Extensive degradation of myelin basic protein isoforms by calpain following traumatic brain injury
暂无分享,去创建一个
F. Tortella | R. Hayes | J. Dave | Kevin K. W. Wang | S. Larner | Wenrong Zheng | M. Liu | Wenrong Zheng | Ming Cheng Liu | Veronica Akle | Jason Kitlen | Barbara O'Steen | Stephen F. Larner | Jitendra R. Dave | Frank C. Tortella | Ronald L. Hayes | Kevin K. W. Wang | Veronica Akle | B. O'Steen | J. Kitlen
[1] H. Berlet,et al. Elucidation of cathepsin B‐like activity associated with extracts of human myelin basic protein , 1985, FEBS letters.
[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] N. Banik,et al. Mechanism of Myelin Breakdown in Experimental Demyelination: A Putative Role for Calpain , 2001, Neurochemical Research.
[4] N. Banik,et al. Peptide bond specificity of calpain: Proteolysis of human myelin basic protein , 1994, Journal of neuroscience research.
[5] Irving Ea,et al. Assessment of white matter injury following prolonged focal cerebral ischaemia in the rat. , 2001 .
[6] R. Talanian,et al. Simultaneous Degradation of αII- and βII-Spectrin by Caspase 3 (CPP32) in Apoptotic Cells* , 1998, The Journal of Biological Chemistry.
[7] D. Graham,et al. Calpain activation and cytoskeletal protein breakdown in the corpus callosum of head-injured patients. , 1999, Journal of neurotrauma.
[8] M. Benuck,et al. Metabolic instability of myelin proteins. Breakdown of basic protein induced by brain cathepsin D. , 1975, European journal of biochemistry.
[9] D. Attwell,et al. NMDA receptors are expressed in oligodendrocytes and activated in ischaemia , 2005, Nature.
[10] J. Morrow,et al. Development and characterization of antibodies specific to caspase-3-produced alpha II-spectrin 120 kDa breakdown product: marker for neuronal apoptosis , 2000, Neurochemistry International.
[11] K. Wang,et al. Development and therapeutic potential of calpain inhibitors. , 1997, Advances in pharmacology.
[12] M. Schwab,et al. Sequential loss of myelin proteins during Wallerian degeneration in the rat spinal cord , 2003, Glia.
[13] J. A. Sloane,et al. Age‐dependent myelin degeneration and proteolysis of oligodendrocyte proteins is associated with the activation of calpain‐1 in the rhesus monkey , 2002, Journal of neurochemistry.
[14] M. Fini,et al. Effects of Matrix Metalloproteinase-9 Gene Knock-Out on Morphological and Motor Outcomes after Traumatic Brain Injury , 2000, The Journal of Neuroscience.
[15] Helen M. Bramlett,et al. Quantitative structural changes in white and gray matter 1 year following traumatic brain injury in rats , 2002, Acta Neuropathologica.
[16] T. Miyatake,et al. Myelin‐Associated Calpain II , 1988, Journal of neurochemistry.
[17] J. Bresnahan,et al. Apoptosis and delayed degeneration after spinal cord injury in rats and monkeys , 1997, Nature Medicine.
[18] K. Williams,et al. Acidic lipids enhance cathepsin D cleavage of the myelin basic protein , 1986, Journal of neuroscience research.
[19] S. Brostoff,et al. Specific cleavage of the A1 protein from myelin with cathepsin D. , 1974, The Journal of biological chemistry.
[20] K. Takahashi,et al. Limited proteolysis of bovine myelin basic protein by calcium-dependent proteinase from bovine spinal cord. , 1989, Journal of biochemistry.
[21] P. Stys,et al. Anoxic and Ischemic Injury of Myelinated Axons in CNS White Matter: From Mechanistic Concepts to Therapeutics , 1998, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.
[22] T. Yamashima,et al. Inhibition of ischaemic hippocampal neuronal death in primates with cathepsin B inhibitor CA‐074: a novel strategy for neuroprotection based on ‘calpain–cathepsin hypothesis’ , 1998 .
[23] S. Waxman. Demyelinating diseases--new pathological insights, new therapeutic targets. , 1998, The New England journal of medicine.
[24] M. Esiri,et al. Axonal damage: a key predictor of outcome in human CNS diseases. , 2003, Brain : a journal of neurology.
[25] D. Okonkwo,et al. Caspase-3-mediated cleavage of amyloid precursor protein and formation of amyloid Beta peptide in traumatic axonal injury. , 2002, Journal of neurotrauma.
[26] A Büki,et al. Cytochrome c Release and Caspase Activation in Traumatic Axonal Injury , 2000, The Journal of Neuroscience.
[27] M. Schwab,et al. Oligodendroglial reaction following spinal cord injury in rat: Transient upregulation of MBP mRNA , 1998, Glia.
[28] T. Saido,et al. A putative mechanism of demyelination in multiple sclerosis by a proteolytic enzyme, calpain. , 1999, Proceedings of the National Academy of Sciences of the United States of America.
[29] D D Blatter,et al. Nonspecific white matter degeneration following traumatic brain injury , 1995, Journal of the International Neuropsychological Society.
[30] INTERNATIONAL SOCIETY FOR NEUROCHEMISTRY , 1976 .
[31] M. Benuck,et al. Specificity of brain cathepsin D: Cleavage of model peptides containing the susceptible phe‐phe regions of myelin basic protein , 1980, Journal of neuroscience research.
[32] M. Fini,et al. Secretion of matrix metalloproteinase-2 and -9 after mechanical trauma injury in rat cortical cultures and involvement of MAP kinase. , 2002, Journal of neurotrauma.
[33] B. Pike,et al. Regional calpain and caspase‐3 proteolysis of α‐spectrin after traumatic brain injury , 1998, Neuroreport.
[34] D. Johnston,et al. Neuronal apoptosis inhibitory protein expression after traumatic brain injury in the mouse. , 2001, Journal of neurotrauma.
[35] J. Trojanowski,et al. The role of calpain-mediated spectrin proteolysis in traumatically induced axonal injury. , 1999, Journal of neuropathology and experimental neurology.
[36] H. Okano,et al. Caspase-mediated oligodendrocyte cell death in the pathogenesis of autoimmune demyelination , 2003, Neuroscience Research.
[37] B. Trapp,et al. NMDA receptors mediate calcium accumulation in myelin during chemical ischaemia , 2006, Nature.
[38] K. Suzuki,et al. In situ capture of mu-calpain activation in platelets. , 1993, The Journal of biological chemistry.
[39] J. Mcdonald,et al. Oligodendrocytes from forebrain are highly vulnerable to AMPA/kainate receptor-mediated excitotoxicity , 1998, Nature Medicine.
[40] M Chopp,et al. Cathepsin B and middle cerebral artery occlusion in the rat. , 1997, Journal of neurosurgery.
[41] G. Clifton,et al. A calpain inhibitor attenuates cortical cytoskeletal protein loss after experimental traumatic brain injury in the rat , 1997, Neuroscience.
[42] G. Lynch,et al. Induction of calpain-mediated spectrin fragments by pathogenic treatments in long-term hippocampal slices. , 1995, The Journal of pharmacology and experimental therapeutics.
[43] M. Fini,et al. Effects of Matrix Metalloproteinase-9 Gene Knock-Out on the Proteolysis of Blood–Brain Barrier and White Matter Components after Cerebral Ischemia , 2001, The Journal of Neuroscience.
[44] J. Povlishock,et al. Traumatically induced altered membrane permeability: its relationship to traumatically induced reactive axonal change. , 1994, Journal of neurotrauma.
[45] A. Omori,et al. Study of expression of myelin basic proteins (MBPs) in developing rat brain using a novel antibody reacting with four major isoforms of MBP , 2002, Journal of neuroscience research.
[46] Kevin K. W Wang,et al. Calpain and caspase: can you tell the difference? , 2000, Trends in Neurosciences.
[47] 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.
[48] W. Poon,et al. The pathological spectrum of diffuse axonal injury in blunt head trauma: assessment with axon and myelin stains , 1994, Clinical Neurology and Neurosurgery.
[49] R. Bullock,et al. Design and statistical issues in multicenter trials of severe head injury , 2001, Neurological research.
[50] M. Salter,et al. NMDA receptors are expressed in developing oligodendrocyte processes and mediate injury , 2005, Nature.
[51] Kevin K W Wang,et al. Selective release of calpain produced alphalI-spectrin (alpha-fodrin) breakdown products by acute neuronal cell death. , 2002, Biological chemistry.
[52] Kevin K W Wang,et al. Selective Release of Calpain Produced αII-Spectrin (α-Fodrin) Breakdown Products by Acute Neuronal Cell Death , 2002 .
[53] B. Pike,et al. Effects of injury severity on regional and temporal mRNA expression levels of calpains and caspases after traumatic brain injury in rats. , 2004, Journal of neurotrauma.
[54] E. Hogan,et al. Calcium‐Stimulated Proteolysis in Myelin: Evidence for a Ca2+‐Activated Neutral Proteinase Associated with Purified Myelin of Rat CNS , 1985, Journal of neurochemistry.
[55] R. Hayes,et al. Neurofilament 68 and neurofilament 200 protein levels decrease after traumatic brain injury. , 1994, Journal of neurotrauma.
[56] 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.