Activation of mu-calpain in developing cortical neurons following methylmercury treatment.
暂无分享,去创建一个
H. Nakanishi | S. Hashioka | K. Murao | T. Saido | Jian Zhang | K. Miyamoto | H. Hao
[1] J. Nascimento,et al. Protection of methylmercury effects on the in vivo dopamine release by NMDA receptor antagonists and nitric oxide synthase inhibitors , 2002, Neuropharmacology.
[2] H. Nakanishi,et al. Involvement of enhanced sensitivity of N-methyl-d-aspartate receptors in vulnerability of developing cortical neurons to methylmercury neurotoxicity , 2001, Brain Research.
[3] A. Kakita,et al. Calpain‐mediated degradation of p35 to p25 in postmortem human and rat brains , 2001, FEBS letters.
[4] B. Zhivotovsky,et al. Antioxidants J811 and 17β‐estradiol protect cerebellar granule cells from methylmercury‐induced apoptotic cell death , 2000, Journal of neuroscience research.
[5] M. Aschner,et al. Methylmercury alters glutamate transport in astrocytes , 2000, Neurochemistry International.
[6] H. Nakanishi,et al. Involvement of caspase 3-like protease in methylmercury-induced apoptosis of primary cultured rat cerebral microglia , 2000, Brain Research.
[7] H. Nakanishi,et al. Glutamate release from microglia via glutamate transporter is enhanced by amyloid-beta peptide , 1999, Neuroscience.
[8] Zhang Ml. Calcium activated neutral protease and its endogenous inhibitor , 1998 .
[9] J. Jordán,et al. Role of Calpain‐ and Interleukin‐1β Converting Enzyme‐Like Proteases in the β‐Amyloid‐Induced Death of Rat Hippocampal Neurons in Culture , 1997 .
[10] Y. Ando,et al. Role of nitric oxide in the cerebellar degeneration during methylmercury intoxication. , 1997, Biochimica et biophysica acta.
[11] M. Goldberg,et al. Calpain Activation Contributes to Dendritic Remodeling after Brief Excitotoxic Injury In Vitro , 1997, The Journal of Neuroscience.
[12] J. Krieglstein,et al. Blockade of calpain proteolytic activity rescues neurons from glutamate excitotoxicity , 1997, Neuroscience Research.
[13] G. Clifton,et al. μ‐Calpain Activation and Calpain‐Mediated Cytoskeletal Proteolysis Following Traumatic Brain Injury , 1996 .
[14] E. Lunney,et al. An alpha-mercaptoacrylic acid derivative is a selective nonpeptide cell-permeable calpain inhibitor and is neuroprotective. , 1996, Proceedings of the National Academy of Sciences of the United States of America.
[15] M. Sakamoto,et al. Comparison of mercury accumulation among the brain, liver, kidney, and the brain regions of rats administered methylmercury in various phases of postnatal development , 1995, Bulletin of environmental contamination and toxicology.
[16] 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.
[17] K. Suzuki,et al. Spatial resolution of fodrin proteolysis in postischemic brain. , 1993, The Journal of biological chemistry.
[18] N. Kassell,et al. Attenuation of AMPA-induced neurotoxicity by a calpain inhibitor , 1993, Brain Research.
[19] M. Aschner,et al. Methylmercury-induced alterations in excitatory amino acid transport in rat primary astrocyte cultures , 1993, Brain Research.
[20] D. Kristt,et al. Inhibition of Amino Acid Transport and Protein Synthesis by HgCl2 and Methylmercury in Astrocytes: Selectivity and Reversibility , 1989, Journal of neurochemistry.
[21] R. Siman,et al. Calpain I activation is specifically related to excitatory amino acid induction of hippocampal damage , 1989, The Journal of neuroscience : the official journal of the Society for Neuroscience.
[22] Robert Siman,et al. Excitatory amino acids activate calpain I and induce structural protein breakdown in vivo , 1988, Neuron.
[23] H. Kawasaki,et al. Calcium‐activated neutral protease and its endogenous inhibitor Activation at the cell membrane and biological function , 1987, FEBS letters.
[24] S. U. Kim,et al. Methylmercury-induced neurotoxicity in cerebral neuron culture is blocked by antioxidants and NMDA receptor antagonists. , 1996, Neurotoxicology.