MicroRNA-155 promotes the pathogenesis of experimental colitis by repressing SHIP-1 expression
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Title
MicroRNA-155 promotes the pathogenesis of experimental colitis by repressing SHIP-1 expression
Authors
Keywords
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Journal
WORLD JOURNAL OF GASTROENTEROLOGY
Volume 23, Issue 6, Pages 976
Publisher
Baishideng Publishing Group Inc.
Online
2017-02-13
DOI
10.3748/wjg.v23.i6.976
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Note: Only part of the references are listed.- Role of Altered Expression of miR-146a, miR-155, and miR-122 in Pediatric Patients with Inflammatory Bowel Disease
- (2016) Nóra J. Béres et al. INFLAMMATORY BOWEL DISEASES
- Different Effects of Three Selected Lactobacillus Strains in Dextran Sulfate Sodium-Induced Colitis in BALB/c Mice
- (2016) Yi Cui et al. PLoS One
- Noncoding RNAs, cytokines, and inflammation-related diseases
- (2015) José Luiz Marques-Rocha et al. FASEB JOURNAL
- The gut microbiota and host health: a new clinical frontier
- (2015) Julian R Marchesi et al. GUT
- Physiological roles of miR-155
- (2015) Ryuichi Mashima IMMUNOLOGY
- Immunopathogenesis of IBD: current state of the art
- (2015) Heitor S. P. de Souza et al. Nature Reviews Gastroenterology & Hepatology
- MicroRNA in inflammatory bowel disease: Translational research and clinical implication
- (2015) Kurt Fisher WORLD JOURNAL OF GASTROENTEROLOGY
- MicroRNAs: new players in IBD
- (2014) R Kalla et al. GUT
- miR-155 deficiency protects mice from experimental colitis by reducing T helper type 1/type 17 responses
- (2014) Udai P. Singh et al. IMMUNOLOGY
- MicroRNA-155 Is Involved in the Pathogenesis of Ulcerative Colitis by Targeting FOXO3a
- (2014) Min Min et al. INFLAMMATORY BOWEL DISEASES
- MicroRNA-155 as a proinflammatory regulator via SHIP-1 down-regulation in acute gouty arthritis
- (2014) Hye Jin et al. ARTHRITIS RESEARCH & THERAPY
- Overexpression of microRNAs-155 and 21 targeting mismatch repair proteins in inflammatory bowel diseases
- (2013) M. Svrcek et al. CARCINOGENESIS
- miR-155: an ancient regulator of the immune system
- (2013) Elena Vigorito et al. IMMUNOLOGICAL REVIEWS
- Triptolide ameliorates ileocolonic anastomosis inflammation in IL-10 deficient mice by mechanism involving suppression of miR-155/SHIP-1 signaling pathway
- (2013) Rong Wu et al. MOLECULAR IMMUNOLOGY
- Cell density during differentiation can alter the phenotype of bone marrow-derived macrophages
- (2013) Chan Lee et al. Cell and Bioscience
- Ulcerative colitis
- (2012) Ingrid Ordás et al. LANCET
- Enzymatic and non-enzymatic activities of SHIP-1 in signal transduction and cancer
- (2011) Claude Condé et al. BIOCHEMICAL PHARMACOLOGY
- Intestinal expression of SHIP in inflammatory bowel diseases
- (2011) Ingrid Arijs et al. GUT
- Inhibitor and activator: dual functions for SHIP in immunity and cancer
- (2010) William G. Kerr Annals of the New York Academy of Sciences
- Role of SHIP in cancer
- (2010) Melisa J. Hamilton et al. EXPERIMENTAL HEMATOLOGY
- SHIP deficiency causes Crohn's disease-like ileitis
- (2010) W. G. Kerr et al. GUT
- MicroRNA Control in the Immune System: Basic Principles
- (2009) Changchun Xiao et al. CELL
- Onco-miR-155 targets SHIP1 to promote TNFα-dependent growth of B cell lymphomas
- (2009) Irene M. Pedersen et al. EMBO Molecular Medicine
- miR-155: On the Crosstalk Between Inflammation and Cancer
- (2009) Esmerina Tili et al. INTERNATIONAL REVIEWS OF IMMUNOLOGY
- Inositol phosphatase SHIP1 is a primary target of miR-155
- (2009) R. M. O'Connell et al. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
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