Accumulation of non‐erythroid αII‐spectrin and calpain‐cleaved αII‐spectrin breakdown products in cerebrospinal fluid after traumatic brain injury in rats
暂无分享,去创建一个
Jeremy J. Flint | Ronald L. Hayes | B. Pike | R. Hayes | Kevin K. W. Wang | J. Flint | Brian R. Pike | Satavisha Dutta | Erik A. Johnson | S. Dutta
[1] K. Raser,et al. Effects of ICE‐like protease and calpain inhibitors on neuronal apoptosis , 1996, Neuroreport.
[2] G. Clifton,et al. Immunohistochemical study of calpain-mediated breakdown products to alpha-spectrin following controlled cortical impact injury in the rat. , 1997, Journal of neurotrauma.
[3] G. Clifton,et al. μ‐Calpain Activation and Calpain‐Mediated Cytoskeletal Proteolysis Following Traumatic Brain Injury , 1996 .
[4] B. Pike,et al. Regional calpain and caspase‐3 proteolysis of α‐spectrin after traumatic brain injury , 1998, Neuroreport.
[5] D. Bozyczko‐Coyne,et al. Prolonged Calpain‐mediated Spectrin Breakdown Occurs Regionally Following Experimental Brain Injury in the Rat , 1996, Journal of neuropathology and experimental neurology.
[6] B. Pike,et al. Temporal Profile of Apoptotic-like Changes in Neurons and Astrocytes Following Controlled Cortical Impact Injury in the Rat , 1999, Experimental Neurology.
[7] R. Siman,et al. Immunolocalization of calpain I-mediated spectrin degradation to vulnerable neurons in the ischemic gerbil brain , 1994, The Journal of neuroscience : the official journal of the Society for Neuroscience.
[8] T A Gennarelli,et al. Animate models of human head injury. , 1994, Journal of neurotrauma.
[9] B. Pike,et al. Temporal relationships between de novo protein synthesis, calpain and caspase 3‐like protease activation, and DNA fragmentation during apoptosis in septo‐hippocampal cultures , 1998, Journal of neuroscience research.
[10] I. Zagon,et al. Brain spectrin: Of mice and men , 1995, Brain Research Bulletin.
[11] Simon C Watkins,et al. Increases in Bcl‐2 and cleavage of caspase‐1 and caspase‐3 in human brain after head injury , 1999, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[12] H. Soininen,et al. Three-year follow-up of cerebrospinal fluid tau, β-amyloid 42 and 40 concentrations in Alzheimer's disease , 2000, Neuroscience Letters.
[13] D. Okonkwo,et al. Cyclosporin A limits calcium-induced axonal damage following traumatic brain injury. , 1999, Neuroreport.
[14] Simon C Watkins,et al. Caspase‐3 Mediated Neuronal Death After Traumatic Brain Injury in Rats , 2000, Journal of neurochemistry.
[15] S. Robinson,et al. Hypothermia blunts acetylcholine increase in CSF of traumatically brain injured rats. , 1993, Molecular and chemical neuropathology.
[16] S. Robinson,et al. The effect of acetylcholine depletion on behavior following traumatic brain injury , 1990, Brain Research.
[17] G. Clifton,et al. Mechanisms of calpain proteolysis following traumatic brain injury: implications for pathology and therapy: implications for pathology and therapy: a review and update. , 1997, Journal of neurotrauma.
[18] Kevin K W Wang,et al. Evidence for Activation of Caspase‐3‐Like Protease in Excitotoxin‐ and Hypoxia/Hypoglycemia‐Injured Neurons , 1998, Journal of neurochemistry.
[19] K. Suzuki,et al. Spatial resolution of fodrin proteolysis in postischemic brain. , 1993, The Journal of biological chemistry.
[20] A. Faden,et al. Combined mechanical trauma and metabolic impairment in vitro induces NMDA receptor‐dependent neuronal cell death and caspase‐3‐dependent apoptosis , 1999, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[21] INTERNATIONAL SOCIETY FOR NEUROCHEMISTRY , 1976 .
[22] R. Bartus,et al. Calpain inhibitor AK295 attenuates motor and cognitive deficits following experimental brain injury in the rat. , 1996, Proceedings of the National Academy of Sciences of the United States of America.
[23] B. Pike,et al. Temporal Profile and Cell Subtype Distribution of Activated Caspase‐3 Following Experimental Traumatic Brain Injury , 2000, Journal of neurochemistry.
[24] R. Grossman,et al. Acetylcholine Metabolism in Intracranial and Lumbar Cerebrospinal Fluid and in Blood , 1980 .
[25] V. Seifert,et al. Fatal secondary increase in serum S-100B protein after severe head injury. Report of three cases. , 1999, Journal of neurosurgery.
[26] R. Rudick,et al. Quantification of Axonal Damage in Traumatic Brain Injury , 1999, Journal of neurochemistry.
[27] B. Pike,et al. Novel Characteristics of Glutamate-Induced Cell Death in Primary Septohippocampal Cultures: Relationship to Calpain and Caspase-3 Protease Activation , 2000, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.
[28] A Büki,et al. Cytochrome c Release and Caspase Activation in Traumatic Axonal Injury , 2000, The Journal of Neuroscience.
[29] J. Morrow,et al. The calmodulin-binding site in alpha-fodrin is near the calcium-dependent protease-I cleavage site. , 1988, The Journal of biological chemistry.
[30] A. Marmarou,et al. Production and clearance of lactate from brain tissue, cerebrospinal fluid, and serum following experimental brain injury. , 1988, Journal of neurosurgery.
[31] R. Raghupathi,et al. Regional and Temporal Alterations in DNA Fragmentation Factor (DFF)‐Like Proteins Following Experimental Brain Trauma in the Rat , 1999, Journal of neurochemistry.
[32] B Pascrell,et al. Traumatic brain injury. The silent epidemic. , 2001, New Jersey medicine : the journal of the Medical Society of New Jersey.
[33] T A Gennarelli,et al. Modification of the cortical impact model to produce axonal injury in the rat cerebral cortex. , 1994, Journal of neurotrauma.
[34] R. Talanian,et al. Simultaneous Degradation of αII- and βII-Spectrin by Caspase 3 (CPP32) in Apoptotic Cells* , 1998, The Journal of Biological Chemistry.
[35] Kevin K W Wang,et al. Activation of apoptosis-linked caspase(s) in NMDA-injured brains in neonatal rats , 2000, Neurochemistry International.
[36] V. Seifert,et al. Serum S-100B protein in severe head injury. , 2000, Neurosurgery.
[37] F. Angileri,et al. Protective effects of moderate hypothermia on behavioral deficits but not necrotic cavitation following cortical impact injury in the rat. , 1998, Journal of neurotrauma.
[38] X. M. Xu,et al. Apoptosis mediates cell death following traumatic injury in rat hippocampal neurons , 1997, Neuroscience.
[39] I. Zagon,et al. Brain spectrin(240/235) and brain spectrin(240/235E): two distinct spectrin subtypes with different locations within mammalian neural cells , 1986, The Journal of cell biology.
[40] R. Bartus,et al. Behavioral Efficacy of Posttraumatic Calpain Inhibition is Not Accompanied by Reduced Spectrin Proteolysis, Cortical Lesion, or Apoptosis , 2000, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.
[41] Ronald L. Hayes,et al. A controlled cortical impact model of traumatic brain injury in the rat , 1991, Journal of Neuroscience Methods.
[42] R. Gilbertsen,et al. Non-erythroid alpha-spectrin breakdown by calpain and interleukin 1 beta-converting-enzyme-like protease(s) in apoptotic cells: contributory roles of both protease families in neuronal apoptosis. , 1996, The Biochemical journal.
[43] S. Wisniewski,et al. Increases in bcl-2 protein in cerebrospinal fluid and evidence for programmed cell death in infants and children after severe traumatic brain injury. , 2000, The Journal of pediatrics.
[44] G. Clifton,et al. mu-calpain activation and calpain-mediated cytoskeletal proteolysis following traumatic brain injury. , 1996, Journal of Neurochemistry.
[45] G. Clifton,et al. A calpain inhibitor attenuates cortical cytoskeletal protein loss after experimental traumatic brain injury in the rat , 1997, Neuroscience.
[46] B. Pike,et al. Stretch injury causes calpain and caspase-3 activation and necrotic and apoptotic cell death in septo-hippocampal cell cultures. , 2000, Journal of neurotrauma.
[47] A. Yakovlev,et al. Activation of CPP32-Like Caspases Contributes to Neuronal Apoptosis and Neurological Dysfunction after Traumatic Brain Injury , 1997, The Journal of Neuroscience.
[48] S. Snyder,et al. Temporal Patterns of Poly(ADP‐Ribose) Polymerase Activation in the Cortex Following Experimental Brain Injury in the Rat , 1999, Journal of neurochemistry.
[49] G. Clifton,et al. Mechanisms of Calpain Proteolysis Following Traumatic Brain Injury: Implications for Pathology and Therapy: A Review and Update , 1997 .