Dextran Sulfate

• 

  Subject Areas on Research

  • A whole animal chemical screen approach to identify modifiers of intestinal neutrophilic inflammation. 
  • Control of Intestinal Inflammation, Colitis-Associated Tumorigenesis, and Macrophage Polarization by Fibrinogen-Like Protein 2. 
  • Dextran sulfate sodium-induced colitis in immunodeficient rats. 
  • Differential inhibition of HIV-1 cell binding and HIV-1-induced syncytium formation by low molecular weight sulphated polysaccharides. 
  • Distinct Kinase-Independent Role of RIPK3 in CD11c+ Mononuclear Phagocytes in Cytokine-Induced Tissue Repair. 
  • Electroactive controlled release thin films. 
  • Engineered biomimetic nanovesicles show intrinsic anti-inflammatory properties for the treatment of inflammatory bowel diseases. 
  • Environmental factors regulate Paneth cell phenotype and host susceptibility to intestinal inflammation in Irgm1-deficient mice. 
  • Fasting prevents experimental murine colitis produced by dextran sulfate sodium and decreases interleukin-1 beta and insulin-like growth factor I messenger ribonucleic acid. 
  • Glutamine therapy improves outcome of in vitro and in vivo experimental colitis models. 
  • IL-10-producing regulatory B10 cells inhibit intestinal injury in a mouse model. 
  • Increased expression of extracellular glutathione peroxidase in mice with dextran sodium sulfate-induced experimental colitis. 
  • Inhibition of the beta-adrenergic receptor kinase by polyanions. 
  • Irgm1-deficient mice exhibit Paneth cell abnormalities and increased susceptibility to acute intestinal inflammation. 
  • Mucosal healing and fibrosis after acute or chronic inflammation in wild type FVB-N mice and C57BL6 procollagen α1(I)-promoter-GFP reporter mice. 
  • NK-1 antagonist reduces colonic inflammation and oxidative stress in dextran sulfate-induced colitis in rats. 
  • Soluble CD4 and dextran sulfate mediate release of gp120 from HIV-1: implications for clinical trials. 
  • Targeting EZH2 histone methyltransferase activity alleviates experimental intestinal inflammation. 
  • The Crohn's Disease Risk Factor IRGM Limits NLRP3 Inflammasome Activation by Impeding Its Assembly and by Mediating Its Selective Autophagy. 
  • The Innate Immune Receptor NLRX1 Functions as a Tumor Suppressor by Reducing Colon Tumorigenesis and Key Tumor-Promoting Signals. 
  • The NLRP3 inflammasome protects against loss of epithelial integrity and mortality during experimental colitis. 
  • The apolipoprotein E-mimetic peptide COG112 inhibits NF-kappaB signaling, proinflammatory cytokine expression, and disease activity in murine models of colitis. 
  • The necroptosis adaptor RIPK3 promotes injury-induced cytokine expression and tissue repair. 
  • Tumor necrosis factor alpha and colitis-associated colon cancer. 
  • Vanilloid receptor-1 containing primary sensory neurones mediate dextran sulphate sodium induced colitis in rats. 
  • rHuKGF ameliorates symptoms in DSS and CD4(+)CD45RB(Hi) T cell transfer mouse models of inflammatory bowel disease.