Toll-like Receptor-Induced Inflammatory Cytokines are Suppressed by Gain of Function or Overexpression of Gαi2 Protein

[1]  D. Wong,et al.  Beneficial Effect of a CXCR4 Agonist in Murine Models of Systemic Inflammation , 2012, Inflammation.

[2]  A. Karsan,et al.  Heterotrimeric Gi/Go proteins modulate endothelial TLR signaling independent of the MyD88-dependent pathway. , 2011, American journal of physiology. Heart and circulatory physiology.

[3]  L. Birnbaumer,et al.  Heterotrimeric Gα(i) proteins are regulated by lipopolysaccharide and are anti-inflammatory in endotoxemia and polymicrobial sepsis. , 2011, Biochimica et biophysica acta.

[4]  A. Bitto,et al.  Beta‐arrestin 2 negatively regulates sepsis‐induced inflammation , 2010, Immunology.

[5]  R. Neubig,et al.  Pleiotropic Phenotype of a Genomic Knock-In of an RGS-Insensitive G184S Gnai2 Allele , 2006, Molecular and Cellular Biology.

[6]  S. Akira,et al.  Pathogen Recognition and Innate Immunity , 2006, Cell.

[7]  W. Janssen,et al.  Oxidants Selectively Reverse TGF-β Suppression of Proinflammatory Mediator Production1 , 2006, The Journal of Immunology.

[8]  L. Birnbaumer,et al.  Lipopolysaccharide- and gram-positive bacteria-induced cellular inflammatory responses: role of heterotrimeric Galpha(i) proteins. , 2005, American journal of physiology. Cell physiology.

[9]  N. Thomson,et al.  TLR2 Agonist Ameliorates Established Allergic Airway Inflammation by Promoting Th1 Response and Not via Regulatory T Cells1 , 2005, The Journal of Immunology.

[10]  H. Karahashi,et al.  Mastoparan, a G Protein Agonist Peptide, Differentially Modulates TLR4- and TLR2-Mediated Signaling in Human Endothelial Cells and Murine Macrophages1 , 2005, The Journal of Immunology.

[11]  J. Platt,et al.  Selective suppression of Toll‐like receptor 4 activation by chemokine receptor 4 , 2005, FEBS letters.

[12]  P. Halushka,et al.  TOLL-LIKE RECEPTOR 4 COUPLED GI PROTEIN SIGNALING PATHWAYS REGULATE EXTRACELLULAR SIGNAL-REGULATED KINASE PHOSPHORYLATION AND AP-1 ACTIVATION INDEPENDENT OF NFκB ACTIVATION , 2004 .

[13]  G. Oster,et al.  Long-term mortality and medical care charges in patients with severe sepsis , 2003, Critical care medicine.

[14]  K. Malcolm,et al.  Cross-talk between ERK and p38 MAPK Mediates Selective Suppression of Pro-inflammatory Cytokines by Transforming Growth Factor-β* , 2002, The Journal of Biological Chemistry.

[15]  S. Akira,et al.  Toll-like receptors: critical proteins linking innate and acquired immunity , 2001, Nature Immunology.

[16]  G. Clermont,et al.  Epidemiology of severe sepsis in the United States: Analysis of incidence, outcome, and associated costs of care , 2001, Critical care medicine.

[17]  K. Triantafilou,et al.  A CD14-independent LPS receptor cluster , 2001, Nature Immunology.

[18]  S. Akira,et al.  Toll-like receptors and their signaling mechanism in innate immunity , 2001, Acta odontologica Scandinavica.

[19]  K. Takeda,et al.  Cutting Edge: Cell Surface Expression and Lipopolysaccharide Signaling Via the Toll-Like Receptor 4-MD-2 Complex on Mouse Peritoneal Macrophages1 , 2000, The Journal of Immunology.

[20]  K. Matsushima,et al.  The molecular pathogenesis of endotoxic shock and organ failure. , 1999, Molecular medicine today.

[21]  M. Ferretti,et al.  Heterotrimeric G proteins physically associated with the lipopolysaccharide receptor CD14 modulate both in vivo and in vitro responses to lipopolysaccharide. , 1998, The Journal of clinical investigation.

[22]  J. Norman,et al.  Why sepsis trials fail. , 1996, JAMA.

[23]  R. Bone.  Why sepsis trials fail. , 1996, JAMA.

[24]  I. Nishimoto,et al.  Insulin-like growth factor-II/mannose 6-phosphate receptor is incapable of activating GTP-binding proteins in response to mannose 6-phosphate, but capable in response to insulin-like growth factor-II. , 1990, Biochemical and biophysical research communications.

[25]  P. Halushka,et al.  Toll-like receptor 4 coupled GI protein signaling pathways regulate extracellular signal-regulated kinase phosphorylation and AP-1 activation independent of NFkappaB activation. , 2004, Shock.