An Immunogenic Peptide in the A-box of HMGB1 Protein Reverses Apoptosis-induced Tolerance through RAGE Receptor*♦
暂无分享,去创建一个
B. Nagar | Y. Durocher | M. Saleh | F. Frank | Jayoung Choi | T. Ferguson | M. A. Hancock | T. Doggett | Philippe M Leblanc | M. Hancock
[1] Jinfeng Liu,et al. Non-canonical inflammasome activation targets caspase-11 , 2011, Nature.
[2] M. Lotze,et al. High-mobility group box 1, oxidative stress, and disease. , 2011, Antioxidants & redox signaling.
[3] K. Tracey,et al. HMGB1 Release and Redox Regulates Autophagy and Apoptosis in Cancer Cells , 2010, Oncogene.
[4] R. Hotchkiss,et al. Sepsis-Induced Apoptosis Leads to Active Suppression of Delayed-Type Hypersensitivity by CD8+ Regulatory T Cells through a TRAIL-Dependent Mechanism , 2010, The Journal of Immunology.
[5] S. Akira,et al. A critical cysteine is required for HMGB1 binding to Toll-like receptor 4 and activation of macrophage cytokine release , 2010, Proceedings of the National Academy of Sciences.
[6] Ming Yan,et al. The axonal repellent, Slit2, inhibits directional migration of circulating neutrophils , 2009, Journal of leukocyte biology.
[7] Yanghua Qin,et al. HMGB1 Enhances the Proinflammatory Activity of Lipopolysaccharide by Promoting the Phosphorylation of MAPK p38 through Receptor for Advanced Glycation End Products1 , 2009, The Journal of Immunology.
[8] S. Akira,et al. HMGB proteins function as universal sentinels for nucleic-acid-mediated innate immune responses , 2009, Nature.
[9] U. Andersson,et al. The alarmin HMGB1 acts in synergy with endogenous and exogenous danger signals to promote inflammation , 2009, Journal of leukocyte biology.
[10] C. Heizmann,et al. Binding of S100 proteins to RAGE: an update. , 2009, Biochimica et biophysica acta.
[11] O. Fortunato,et al. Extracellular high mobility group box-1 inhibits R5 and X4 HIV-1 strains replication in mononuclear phagocytes without induction of chemokines and cytokines , 2009, AIDS.
[12] S. Yamada,et al. Proteolytic Cleavage of High Mobility Group Box 1 Protein by Thrombin–Thrombomodulin Complexes , 2008, Arteriosclerosis, thrombosis, and vascular biology.
[13] R. Hotchkiss,et al. BIM siRNA DECREASES LYMPHOCYTE APOPTOSIS AND IMPROVES SURVIVAL IN SEPSIS , 2008, Shock.
[14] D. Green,et al. Induction of immunological tolerance by apoptotic cells requires caspase-dependent oxidation of high-mobility group box-1 protein. , 2008, Immunity.
[15] M. Moss,et al. The epidemiology of sepsis. , 2008, Current pharmaceutical design.
[16] Jeon-Soo Shin,et al. High Mobility Group Box 1 Protein Binding to Lipopolysaccharide Facilitates Transfer of Lipopolysaccharide to CD14 and Enhances Lipopolysaccharide-Mediated TNF-α Production in Human Monocytes1 , 2008, The Journal of Immunology.
[17] E. Abraham,et al. HMGB1 Develops Enhanced Proinflammatory Activity by Binding to Cytokines1 , 2008, The Journal of Immunology.
[18] W. Shao,et al. The Caspase-1 Digestome Identifies the Glycolysis Pathway as a Target during Infection and Septic Shock*♦ , 2007, Journal of Biological Chemistry.
[19] L. Moldawer,et al. INCREASED MORTALITY AND ALTERED IMMUNITY IN NEONATAL SEPSIS PRODUCED BY GENERALIZED PERITONITIS , 2007, Shock.
[20] L. Audoly,et al. Toll-like receptor 9–dependent activation by DNA-containing immune complexes is mediated by HMGB1 and RAGE , 2007, Nature Immunology.
[21] R. Hotchkiss,et al. Apoptosis and caspases regulate death and inflammation in sepsis , 2006, Nature Reviews Immunology.
[22] L. Doughty,et al. In vivo delivery of caspase-8 or Fas siRNA improves the survival of septic mice. , 2005, Blood.
[23] Kevin J. Tracey,et al. High-mobility group box 1 protein (HMGB1): nuclear weapon in the immune arsenal , 2005, Nature Reviews Immunology.
[24] R. Hotchkiss,et al. INCREASED LYMPHOID TISSUE APOPTOSIS IN BABOONS WITH BACTEREMIC SHOCK , 2004, Shock.
[25] K. Tracey,et al. Reversing established sepsis with antagonists of endogenous high-mobility group box 1 , 2003, Proceedings of the National Academy of Sciences of the United States of America.
[26] I. Chaudry,et al. Inhibition of Fas/Fas ligand signaling improves septic survival: differential effects on macrophage apoptotic and functional capacity , 2003, Journal of leukocyte biology.
[27] D. Mannino,et al. The epidemiology of sepsis in the United States from 1979 through 2000. , 2003, The New England journal of medicine.
[28] F. Martinon,et al. The inflammasome: a molecular platform triggering activation of inflammatory caspases and processing of proIL-beta. , 2002, Molecular cell.
[29] Miau-Rong Lee,et al. Apoptosis contributes to the decrement in numbers of alveolar macrophages from rats with polymicrobial sepsis. , 2002, Journal of microbiology, immunology, and infection = Wei mian yu gan ran za zhi.
[30] M. Adib-Conquy,et al. Mitochondrial membrane potential and apoptosis peripheral blood monocytes in severe human sepsis. , 2001, American journal of respiratory and critical care medicine.
[31] E. Melloni,et al. Extracellular processing of amphoterin generates a peptide active on erythroleukaemia cell differentiation. , 2001, The Biochemical journal.
[32] K. Tracey,et al. High Mobility Group 1 Protein (Hmg-1) Stimulates Proinflammatory Cytokine Synthesis in Human Monocytes , 2000, The Journal of experimental medicine.
[33] D. Myszka,et al. Improving biosensor analysis , 1999, Journal of molecular recognition : JMR.
[34] K. Tracey,et al. HMG-1 as a late mediator of endotoxin lethality in mice. , 1999, Science.
[35] I. Chaudry,et al. Differential induction of apoptosis in lymphoid tissues during sepsis: variation in onset, frequency, and the nature of the mediators. , 1996, Blood.
[36] J. Meakins,et al. The Delayed Hypersensitivity Response and Host Resistance in Surgical Patients: 20 Years Later , 1995, Annals of surgery.
[37] J. Bancewicz,et al. Failure of delayed hypersensitivity skin testing to predict postoperative sepsis and mortality , 1982, British medical journal.
[38] G. Richards,et al. The epidemiology of sepsis. , 1973, Clinical orthopaedics and related research.
[39] Hong Wang,et al. Structural Basis for the Proinflammatory Cytokine Activity of High Mobility Group Box 1 , 2003, Molecular medicine.