Treatment with N-tosyl-l-phenylalanine chloromethyl ketone after the onset of collagen-induced arthritis reduces joint erosion and NF-kappaB activation.

[1]  Georg Schett,et al.  IκB kinase (IKK)β, but not IKKα, is a critical mediator of osteoclast survival and is required for inflammation-induced bone loss , 2005, The Journal of experimental medicine.

[2]  G. Firestein.  NF‐κB: Holy Grail for rheumatoid arthritis? , 2004 .

[3]  Koji Okabe,et al.  Selective inhibition of NF-κB blocks osteoclastogenesis and prevents inflammatory bone destruction in vivo , 2004, Nature Medicine.

[4]  Kyung-Su Park,et al.  Induction of IL-10-producing CD4+CD25+ T cells in animal model of collagen-induced arthritis by oral administration of type II collagen , 2004, Arthritis research & therapy.

[5]  J. Clohisy,et al.  Direct Inhibition of NF-κB Blocks Bone Erosion Associated with Inflammatory Arthritis1 , 2003, The Journal of Immunology.

[6]  K. Hruska,et al.  Activin A stimulates IκB‐α/NFκB and rank expression for osteoclast differentiation, but not AKT survival pathway in osteoclast precursors , 2003 .

[7]  David L. Lacey,et al.  Osteoclast differentiation and activation , 2003, Nature.

[8]  J. Choi,et al.  Dual effect of oxidative stress on NF-κB activation in HeLa cells , 2002, Experimental & Molecular Medicine.

[9]  L. Joosten,et al.  Therapeutic effect of neutralizing endogenous IL-18 activity in the collagen-induced model of arthritis. , 2001, The Journal of clinical investigation.

[10]  G. Panayi,et al.  Cytokine pathways and joint inflammation in rheumatoid arthritis. , 2001, The New England journal of medicine.

[11]  W. B. van den Berg.  Anti-cytokine therapy in chronic destructive arthritis , 2000, Arthritis research.

[12]  P. Tak,et al.  The Effect of a T Cell-Specific NF-κB Inhibitor on In Vitro Cytokine Production and Collagen-Induced Arthritis1 , 2000, The Journal of Immunology.

[13]  J. Fratkin,et al.  N-tosyl-L-phenylalanyl-chloromethylketone reduces hypoxic-ischemic brain injury in rat pups. , 2000, European journal of pharmacology.

[14]  Josef M. Penninger,et al.  Activated T cells regulate bone loss and joint destruction in adjuvant arthritis through osteoprotegerin ligand , 1999, Nature.

[15]  K. Jeon,et al.  Nuclear factor kappaB (NF-kappaB) pathway as a therapeutic target in rheumatoid arthritis. , 1999, Journal of Korean medical science.

[16]  G. Boivin,et al.  Association of the course of collagen-induced arthritis with distinct patterns of cytokine and chemokine messenger RNA expression. , 1999, Arthritis and rheumatism.

[17]  Ulrich Siebenlist,et al.  Requirement for NF-κB in osteoclast and B-cell development , 1997 .

[18]  J. Caamaño,et al.  Osteopetrosis in mice lacking NF-κB1 and NF-κB2 , 1997, Nature Medicine.

[19]  A. Kang,et al.  Collagen-induced arthritis, an animal model of autoimmunity. , 1997, Life sciences.

[20]  M. Karin,et al.  Nuclear factor-kappaB: a pivotal transcription factor in chronic inflammatory diseases. , 1997, The New England journal of medicine.

[21]  E. Gravallese,et al.  Nuclear factor-kappa B in rheumatoid synovium. Localization of p50 and p65. , 1995, Arthritis and rheumatism.

[22]  L. Ignarro,et al.  Serine and cysteine proteinase inhibitors prevent nitric oxide production by activated macrophages by interfering with transcription of the inducible NO synthase gene. , 1995, Biochemical and biophysical research communications.

[23]  B. Rovin,et al.  Activation of nuclear factor-κB correlates with MCP-1 expression by human mesangial cells , 1995 .

[24]  K. Baek,et al.  Chloromethyl ketones block induction of nitric oxide synthase in murine macrophages by preventing activation of nuclear factor-kappa B. , 1995, Journal of immunology.

[25]  S. Haskill,et al.  Interleukin 1-induced phosphorylation of MAD3, the major inhibitor of nuclear factor kappa B of HeLa cells. Interference in signalling by the proteinase inhibitors 3,4-dichloroisocoumarin and tosylphenylalanyl chloromethylketone. , 1995, The Biochemical journal.

[26]  A. Yaron,et al.  In vivo stimulation of I kappa B phosphorylation is not sufficient to activate NF-kappa B , 1995, Molecular and cellular biology.

[27]  M. Karin,et al.  Phosphorylation of I kappa B alpha precedes but is not sufficient for its dissociation from NF-kappa B , 1995, Molecular and cellular biology.

[28]  I. Verma,et al.  Tumor necrosis factor alpha-induced phosphorylation of I kappa B alpha is a signal for its degradation but not dissociation from NF-kappa B. , 1994, Proceedings of the National Academy of Sciences of the United States of America.

[29]  A. Baldwin,et al.  Inducible phosphorylation of I kappa B alpha is not sufficient for its dissociation from NF-kappa B and is inhibited by protease inhibitors. , 1994, Proceedings of the National Academy of Sciences of the United States of America.

[30]  N. Mackman.  Protease inhibitors block lipopolysaccharide induction of tissue factor gene expression in human monocytic cells by preventing activation of c-Rel/p65 heterodimers. , 1994, The Journal of biological chemistry.

[31]  I. Verma,et al.  Autoregulation of I kappa B alpha activity. , 1994, Proceedings of the National Academy of Sciences of the United States of America.

[32]  S. Goodbourn,et al.  Proteolytic degradation of MAD3 (IϰBα) and enhanced processing of the NF-ϰB precursor p105 are obligatory steps in the activation of NF-ϰB , 1993 .

[33]  Y. Ben-Neriah,et al.  Rapid proteolysis of IκB-α is necessary for activation of transcription factor NF-κB , 1993, Nature.

[34]  Josef M. Penninger,et al.  Activated T cells regulate bone loss and joint destruction in adjuvant arthritis through osteoprotegerin ligand , 1999, Nature.

[35]  A. Manning,et al.  AP-1 and NF-kappaB regulation in rheumatoid arthritis and murine collagen-induced arthritis. , 1998, Autoimmunity.

[36]  P. Baeuerle,et al.  Activation of the transcription factor NF-kB in inflamed synovial tissue , 1996 .

[37]  O. Kwon,et al.  Pro-tumour necrosis factor cleavage enzyme in macrophage membrane/particulate. , 1993, Immunology.