Toll-like Receptor-Induced Inflammatory Cytokines are Suppressed by Gain of Function or Overexpression of Gαi2 Protein
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R. Neubig | Pengfei Li | B. Zingarelli | P. Halushka | J. Cook | K. Borg | Hongkuan Fan
[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.