Early-stage blocking of Notch signaling inhibits the depletion of goblet cells in dextran sodium sulfate-induced colitis in mice

[1]  L. Augenlicht,et al.  Intestinal deletion of Pofut1 in the mouse inactivates notch signaling and causes enterocolitis. , 2008, Gastroenterology.

[2]  Xi C. He,et al.  Current view: intestinal stem cells and signaling. , 2008, Gastroenterology.

[3]  E. Mizoguchi,et al.  Inflammatory bowel disease, past, present and future: lessons from animal models , 2008, Journal of Gastroenterology.

[4]  A. Nusrat,et al.  Role of the intestinal barrier in inflammatory bowel disease. , 2008, World journal of gastroenterology.

[5]  S. Kaufmann,et al.  Notch signaling is activated by TLR stimulation and regulates macrophage functions , 2008, European journal of immunology.

[6]  H. Zoghbi,et al.  Intestine-specific ablation of mouse atonal homolog 1 (Math1) reveals a role in cellular homeostasis. , 2007, Gastroenterology.

[7]  J. Roman,et al.  Matrix metalloproteinase-9 regulates MUC-2 expression through its effect on goblet cell differentiation. , 2007, Gastroenterology.

[8]  S. Chiba.  Concise Review: Notch Signaling in Stem Cell Systems , 2006 .

[9]  M. Radomski,et al.  Role of Matrix Metalloproteinases in Intestinal Inflammation , 2006, Journal of Pharmacology and Experimental Therapeutics.

[10]  J. Meijerink,et al.  Muc2-deficient mice spontaneously develop colitis, indicating that MUC2 is critical for colonic protection. , 2006, Gastroenterology.

[11]  C. Cherbut,et al.  MUC Genes Are Differently Expressed During Onset and Maintenance of Inflammation in Dextran Sodium Sulfate-Treated Mice , 2006, Digestive Diseases and Sciences.

[12]  Yuji Naito,et al.  Role of matrix metalloproteinases in inflammatory bowel disease. , 2005, Molecular aspects of medicine.

[13]  M. Koopmans,et al.  Homeostasis and function of goblet cells during rotavirus infection in mice. , 2005, Virology.

[14]  Hans Clevers,et al.  Notch/γ-secretase inhibition turns proliferative cells in intestinal crypts and adenomas into goblet cells , 2005, Nature.

[15]  E. Siemers,et al.  Safety, Tolerability, and Changes in Amyloid β Concentrations After Administration of a γ-Secretase Inhibitor in Volunteers , 2005 .

[16]  J. Lamb,et al.  Notch1 co‐localizes with CD4 on activated T cells and Notch signaling is required for IL‐10 production , 2005, European journal of immunology.

[17]  David W. Smith,et al.  Dynamics of β-Amyloid Reductions in Brain, Cerebrospinal Fluid, and Plasma of β-Amyloid Precursor Protein Transgenic Mice Treated with a γ-Secretase Inhibitor , 2005, Journal of Pharmacology and Experimental Therapeutics.

[18]  Francois Pognan,et al.  Modulation of notch processing by gamma-secretase inhibitors causes intestinal goblet cell metaplasia and induction of genes known to specify gut secretory lineage differentiation. , 2004, Toxicological sciences : an official journal of the Society of Toxicology.

[19]  E. Siemers,et al.  P4-333 Safety, tolerability, and changes in plasma and cerebrospinal fluid amyloid beta concentrations after administration of a functional gamma-secretase inhibitor in healthy volunteers , 2004, Neurobiology of Aging.

[20]  Richard A Flavell,et al.  Instruction of Distinct CD4 T Helper Cell Fates by Different Notch Ligands on Antigen-Presenting Cells , 2004, Cell.

[21]  Jay S. Fine,et al.  Chronic Treatment with the γ-Secretase Inhibitor LY-411,575 Inhibits β-Amyloid Peptide Production and Alters Lymphopoiesis and Intestinal Cell Differentiation* , 2004, Journal of Biological Chemistry.

[22]  W. H. Jordan,et al.  Adipsin, a Biomarker of Gastrointestinal Toxicity Mediated by a Functional γ-Secretase Inhibitor* , 2003, Journal of Biological Chemistry.

[23]  D. Roberts,et al.  Development and differentiation of the intestinal epithelium , 2003, Cellular and Molecular Life Sciences CMLS.

[24]  M. Baron,et al.  An overview of the Notch signalling pathway. , 2003, Seminars in cell & developmental biology.

[25]  T. Iwatsubo,et al.  The role of presenilin cofactors in the γ-secretase complex , 2003, Nature.

[26]  S. Sisodia,et al.  The Notch Ligands, Delta1 and Jagged2, Are Substrates for Presenilin-dependent “γ-Secretase” Cleavage* , 2003, The Journal of Biological Chemistry.

[27]  Harald Steiner,et al.  Presenilin-dependent Intramembrane Proteolysis of CD44 Leads to the Liberation of Its Intracellular Domain and the Secretion of an Aβ-like Peptide* , 2002, The Journal of Biological Chemistry.

[28]  J. Dekker,et al.  Epithelial proliferation, cell death, and gene expression in experimental colitis: alterations in carbonic anhydrase I, mucin MUC2, and trefoil factor 3 expression , 2002, International Journal of Colorectal Disease.

[29]  G. Serban,et al.  A presenilin‐1/γ‐secretase cleavage releases the E‐cadherin intracellular domain and regulates disassembly of adherens junctions , 2002, The EMBO journal.

[30]  H. Zoghbi,et al.  Requirement of Math1 for Secretory Cell Lineage Commitment in the Mouse Intestine , 2001, Science.

[31]  D. Roberts,et al.  Epithelial Cell Differentiation--a Mather of Choice , 2001, Science.

[32]  C. Probert,et al.  Mucins and inflammatory bowel disease , 2000, Postgraduate medical journal.

[33]  F. D. Miller,et al.  Functional gamma‐secretase inhibitors reduce beta‐amyloid peptide levels in brain , 2000, Journal of neurochemistry.

[34]  K. Tomita,et al.  The bHLH Gene Hes1 Regulates Differentiation of Multiple Cell Types , 2000, Molecules and cells.

[35]  D. Podolsky,et al.  A paradoxical reduction in susceptibility to colonic injury upon targeted transgenic ablation of goblet cells. , 1999, The Journal of clinical investigation.

[36]  C. J. Taylor,et al.  Matrix metalloproteinase levels are elevated in inflammatory bowel disease. , 1999, Gastroenterology.

[37]  S. Artavanis-Tsakonas,et al.  Notch Signaling : Cell Fate Control and Signal Integration in Development , 1999 .

[38]  William J. Ray,et al.  A presenilin-1-dependent γ-secretase-like protease mediates release of Notch intracellular domain , 1999, Nature.

[39]  J. Pearson,et al.  The MUC2 gene product: a human intestinal mucin. , 1998, The international journal of biochemistry & cell biology.

[40]  J. Dekker,et al.  63 DISEASE‐RELATED QUANTITATIVE ALTERATIONS IN MUC2 SYNTHESIS IN ULCERATIVE COLITIS ARE REGULATED AT THE TRANSLATIONAL LEVEL , 1996, Journal of Pediatric Gastroenterology and Nutrition.

[41]  J. Dekker,et al.  MUC2 is the prominent colonic mucin expressed in ulcerative colitis. , 1996, Gut.

[42]  Christel Brou,et al.  Signalling downstream of activated mammalian Notch , 1995, Nature.

[43]  H. Cooper,et al.  Clinicopathologic study of dextran sulfate sodium experimental murine colitis. , 1993, Laboratory investigation; a journal of technical methods and pathology.

[44]  D. A. McCormick,et al.  Mucin depletion in inflammatory bowel disease. , 1990, Journal of clinical pathology.

[45]  Guoxing Wang,et al.  Differences in goblet cell differentiation between Crohn's disease and ulcerative colitis. , 2009, Differentiation; research in biological diversity.

[46]  Tetsuya Nakamura,et al.  Requirement of Notch activation during regeneration of the intestinal epithelia. , 2009, American journal of physiology. Gastrointestinal and liver physiology.

[47]  伊藤 令子.  Interferon-gamma is causatively involved in experimental inflammatory bowel disease in mice , 2007 .

[48]  C. Albright,et al.  Gamma-secretase inhibitors for Alzheimer's disease: balancing efficacy and toxicity. , 2006, Drugs in R&D.

[49]  S. Chiba.  Notch signaling in stem cell systems. , 2006, Stem cells.

[50]  C. Albright,et al.  γ-Secretase Inhibitors for Alzheimer’s Disease , 2006 .

[51]  E. Siemers,et al.  Safety, tolerability, and changes in amyloid beta concentrations after administration of a gamma-secretase inhibitor in volunteers. , 2005, Clinical neuropharmacology.

[52]  J. Hendrick,et al.  Dynamics of {beta}-amyloid reductions in brain, cerebrospinal fluid, and plasma of {beta}-amyloid precursor protein transgenic mice treated with a {gamma}-secretase inhibitor. , 2005, The Journal of pharmacology and experimental therapeutics.

[53]  G. Higgins,et al.  Chronic treatment with the gamma-secretase inhibitor LY-411,575 inhibits beta-amyloid peptide production and alters lymphopoiesis and intestinal cell differentiation. , 2004, The Journal of biological chemistry.

[54]  T. Iwatsubo,et al.  The role of presenilin cofactors in the gamma-secretase complex. , 2003, Nature.

[55]  Ryoichiro Kageyama,et al.  Control of endodermal endocrine development by Hes-1 , 2000, Nature Genetics.

[56]  福島 敦樹.  2 季節性アレルギー性結膜炎の発症機構Lessons from animal models (10 アレルギー性鼻炎, アレルギー性結膜炎の病態と治療) , 1999 .