Glutamine deprivation-mediated cell shrinkage induces ligand-independent CD95 receptor signaling and apoptosis
暂无分享,去创建一个
[1] P. Krammer,et al. CD95's deadly mission in the immune system , 2000, Nature.
[2] D. Choi,et al. Ions, cell volume, and apoptosis. , 2000, Proceedings of the National Academy of Sciences of the United States of America.
[3] Y Ishizaki,et al. Normotonic cell shrinkage because of disordered volume regulation is an early prerequisite to apoptosis. , 2000, Proceedings of the National Academy of Sciences of the United States of America.
[4] D. Palmieri,et al. Insight into the mechanism of asparaginase-induced depletion of antithrombin III in treatment of childhood acute lymphoblastic leukemia. , 2000, Leukemia research.
[5] P. Golstein. FasL Binds Preassembled Fas , 2000, Science.
[6] C. Bortner,et al. Protein Kinase C (PKC) Inhibits Fas Receptor-induced Apoptosis through Modulation of the Loss of K+ and Cell Shrinkage , 2000, The Journal of Biological Chemistry.
[7] J K Frederiksen,et al. Fas preassociation required for apoptosis signaling and dominant inhibition by pathogenic mutations. , 2000, Science.
[8] D. Lawrence,et al. Apo2L/TRAIL-dependent recruitment of endogenous FADD and caspase-8 to death receptors 4 and 5. , 2000, Immunity.
[9] H. Zhu,et al. Cloning and Functional Identification of a Neuronal Glutamine Transporter* , 2000, The Journal of Biological Chemistry.
[10] A. Signore,et al. Identification and Characterization of a Ligand-independent Oligomerization Domain in the Extracellular Region of the CD95 Death Receptor* , 1999, The Journal of Biological Chemistry.
[11] G. Evan,et al. c-Myc-induced sensitization to apoptosis is mediated through cytochrome c release. , 1999, Genes & development.
[12] Y. Aizawa,et al. Graft-versus-leukemia effect and graft-versus-host disease can be differentiated by cytotoxic mechanisms in a murine model of allogeneic bone marrow transplantation , 1999 .
[13] E. Solary,et al. Fas Ligand-independent, FADD-mediated Activation of the Fas Death Pathway by Anticancer Drugs* , 1999, The Journal of Biological Chemistry.
[14] M. Amylon,et al. Intensive high-dose asparaginase consolidation improves survival for pediatric patients with T cell acute lymphoblastic leukemia and advanced stage lymphoblastic lymphoma: a Pediatric Oncology Group study , 1999, Leukemia.
[15] G. Griffiths,et al. Degranulation plays an essential part in regulating cell surface expression of Fas ligand in T cells and natural killer cells , 1999, Nature Medicine.
[16] G. Gores,et al. Toxic bile salts induce rodent hepatocyte apoptosis via direct activation of Fas. , 1999, The Journal of clinical investigation.
[17] A. Fornace,et al. Ultraviolet-irradiation-induced apoptosis is mediated via ligand independent activation of tumor necrosis factor receptor 1 , 1998, Oncogene.
[18] Xiaodong Wang,et al. Bid, a Bcl2 Interacting Protein, Mediates Cytochrome c Release from Mitochondria in Response to Activation of Cell Surface Death Receptors , 1998, Cell.
[19] Junying Yuan,et al. Cleavage of BID by Caspase 8 Mediates the Mitochondrial Damage in the Fas Pathway of Apoptosis , 1998, Cell.
[20] T. Ko,et al. Glutamine deprivation induces apoptosis in intestinal epithelial cells. , 1998, Surgery.
[21] H. Müller,et al. Use of L-asparaginase in childhood ALL. , 1998, Critical reviews in oncology/hematology.
[22] F. Lang,et al. Tyrosine kinase-dependent activation of a chloride channel in CD95-induced apoptosis in T lymphocytes. , 1998, Proceedings of the National Academy of Sciences of the United States of America.
[23] J. Sheridan,et al. Identification of a ligand for the death-domain-containing receptor Apo3 , 1998, Current Biology.
[24] M. Peter,et al. Two CD95 (APO‐1/Fas) signaling pathways , 1998, The EMBO journal.
[25] M. Moreno,et al. Apoptosis induced by a chimeric Fas/FLICE receptor: lack of requirement for Fas- or FADD-binding proteins. , 1998, Journal of immunology.
[26] P. Scheurich,et al. Dominant-negative FADD inhibits TNFR60-, Fas/Apo1- and TRAIL-R/Apo2-mediated cell death but not gene induction , 1998, Current Biology.
[27] Thomas A. Luger,et al. Ultraviolet Light Induces Apoptosis via Direct Activation of CD95 (Fas/APO-1) Independently of Its Ligand CD95L , 1998, The Journal of cell biology.
[28] G. Evan,et al. Requirement for the CD95 receptor-ligand pathway in c-Myc-induced apoptosis. , 1997, Science.
[29] T. Ueno,et al. Cell cycle arrest and apoptosis of leukemia cells induced by L-asparaginase , 1997, Leukemia.
[30] A. Chinnaiyan,et al. Ultraviolet Radiation-induced Apoptosis Is Mediated by Activation of CD-95 (Fas/APO-1)* , 1997, The Journal of Biological Chemistry.
[31] B. Dörken,et al. Differential CD95 expression and function in T and B lineage acute lymphoblastic leukemia cells , 1997, Leukemia.
[32] V. Dixit,et al. A Novel Family of Viral Death Effector Domain-containing Molecules That Inhibit Both CD-95- and Tumor Necrosis Factor Receptor-1-induced Apoptosis* , 1997, The Journal of Biological Chemistry.
[33] E. Newsholme,et al. Aspects of glutamine metabolism in human tumour cells , 1997, Biochemistry and molecular biology international.
[34] J. Bertin,et al. Death effector domain-containing herpesvirus and poxvirus proteins inhibit both Fas- and TNFR1-induced apoptosis. , 1997, Proceedings of the National Academy of Sciences of the United States of America.
[35] Stephen J. Elledge,et al. Cell Cycle Checkpoints: Preventing an Identity Crisis , 1996, Science.
[36] Michael Karin,et al. Ultraviolet Light and Osmotic Stress: Activation of the JNK Cascade Through Multiple Growth Factor and Cytokine Receptors , 1996, Science.
[37] G. Guidotti,et al. Cell susceptibility to apoptosis by glutamine deprivation and rescue: Survival and apoptotic death in cultured lymphoma‐leukemia cell lines , 1996, Journal of cellular physiology.
[38] C. Bortner,et al. Absence of volume regulatory mechanisms contributes to the rapid activation of apoptosis in thymocytes. , 1996, The American journal of physiology.
[39] H. Jürgens,et al. Monitoring of asparaginase activity and asparagine levels in children on different asparaginase preparations. , 1996, European journal of cancer.
[40] M. Peter,et al. Cytotoxicity‐dependent APO‐1 (Fas/CD95)‐associated proteins form a death‐inducing signaling complex (DISC) with the receptor. , 1995, The EMBO journal.
[41] P. Krammer,et al. Regulation of cell surface APO‐1/Fas (CD95) ligand expression by metalloproteases , 1995, European journal of immunology.
[42] V. Dall’Asta,et al. Response of human fibroblasts to hypertonic stress. Cell shrinkage is counteracted by an enhanced active transport of neutral amino acids. , 1994, The Journal of biological chemistry.
[43] L. Filgueira,et al. Exogenous glutamine requirement is confined to late events of T cell activation , 1993, Journal of cellular biochemistry.
[44] H. Mikawa,et al. The Inhibition of Lymphocyte Blastogenesis by Asparaginase: Critical Role of Glutamine in both T and B Lymphocyte Transformation , 1992, Acta paediatrica Japonica : Overseas edition.
[45] G. Guidotti,et al. Amino Acid Transporters: Systematic Approach and Principles of Control , 1992 .
[46] D. Häussinger,et al. Mammalian Amino Acid Transport , 1992, Springer US.
[47] G. Guidotti,et al. Role of Amino Acid Transport System A in the Control of Cell Volume in Cultured Human Fibroblasts , 1991 .
[48] H. Mikawa,et al. Metabolic basis for differential glutamine requirements of human leukemia cell lines , 1990, Journal of cellular physiology.
[49] U. Stephani,et al. Electrolytes, Amino Acids and Proteins in Lumbar CSF during the Treatment of Acute Leukemia in Childhood , 1990, Acta paediatrica Scandinavica.
[50] E. Newsholme,et al. The effect of glutamine concentration on the activity of carbamoyl-phosphate synthase II and on the incorporation of [3H]thymidine into DNA in rat mesenteric lymphocytes stimulated by phytohaemagglutinin. , 1989, The Biochemical journal.
[51] E. Roth,et al. Asparaginase‐induced derangements of glutamine metabolism: the pathogenetic basis for some drug‐related side‐effects , 1988, European journal of clinical investigation.
[52] M. Ardawi. Glutamine and glucose metabolism in human peripheral lymphocytes. , 1988, Metabolism: clinical and experimental.
[53] R. Law,et al. Are ninhydrin‐positive substances volume‐regulatory osmolytes in rat renal papillary cells? , 1987, The Journal of physiology.
[54] K. Brand. Glutamine and glucose metabolism during thymocyte proliferation. Pathways of glutamine and glutamate metabolism. , 1985, The Biochemical journal.
[55] H. R. Zielke,et al. Glutamine: a major energy source for cultured mammalian cells. , 1984, Federation proceedings.
[56] L. Reitzer,et al. Evidence that glutamine, not sugar, is the major energy source for cultured HeLa cells. , 1979, The Journal of biological chemistry.
[57] D C Teller,et al. Physical properties of antitumor glutaminase-asparaginase from Pseudomonas 7A. , 1976, The Journal of biological chemistry.
[58] A. Spiers,et al. Bacterial glutaminase in treatment of acute leukaemia. , 1976, British medical journal.
[59] J. Roberts. Purification and properties of a highly potent antitumor glutaminase-asparaginase from Pseudomonas 7Z. , 1976, The Journal of biological chemistry.
[60] H. G. Windmueller,et al. Uptake and metabolism of plasma glutamine by the small intestine. , 1974, The Journal of biological chemistry.
[61] H. Morris,et al. The role of glutamine in the oxidative metabolism of malignant cells. , 1972, Cancer research.
[62] W. Dolowy,et al. Isolation, crystallization, and properties of Achromobacteraceae glutaminase-asparaginase with antitumor activity. , 1972, The Journal of biological chemistry.
[63] D. Herbert,et al. A new L-asparaginase with antitumour activity? , 1968, Lancet.
[64] L. Mashburn,et al. TUMOR INHIBITORY EFFECT OF L-ASPARAGINASE FROM ESCHERICHIA COLI. , 1964, Archives of biochemistry and biophysics.