Molecular mechanisms of sulfasalazine‐induced T‐cell apoptosis
暂无分享,去创建一个
G. Kroemer | S. Fulda | R. Schmid | G. Adler | S. Liptay | S. Bourteele | K. Ferri | M. Schanbacher | K. Debatin
[1] R. Schmid,et al. Suppression of NF-κB activity by sulfasalazine is mediated by direct inhibition of IκB kinases α and β , 2000 .
[2] G. Kroemer,et al. Apoptosis Control in Syncytia Induced by the HIV Type 1–Envelope Glycoprotein Complex , 2000, The Journal of experimental medicine.
[3] Tak W. Mak,et al. Two Distinct Pathways Leading to Nuclear Apoptosis , 2000, The Journal of experimental medicine.
[4] Robert L Moritz,et al. Identification of DIABLO, a Mammalian Protein that Promotes Apoptosis by Binding to and Antagonizing IAP Proteins , 2000, Cell.
[5] Xiaodong Wang,et al. Smac, a Mitochondrial Protein that Promotes Cytochrome c–Dependent Caspase Activation by Eliminating IAP Inhibition , 2000, Cell.
[6] Guido Kroemer,et al. Apoptosis‐inducing factor (AIF): a ubiquitous mitochondrial oxidoreductase involved in apoptosis , 2000, FEBS letters.
[7] R. Schmid,et al. NF-κB/Rel/IκB: Implications in gastrointestinal diseases , 2000 .
[8] Y Li,et al. [Mitochondria and apoptosis]. , 2000, Zhonghua yu fang yi xue za zhi [Chinese journal of preventive medicine].
[9] P. Krammer,et al. The CD95 (APO-1/Fas) and the TRAIL (APO-2L) apoptosis systems. , 2000, Experimental cell research.
[10] A. Strasser,et al. Ionizing Radiation and Chemotherapeutic Drugs Induce Apoptosis in Lymphocytes in the Absence of FAS or Fadd/Mort1 Signaling Implications for Cancer Therapy , 2000 .
[11] R. Schmid,et al. Inhibition of nuclear factor kappa B and induction of apoptosis in T‐lymphocytes by sulfasalazine , 1999, British journal of pharmacology.
[12] S. Korsmeyer,et al. BCL-2 family members and the mitochondria in apoptosis. , 1999, Genes & development.
[13] Masashi Narita,et al. Bcl-2 family proteins regulate the release of apoptogenic cytochrome c by the mitochondrial channel VDAC , 1999, Nature.
[14] M. Peter,et al. Apoptosis signaling in lymphocytes. , 1999, Current opinion in immunology.
[15] Y. Tao,et al. NF-κB functions as both a proapoptotic and antiapoptotic regulatory factor within a single cell type , 1999, Cell Death and Differentiation.
[16] R. Tersigni,et al. Lamina propria T cells in Crohn's disease and other gastrointestinal inflammation show defective CD2 pathway-induced apoptosis. , 1999, Gastroenterology.
[17] M. Schwab,et al. MycN sensitizes neuroblastoma cells for drug-induced apoptosis , 1999, Oncogene.
[18] Ruedi Aebersold,et al. Molecular characterization of mitochondrial apoptosis-inducing factor , 1999, Nature.
[19] I. Herr,et al. JNK/SAPK activity is not sufficient for anticancer therapy‐induced apoptosis involving CD95‐L, TRAIL and TNF‐α , 1999, International journal of cancer.
[20] S. Korsmeyer,et al. Regulated Targeting of BAX to Mitochondria , 1998, The Journal of cell biology.
[21] T. Griffith,et al. TRAIL: a molecule with multiple receptors and control mechanisms. , 1998, Current opinion in immunology.
[22] J C Reed,et al. Bax and adenine nucleotide translocator cooperate in the mitochondrial control of apoptosis. , 1998, Science.
[23] S. Korsmeyer,et al. Enforced dimerization of BAX results in its translocation, mitochondrial dysfunction and apoptosis , 1998, The EMBO journal.
[24] John Calvin Reed,et al. Bcl-2 family proteins as ion-channels , 1998, Cell Death and Differentiation.
[25] J C Reed,et al. Bax directly induces release of cytochrome c from isolated mitochondria. , 1998, Proceedings of the National Academy of Sciences of the United States of America.
[26] G. Kroemer,et al. Disruption of the outer mitochondrial membrane as a result of large amplitude swelling: the impact of irreversible permeability transition , 1998, FEBS letters.
[27] R. Schmid,et al. Sulfasalazine: a potent and specific inhibitor of nuclear factor kappa B. , 1998, The Journal of clinical investigation.
[28] S. Nagata,et al. A caspase-activated DNase that degrades DNA during apoptosis, and its inhibitor ICAD , 1998, Nature.
[29] Yi-Te Hsu,et al. Movement of Bax from the Cytosol to Mitochondria during Apoptosis , 1997, The Journal of cell biology.
[30] M. V. Heiden,et al. Bcl-xL Regulates the Membrane Potential and Volume Homeostasis of Mitochondria , 1997, Cell.
[31] S. Srinivasula,et al. Cytochrome c and dATP-Dependent Formation of Apaf-1/Caspase-9 Complex Initiates an Apoptotic Protease Cascade , 1997, Cell.
[32] I. Herr,et al. The CD95 (APO-1/Fas) system mediates drug-induced apoptosis in neuroblastoma cells. , 1997, Cancer research.
[33] W. Earnshaw,et al. Comparison of apoptosis in wild-type and Fas-resistant cells: chemotherapy-induced apoptosis is not dependent on Fas/Fas ligand interactions. , 1997, Blood.
[34] G. Kroemer. The proto-oncogene Bcl-2 and its role in regulating apoptosis , 1997, Nature Medicine.
[35] G. Kroemer,et al. The Central Executioner of Apoptosis: Multiple Connections between Protease Activation and Mitochondria in Fas/APO-1/CD95- and Ceramide-induced Apoptosis , 1997, The Journal of experimental medicine.
[36] Xiaodong Wang,et al. DFF, a Heterodimeric Protein That Functions Downstream of Caspase-3 to Trigger DNA Fragmentation during Apoptosis , 1997, Cell.
[37] Y. Hsu,et al. Cytosol-to-membrane redistribution of Bax and Bcl-X(L) during apoptosis. , 1997, Proceedings of the National Academy of Sciences of the United States of America.
[38] Dean P. Jones,et al. Prevention of Apoptosis by Bcl-2: Release of Cytochrome c from Mitochondria Blocked , 1997, Science.
[39] D. Green,et al. The Release of Cytochrome c from Mitochondria: A Primary Site for Bcl-2 Regulation of Apoptosis , 1997, Science.
[40] S. Nagata,et al. Apoptosis by Death Factor , 1997, Cell.
[41] P. Emery,et al. Inhibition of T cell apoptosis in the rheumatoid synovium. , 1997, The Journal of clinical investigation.
[42] G. Anderson. Resolution of chronic inflammation by therapeutic induction of apoptosis. , 1996, Trends in pharmacological sciences.
[43] G. Kroemer,et al. Bcl-2 inhibits the mitochondrial release of an apoptogenic protease , 1996, The Journal of experimental medicine.
[44] I. Herr,et al. Involvement of the CD95 (APO–1/Fas) receptor/ligand system in drug–induced apoptosis in leukemia cells , 1996, Nature Medicine.
[45] A. Strasser,et al. Bcl‐2 and Fas/APO‐1 regulate distinct pathways to lymphocyte apoptosis. , 1995, The EMBO journal.
[46] Patrick R. Griffin,et al. Identification and inhibition of the ICE/CED-3 protease necessary for mammalian apoptosis , 1995, Nature.
[47] Muneesh Tewari,et al. Yama/CPP32β, a mammalian homolog of CED-3, is a CrmA-inhibitable protease that cleaves the death substrate poly(ADP-ribose) polymerase , 1995, Cell.
[48] H. Ishii,et al. Restricted usage of immunoglobulin heavy chain variable region (VH3) in B cell clones producing anti-colon antibodies in ulcerative colitis , 1995 .
[49] C. Thompson,et al. Apoptosis in the pathogenesis and treatment of disease , 1995, Science.
[50] D. Munn,et al. Activation-induced apoptosis in human macrophages: developmental regulation of a novel cell death pathway by macrophage colony- stimulating factor and interferon gamma , 1995, The Journal of experimental medicine.
[51] J. Mountz,et al. Autoimmune disease. A problem of defective apoptosis. , 1994, Arthritis and rheumatism.
[52] C. Bloch,et al. Bcl-2 inhibits chemotherapy-induced apoptosis in neuroblastoma. , 1994, Cancer research.
[53] A. Modica,et al. Detection and characterization of apoptotic peripheral blood lymphocytes in human immunodeficiency virus infection and cancer chemotherapy by a novel flow immunocytometric method. , 1994, Blood.
[54] T. Honjo,et al. The bcl-2 gene product inhibits clonal deletion of self-reactive B lymphocytes in the periphery but not in the bone marrow , 1993, The Journal of experimental medicine.
[55] P. Krammer,et al. Activation interferes with the APO-1 pathway in mature human T cells. , 1993, International immunology.
[56] O. Janssen,et al. Induction of activation-driven death (apoptosis) in activated but not resting peripheral blood T cells. , 1993, Journal of immunology.
[57] C. Haslett. Resolution of acute inflammation and the role of apoptosis in the tissue fate of granulocytes. , 1992, Clinical science.
[58] Gary J. Nabel,et al. Cloning of an NF-κB subunit which stimulates HIV transcription in synergy with p65 , 1991, Nature.
[59] H. Macdonald,et al. Programmed death of autoreactive thymocytes , 1990, Nature.
[60] D. Heijde,et al. EFFECTS OF HYDROXYCHLOROQUINE AND SULPHASALAZINE ON PROGRESSION OF JOINT DAMAGE IN RHEUMATOID ARTHRITIS , 1989, The Lancet.
[61] S. Korsmeyer,et al. bcl-2-Immunoglobulin transgenic mice demonstrate extended B cell survival and follicular lymphoproliferation , 1989, Cell.
[62] B. McConkey,et al. Comparison between penicillamine and sulphasalazine in rheumatoid arthritis: Leeds-Birmingham trial. , 1983, British medical journal.
[63] J. McManus,et al. The metabolism of salicylazosulphapyridine in ulcerative colitis , 1973, Gut.
[64] M. Peppercorn,et al. Distribution studies of salicylazosulfapyridine and its metabolites. , 1973, Gastroenterology.
[65] D. Isenberg,et al. Apoptosis in human autoimmune diseases. , 1999, International reviews of immunology.
[66] K O'Rourke,et al. Yama/CPP32 beta, a mammalian homolog of CED-3, is a CrmA-inhibitable protease that cleaves the death substrate poly(ADP-ribose) polymerase. , 1995, Cell.
[67] P. Andrews,et al. Cloning of an NF-kappa B subunit which stimulates HIV transcription in synergy with p65. , 1991, Nature.
[68] H. Cox,et al. Letter: Moorgate tube disaster: disputed alcohol findings. , 1975, Lancet.
[69] O. Bonnevie,et al. The prophylactic effect of salazosulphapyridine in ulcerative colitis during long-term treatment. A double-blind trial on patients asymptomatic for one year. , 1973, Scandinavian journal of gastroenterology.