original
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Loading RightsCell Calcium, ISSN 0143-4160, 2014, Volume 55, Issue 6, pp. 355 - 361
Abstract Fluid and electrolyte releasing from secretory epithelia are elaborately regulated by orchestrated activity of ion channels. The activity of chloride...
Advanced Basic Science | Salivary gland acinar cell | Anoctamin1 | Ca2+-activated Cl− channel | TMEM16A | Airway epithelium | Fluid secretion | Intestinal epithelium | AIRWAY MUCUS FUNCTION | ION-TRANSPORT | PROTEIN-KINASE | CELL BIOLOGY | GLAND ACINAR-CELLS | Ca2+-activated Cl- channel | CA2+-ACTIVATED CL-CHANNELS | CALCIUM | INTESTINAL CRYPT | CYSTIC-FIBROSIS | ACTIVATED CHLORIDE CHANNELS | Intestinal Mucosa - metabolism | Epithelium - metabolism | Signal Transduction | Calcium - metabolism | Humans | Intestinal Mucosa - secretion | Epithelium - secretion | Salivary Glands - secretion | Cystic Fibrosis Transmembrane Conductance Regulator - metabolism | Chloride Channels - metabolism | Mucins - metabolism | Respiratory Mucosa - metabolism | Cyclic AMP - metabolism | Salivary Glands - metabolism | Respiratory Mucosa - secretion | Cystic fibrosis
Advanced Basic Science | Salivary gland acinar cell | Anoctamin1 | Ca2+-activated Cl− channel | TMEM16A | Airway epithelium | Fluid secretion | Intestinal epithelium | AIRWAY MUCUS FUNCTION | ION-TRANSPORT | PROTEIN-KINASE | CELL BIOLOGY | GLAND ACINAR-CELLS | Ca2+-activated Cl- channel | CA2+-ACTIVATED CL-CHANNELS | CALCIUM | INTESTINAL CRYPT | CYSTIC-FIBROSIS | ACTIVATED CHLORIDE CHANNELS | Intestinal Mucosa - metabolism | Epithelium - metabolism | Signal Transduction | Calcium - metabolism | Humans | Intestinal Mucosa - secretion | Epithelium - secretion | Salivary Glands - secretion | Cystic Fibrosis Transmembrane Conductance Regulator - metabolism | Chloride Channels - metabolism | Mucins - metabolism | Respiratory Mucosa - metabolism | Cyclic AMP - metabolism | Salivary Glands - metabolism | Respiratory Mucosa - secretion | Cystic fibrosis
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IFN-gamma-Mediated Induction of an Apical IL-10 Receptor on Polarized Intestinal Epithelia
JOURNAL OF IMMUNOLOGY, ISSN 0022-1767, 02/2014, Volume 192, Issue 3, pp. 1267 - 1276
Cytokines secreted at sites of inflammation impact the onset, progression, and resolution of inflammation. In this article, we investigated potential...
RECOMBINANT HUMAN INTERLEUKIN-10 | INFLAMMATORY-BOWEL-DISEASE | TGF-BETA | INDUCIBLE FACTOR-I | EXPERIMENTAL COLITIS | INTERFERON-GAMMA | BARRIER FUNCTION | IMMUNOLOGY | ACTIVE CROHNS-DISEASE | HYPOXIA | T-CELLS | Cell Polarity | Intestinal Mucosa - metabolism | Epithelial Cells - metabolism | Fluorescein-5-isothiocyanate - pharmacokinetics | Epithelial Cells - drug effects | Humans | Interleukin-10 Receptor alpha Subunit - biosynthesis | Interleukin-10 - physiology | Dextrans - pharmacokinetics | Colitis - chemically induced | Interferon-gamma - genetics | Cytokines - genetics | STAT3 Transcription Factor - metabolism | Cell Line | Mice, Inbred C57BL | Gene Expression Regulation | Epithelial Cells - ultrastructure | Interferon-gamma - physiology | Suppressor of Cytokine Signaling Proteins - genetics | Fluorescein-5-isothiocyanate - analogs & derivatives | Permeability | Recombinant Proteins - pharmacology | Dextran Sulfate - toxicity | Suppressor of Cytokine Signaling 3 Protein | Animals | Interleukin-10 Receptor alpha Subunit - genetics | Colitis - metabolism | Mice | Suppressor of Cytokine Signaling Proteins - biosynthesis | Cytokines - biosynthesis | Interferon-gamma - biosynthesis | Interferon-gamma - pharmacology
RECOMBINANT HUMAN INTERLEUKIN-10 | INFLAMMATORY-BOWEL-DISEASE | TGF-BETA | INDUCIBLE FACTOR-I | EXPERIMENTAL COLITIS | INTERFERON-GAMMA | BARRIER FUNCTION | IMMUNOLOGY | ACTIVE CROHNS-DISEASE | HYPOXIA | T-CELLS | Cell Polarity | Intestinal Mucosa - metabolism | Epithelial Cells - metabolism | Fluorescein-5-isothiocyanate - pharmacokinetics | Epithelial Cells - drug effects | Humans | Interleukin-10 Receptor alpha Subunit - biosynthesis | Interleukin-10 - physiology | Dextrans - pharmacokinetics | Colitis - chemically induced | Interferon-gamma - genetics | Cytokines - genetics | STAT3 Transcription Factor - metabolism | Cell Line | Mice, Inbred C57BL | Gene Expression Regulation | Epithelial Cells - ultrastructure | Interferon-gamma - physiology | Suppressor of Cytokine Signaling Proteins - genetics | Fluorescein-5-isothiocyanate - analogs & derivatives | Permeability | Recombinant Proteins - pharmacology | Dextran Sulfate - toxicity | Suppressor of Cytokine Signaling 3 Protein | Animals | Interleukin-10 Receptor alpha Subunit - genetics | Colitis - metabolism | Mice | Suppressor of Cytokine Signaling Proteins - biosynthesis | Cytokines - biosynthesis | Interferon-gamma - biosynthesis | Interferon-gamma - pharmacology
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Loading RightsNature, ISSN 0028-0836, 04/2016, Volume 532, Issue 7597, pp. 117 - 121
Colonic epithelial cells are covered by thick inner and outer mucus layers(1,2). The inner mucus layer is free of commensal microbiota, which contributes to...
BACTERIA | HOMEOSTASIS | LECTIN | MUCIN | MULTIDISCIPLINARY SCIENCES | GUT | HOST | PANETH CELLS | INTESTINE | MUCUS LAYERS | MOLECULES | Inflammation - chemically induced | Dextran Sulfate | Intestinal Mucosa - metabolism | Proteus mirabilis - metabolism | Colitis - genetics | Humans | Intestinal Mucosa - secretion | Homeostasis | Male | Gram-Negative Bacteria - metabolism | Intestinal Mucosa - cytology | GPI-Linked Proteins - deficiency | Inflammation - drug therapy | Colitis - chemically induced | Epithelium - microbiology | Female | GPI-Linked Proteins - secretion | Colitis - drug therapy | Proteus mirabilis - pathogenicity | Gram-Negative Bacteria - physiology | Caco-2 Cells | Symbiosis | Cell Line | Intestinal Mucosa - microbiology | GPI-Linked Proteins - metabolism | Bacterial Adhesion | Gram-Negative Bacteria - drug effects | Animals | Gram-Negative Bacteria - pathogenicity | Inflammation - genetics | Colon - microbiology | Mice | Flagella | Proteus mirabilis - drug effects | GPI-Linked Proteins - genetics | Physiological aspects | Colon (Anatomy) | Microbiota (Symbiotic organisms) | Epithelial cells | Proteins | Inflammatory bowel disease | Motility | Pathogenesis | Large intestine | Rodents | Bacteria | Inflammation | Colon | Small intestine | Molecular weight
BACTERIA | HOMEOSTASIS | LECTIN | MUCIN | MULTIDISCIPLINARY SCIENCES | GUT | HOST | PANETH CELLS | INTESTINE | MUCUS LAYERS | MOLECULES | Inflammation - chemically induced | Dextran Sulfate | Intestinal Mucosa - metabolism | Proteus mirabilis - metabolism | Colitis - genetics | Humans | Intestinal Mucosa - secretion | Homeostasis | Male | Gram-Negative Bacteria - metabolism | Intestinal Mucosa - cytology | GPI-Linked Proteins - deficiency | Inflammation - drug therapy | Colitis - chemically induced | Epithelium - microbiology | Female | GPI-Linked Proteins - secretion | Colitis - drug therapy | Proteus mirabilis - pathogenicity | Gram-Negative Bacteria - physiology | Caco-2 Cells | Symbiosis | Cell Line | Intestinal Mucosa - microbiology | GPI-Linked Proteins - metabolism | Bacterial Adhesion | Gram-Negative Bacteria - drug effects | Animals | Gram-Negative Bacteria - pathogenicity | Inflammation - genetics | Colon - microbiology | Mice | Flagella | Proteus mirabilis - drug effects | GPI-Linked Proteins - genetics | Physiological aspects | Colon (Anatomy) | Microbiota (Symbiotic organisms) | Epithelial cells | Proteins | Inflammatory bowel disease | Motility | Pathogenesis | Large intestine | Rodents | Bacteria | Inflammation | Colon | Small intestine | Molecular weight
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Loading RightsJournal of Virology, ISSN 0022-538X, 03/2012, Volume 86, Issue 5, pp. 2556 - 2570
Article Usage Stats Services JVI Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley...
CHEMOKINE RECEPTOR EXPRESSION | VIROLOGY | BREAST-MILK MACROPHAGES | LYMPHOCYTE SUBSETS | HUMAN-IMMUNODEFICIENCY-VIRUS | TO-CHILD TRANSMISSION | AMNIOTIC-FLUID | CORECEPTOR EXPRESSION | SUBCLINICAL MASTITIS | LANGERHANS CELLS | PRIMARY INFECTION | HIV Infections - virology | Humans | Middle Aged | Mouth Mucosa - immunology | Male | Intestinal Mucosa - virology | Infectious Disease Transmission, Vertical | Epithelium - virology | T-Lymphocytes - virology | Fetal Diseases - virology | Epithelium - immunology | HIV Infections - immunology | HIV-1 - physiology | Macrophages - virology | Intestinal Mucosa - immunology | Mouth Mucosa - virology | Adult | Female | HIV Infections - transmission | T-Lymphocytes - immunology | Macrophages - immunology | Virus-Cell Interactions
CHEMOKINE RECEPTOR EXPRESSION | VIROLOGY | BREAST-MILK MACROPHAGES | LYMPHOCYTE SUBSETS | HUMAN-IMMUNODEFICIENCY-VIRUS | TO-CHILD TRANSMISSION | AMNIOTIC-FLUID | CORECEPTOR EXPRESSION | SUBCLINICAL MASTITIS | LANGERHANS CELLS | PRIMARY INFECTION | HIV Infections - virology | Humans | Middle Aged | Mouth Mucosa - immunology | Male | Intestinal Mucosa - virology | Infectious Disease Transmission, Vertical | Epithelium - virology | T-Lymphocytes - virology | Fetal Diseases - virology | Epithelium - immunology | HIV Infections - immunology | HIV-1 - physiology | Macrophages - virology | Intestinal Mucosa - immunology | Mouth Mucosa - virology | Adult | Female | HIV Infections - transmission | T-Lymphocytes - immunology | Macrophages - immunology | Virus-Cell Interactions
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Loading RightsGastroenterology, ISSN 0016-5085, 11/2017, Volume 153, Issue 5, pp. 1338 - 1350.e3
Diarrhea associated with inflammatory bowel diseases has been associated with increased levels of inflammatory cytokines, including tumor necrosis factor...
NaCl Absorption | Intestinal Inflammation | Ion Transporter | Mouse Model | DIARRHEA | IFN-GAMMA | BARRIER | MECHANISMS | INHIBITION | IN-VIVO | GENE-EXPRESSION | MICE | ADENOMA DRA | GASTROENTEROLOGY & HEPATOLOGY | INFLAMMATORY BOWEL DISEASES | Chloride-Bicarbonate Antiporters - genetics | Intestinal Mucosa - metabolism | Epithelial Cells - metabolism | Epithelial Cells - drug effects | Humans | Intestinal Absorption - drug effects | NF-kappa B - metabolism | Inflammatory Bowel Diseases - metabolism | Intestinal Mucosa - drug effects | Dose-Response Relationship, Drug | Transfection | RNA Interference | Time Factors | Antiporters - genetics | Inflammatory Bowel Diseases - genetics | Inflammatory Bowel Diseases - complications | Caco-2 Cells | Promoter Regions, Genetic | Down-Regulation | Mice, Inbred C57BL | Antiporters - metabolism | Epithelial Cells - pathology | HT29 Cells | Tumor Necrosis Factor-alpha - pharmacology | Chloride-Bicarbonate Antiporters - metabolism | Animals | NF-kappa B - genetics | Diarrhea - genetics | Diarrhea - etiology | Diarrhea - metabolism | Mice | Intestinal Mucosa - pathology
NaCl Absorption | Intestinal Inflammation | Ion Transporter | Mouse Model | DIARRHEA | IFN-GAMMA | BARRIER | MECHANISMS | INHIBITION | IN-VIVO | GENE-EXPRESSION | MICE | ADENOMA DRA | GASTROENTEROLOGY & HEPATOLOGY | INFLAMMATORY BOWEL DISEASES | Chloride-Bicarbonate Antiporters - genetics | Intestinal Mucosa - metabolism | Epithelial Cells - metabolism | Epithelial Cells - drug effects | Humans | Intestinal Absorption - drug effects | NF-kappa B - metabolism | Inflammatory Bowel Diseases - metabolism | Intestinal Mucosa - drug effects | Dose-Response Relationship, Drug | Transfection | RNA Interference | Time Factors | Antiporters - genetics | Inflammatory Bowel Diseases - genetics | Inflammatory Bowel Diseases - complications | Caco-2 Cells | Promoter Regions, Genetic | Down-Regulation | Mice, Inbred C57BL | Antiporters - metabolism | Epithelial Cells - pathology | HT29 Cells | Tumor Necrosis Factor-alpha - pharmacology | Chloride-Bicarbonate Antiporters - metabolism | Animals | NF-kappa B - genetics | Diarrhea - genetics | Diarrhea - etiology | Diarrhea - metabolism | Mice | Intestinal Mucosa - pathology
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Epithelia Use Butyrophilin-like Molecules to Shape Organ-Specific γδ T Cell Compartments
Cell, ISSN 0092-8674, 09/2016, Volume 167, Issue 1, pp. 203 - 218.e17
Many body surfaces harbor organ-specific γδ T cell compartments that contribute to tissue integrity. Thus, murine dendritic epidermal T cells (DETCs) uniquely...
Animals | Butyrophilins - immunology | Butyrophilins - genetics | Intestinal Mucosa - immunology | Humans | Mice, Inbred C57BL | Receptors, Antigen, T-Cell, gamma-delta - immunology | T-Lymphocytes - immunology | Thymus Gland - immunology | Mice | Gene Knockout Techniques | Thymus Gland | Life Sciences | Intestinal Mucosa | Immunology | T-Lymphocytes | Butyrophilins | Receptors, Antigen, T-Cell, gamma-delta
Animals | Butyrophilins - immunology | Butyrophilins - genetics | Intestinal Mucosa - immunology | Humans | Mice, Inbred C57BL | Receptors, Antigen, T-Cell, gamma-delta - immunology | T-Lymphocytes - immunology | Thymus Gland - immunology | Mice | Gene Knockout Techniques | Thymus Gland | Life Sciences | Intestinal Mucosa | Immunology | T-Lymphocytes | Butyrophilins | Receptors, Antigen, T-Cell, gamma-delta
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Loading RightsAnnual Review of Pathology: Mechanisms of Disease, ISSN 1553-4006, 2012, Volume 7, Issue 1, pp. 35 - 60
Epithelial cells form protective barriers that physically separate an organism from the outside world. Rather than being merely static, impregnable shields,...
Homeostasis | Inflammatory bowel diseases | Proliferation | Differentiation | Apoptosis | LIGHT-CHAIN KINASE | differentiation | inflammatory bowel diseases | proliferation | INTESTINAL STEM-CELLS | HUMAN COLON-CARCINOMA | BARRIER FUNCTION | apoptosis | PATHOLOGY | BETA-CATENIN | BOWEL-DISEASE | GLYCOGEN-SYNTHASE KINASE-3-BETA | homeostasis | TUMOR-NECROSIS-FACTOR | INTERFERON-GAMMA | NF-KAPPA-B | Inflammation - pathology | Intestinal Mucosa - metabolism | Intestinal Mucosa - physiopathology | Epithelial Cells - metabolism | Cytokines - metabolism | Signal Transduction | Humans | Epithelial Cells - pathology | Inflammatory Bowel Diseases - metabolism | Inflammation - metabolism | Animals | Inflammatory Bowel Diseases - pathology | Inflammation - physiopathology | Intestinal Mucosa - pathology | Physiological aspects | Cellular signal transduction | Genetic aspects | Research | Risk factors | Basic Medicine | Medical and Health Sciences | Medicin och hälsovetenskap | Medicinska och farmaceutiska grundvetenskaper | Cell and Molecular Biology | Cell- och molekylärbiologi
Homeostasis | Inflammatory bowel diseases | Proliferation | Differentiation | Apoptosis | LIGHT-CHAIN KINASE | differentiation | inflammatory bowel diseases | proliferation | INTESTINAL STEM-CELLS | HUMAN COLON-CARCINOMA | BARRIER FUNCTION | apoptosis | PATHOLOGY | BETA-CATENIN | BOWEL-DISEASE | GLYCOGEN-SYNTHASE KINASE-3-BETA | homeostasis | TUMOR-NECROSIS-FACTOR | INTERFERON-GAMMA | NF-KAPPA-B | Inflammation - pathology | Intestinal Mucosa - metabolism | Intestinal Mucosa - physiopathology | Epithelial Cells - metabolism | Cytokines - metabolism | Signal Transduction | Humans | Epithelial Cells - pathology | Inflammatory Bowel Diseases - metabolism | Inflammation - metabolism | Animals | Inflammatory Bowel Diseases - pathology | Inflammation - physiopathology | Intestinal Mucosa - pathology | Physiological aspects | Cellular signal transduction | Genetic aspects | Research | Risk factors | Basic Medicine | Medical and Health Sciences | Medicin och hälsovetenskap | Medicinska och farmaceutiska grundvetenskaper | Cell and Molecular Biology | Cell- och molekylärbiologi
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Loading RightsCancer Research, ISSN 0008-5472, 11/2017, Volume 77, Issue 21, pp. 5741 - 5754
The trans-sulfuration enzyme cystathionine-beta-synthase (CBS) and its product hydrogen sulfide (H2S) are aberrantly upregulated in colorectal cancers, where...
SULFHYDRATION | INHIBITION | SET ENRICHMENT ANALYSIS | ANGIOGENESIS | ONCOLOGY | BIOENERGETICS | CELL-PROLIFERATION | HYDROGEN-SULFIDE | CANCER | EXPRESSION | MODULATION | Hydrogen Sulfide - metabolism | Up-Regulation | Intestinal Mucosa - metabolism | Adenomatous Polyps - genetics | Humans | Gene Expression Regulation, Neoplastic | Male | Transplantation, Heterologous | Carcinogenesis - metabolism | Cell Movement - genetics | Female | Cystathionine beta-Synthase - genetics | Cell Line | Colon - pathology | HCT116 Cells | Carcinogenesis - genetics | Gene Expression Profiling - methods | Cystathionine beta-Synthase - metabolism | Metabolomics - methods | Colon - metabolism | Mice, Knockout | Animals | Mice, Nude | Adenomatous Polyps - metabolism | Intestinal Mucosa - pathology | Phosphates | Mesenchyme | Epithelial cells | Colorectal carcinoma | p53 Protein | Genes | Colorectal cancer | Sphingolipids | Phospholipids | Adenoma | Carcinogenesis | E-cadherin | K-Ras protein | Hydrogen sulfide | Carcinogens | Colon cancer | Metabolites | Bioenergetics | Pentose | Cell adhesion | Extracellular matrix | Colon | Autocrine signalling | Lipogenesis | Sugars | NF-κB protein | Bile acids | Metabolism | Gene expression | Ablation | Intermediates | Pentose phosphate pathway | Glycolysis | Hypoxia | Anoikis | Mice | Aberration | Cancer | cancer metabolism | transsulfuration pathway | cystathionine-βsynthase | hydrogen sulfide | adenoma to carcinoma sequence
SULFHYDRATION | INHIBITION | SET ENRICHMENT ANALYSIS | ANGIOGENESIS | ONCOLOGY | BIOENERGETICS | CELL-PROLIFERATION | HYDROGEN-SULFIDE | CANCER | EXPRESSION | MODULATION | Hydrogen Sulfide - metabolism | Up-Regulation | Intestinal Mucosa - metabolism | Adenomatous Polyps - genetics | Humans | Gene Expression Regulation, Neoplastic | Male | Transplantation, Heterologous | Carcinogenesis - metabolism | Cell Movement - genetics | Female | Cystathionine beta-Synthase - genetics | Cell Line | Colon - pathology | HCT116 Cells | Carcinogenesis - genetics | Gene Expression Profiling - methods | Cystathionine beta-Synthase - metabolism | Metabolomics - methods | Colon - metabolism | Mice, Knockout | Animals | Mice, Nude | Adenomatous Polyps - metabolism | Intestinal Mucosa - pathology | Phosphates | Mesenchyme | Epithelial cells | Colorectal carcinoma | p53 Protein | Genes | Colorectal cancer | Sphingolipids | Phospholipids | Adenoma | Carcinogenesis | E-cadherin | K-Ras protein | Hydrogen sulfide | Carcinogens | Colon cancer | Metabolites | Bioenergetics | Pentose | Cell adhesion | Extracellular matrix | Colon | Autocrine signalling | Lipogenesis | Sugars | NF-κB protein | Bile acids | Metabolism | Gene expression | Ablation | Intermediates | Pentose phosphate pathway | Glycolysis | Hypoxia | Anoikis | Mice | Aberration | Cancer | cancer metabolism | transsulfuration pathway | cystathionine-βsynthase | hydrogen sulfide | adenoma to carcinoma sequence
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Loading RightsAnnual Review of Nutrition, ISSN 0199-9885, 08/2011, Volume 31, Issue 1, pp. 177 - 201
Until recently, the transport of folates into cells and across epithelia has been interpreted primarily within the context of two transporters with high...
Heme carrier protein-1 (HCP1) | Reduced folate carrier (RFC) (SLC19A1) | Intestinal folate absorption | Proton-coupled folate transporter (PCFT) (SLC46A1) | Cerebral folate deficiency (CFD) | Hereditary folate malabsorption (HFM) | intestinal folate absorption | ORGANIC ANION TRANSPORTER | MULTIDRUG-RESISTANCE PROTEINS | heme carrier protein-1 (HCP1) | RECEPTOR-TYPE BETA | BINDING-PROTEIN | FUNCTIONAL-CHARACTERIZATION | CEREBROSPINAL-FLUID | hereditary folate malabsorption (HFM) | CARRIER-MEDIATED TRANSPORT | FOLIC-ACID | NUTRITION & DIETETICS | METHOTREXATE TRANSPORT | proton-coupled folate transporter (PCFT) (SLC46A1) | POLYPEPTIDE OATP-B | reduced folate carrier (RFC) (SLC19A1) | cerebral folate deficiency (CFD) | Folic Acid Deficiency - metabolism | Folic Acid - analogs & derivatives | Epithelium - enzymology | Epithelium - metabolism | Humans | Liver - metabolism | Choroid Plexus - metabolism | Male | Reduced Folate Carrier Protein - metabolism | Intestinal Absorption | Placenta - metabolism | Pregnancy | Cell Membrane - enzymology | Kidney - metabolism | Animals | Biological Transport | Folic Acid - metabolism | Proton-Coupled Folate Transporter - metabolism | Female | Cell Membrane - metabolism | Physiological aspects | Research | Epithelium | Biological transport | Folic acid
Heme carrier protein-1 (HCP1) | Reduced folate carrier (RFC) (SLC19A1) | Intestinal folate absorption | Proton-coupled folate transporter (PCFT) (SLC46A1) | Cerebral folate deficiency (CFD) | Hereditary folate malabsorption (HFM) | intestinal folate absorption | ORGANIC ANION TRANSPORTER | MULTIDRUG-RESISTANCE PROTEINS | heme carrier protein-1 (HCP1) | RECEPTOR-TYPE BETA | BINDING-PROTEIN | FUNCTIONAL-CHARACTERIZATION | CEREBROSPINAL-FLUID | hereditary folate malabsorption (HFM) | CARRIER-MEDIATED TRANSPORT | FOLIC-ACID | NUTRITION & DIETETICS | METHOTREXATE TRANSPORT | proton-coupled folate transporter (PCFT) (SLC46A1) | POLYPEPTIDE OATP-B | reduced folate carrier (RFC) (SLC19A1) | cerebral folate deficiency (CFD) | Folic Acid Deficiency - metabolism | Folic Acid - analogs & derivatives | Epithelium - enzymology | Epithelium - metabolism | Humans | Liver - metabolism | Choroid Plexus - metabolism | Male | Reduced Folate Carrier Protein - metabolism | Intestinal Absorption | Placenta - metabolism | Pregnancy | Cell Membrane - enzymology | Kidney - metabolism | Animals | Biological Transport | Folic Acid - metabolism | Proton-Coupled Folate Transporter - metabolism | Female | Cell Membrane - metabolism | Physiological aspects | Research | Epithelium | Biological transport | Folic acid
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