Activation of calpain in cultured neurons overexpressing Alzheimer amyloid precursor protein.
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[1] T. Hara,et al. Cell death induced by a caspase-cleaved transmembrane fragment of the Alzheimer amyloid precursor protein , 2002, Cell Death and Differentiation.
[2] P. Nicotera,et al. Calpain inhibitors prevent nitric oxide-triggered excitotoxic apoptosis , 2001, Neuroreport.
[3] B. Pike,et al. Concurrent Assessment of Calpain and Caspase-3 Activation after Oxygen–Glucose Deprivation in Primary Septo-Hippocampal Cultures , 2001, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.
[4] Changlian Zhu,et al. Synergistic Activation of Caspase-3 by m-Calpain after Neonatal Hypoxia-Ischemia , 2001, The Journal of Biological Chemistry.
[5] R. Neve,et al. Alzheimer’s disease: a dysfunction of the amyloid precursor protein 1 1 Published on the World Wide Web on 11 September 2000. , 2000, Brain Research.
[6] R. Hata,et al. Caspase-3 activation and inflammatory responses in rat hippocampus inoculated with a recombinant adenovirus expressing the Alzheimer amyloid precursor protein. , 2000, Brain research. Molecular brain research.
[7] Junying Yuan,et al. Cross-Talk between Two Cysteine Protease Families , 2000, The Journal of cell biology.
[8] Y. Suh,et al. Carboxyl‐terminal fragment of Alzheimer's APP destabilizes calcium homeostasis and renders neuronal cells vulnerable to excitotoxicity , 2000, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[9] Peng Li,et al. Direct Cleavage by the Calcium-activated Protease Calpain Can Lead to Inactivation of Caspases* , 2000, The Journal of Biological Chemistry.
[10] K. Jellinger,et al. Activation of caspase-3 in single neurons and autophagic granules of granulovacuolar degeneration in Alzheimer's disease. Evidence for apoptotic cell death. , 1999, The American journal of pathology.
[11] R. Neve,et al. Enhanced BK-induced calcium responsiveness in PC12 cells expressing the C100 fragment of the amyloid precursor protein. , 1999, Brain research. Molecular brain research.
[12] K. Wang,et al. Procaspase-3 and poly(ADP)ribose polymerase (PARP) are calpain substrates. , 1999, Biochemical and biophysical research communications.
[13] C. Martínez-A,et al. Implication of calpain in caspase activation during B cell clonal deletion , 1999, The EMBO journal.
[14] D. Holtzman,et al. In situ immunodetection of neuronal caspase-3 activation in Alzheimer disease. , 1999, Journal of neuropathology and experimental neurology.
[15] K. Yoshikawa,et al. Activation of Neuronal Caspase-3 by Intracellular Accumulation of Wild-Type Alzheimer Amyloid Precursor Protein , 1999, Journal of Neuroscience.
[16] L. Mucke,et al. Wild-type but not Alzheimer-mutant amyloid precursor protein confers resistance against p53-mediated apoptosis. , 1999, Proceedings of the National Academy of Sciences of the United States of America.
[17] E. Newcomb,et al. Caspase-dependent Activation of Calpain during Drug-induced Apoptosis* , 1999, The Journal of Biological Chemistry.
[18] J. Shioi,et al. Overexpression in Neurons of Human Presenilin-1 or a Presenilin-1 Familial Alzheimer Disease Mutant Does Not Enhance Apoptosis , 1998, The Journal of Neuroscience.
[19] D. Green,et al. Calpain activation is upstream of caspases in radiation-induced apoptosis , 1998, Cell Death and Differentiation.
[20] R. Oppenheim,et al. Increased Production of Amyloid Precursor Protein Provides a Substrate for Caspase-3 in Dying Motoneurons , 1998, The Journal of Neuroscience.
[21] R. Simon,et al. Induction of Caspase-3-Like Protease May Mediate Delayed Neuronal Death in the Hippocampus after Transient Cerebral Ischemia , 1998, The Journal of Neuroscience.
[22] M. Moskowitz,et al. Activation and Cleavage of Caspase-3 in Apoptosis Induced by Experimental Cerebral Ischemia , 1998, The Journal of Neuroscience.
[23] H. Okamura,et al. Degeneration In Vivo of Rat Hippocampal Neurons by Wild-Type Alzheimer Amyloid Precursor Protein Overexpressed by Adenovirus-Mediated Gene Transfer , 1998, The Journal of Neuroscience.
[24] Hui Zheng,et al. The β-Amyloid Precursor Protein of Alzheimer’s Disease Enhances Neuron Viability and Modulates Neuronal Polarity , 1997, The Journal of Neuroscience.
[25] M. Mattson. Cellular actions of beta-amyloid precursor protein and its soluble and fibrillogenic derivatives. , 1997, Physiological reviews.
[26] R. Nixon,et al. Active site-directed antibodies identify calpain II as an early-appearing and pervasive component of neurofibrillary pathology in Alzheimer's disease , 1997, Brain Research.
[27] A. Ogura,et al. Glutamate responsiveness enhanced in neurones expressing amyloid precursor protein , 1997, Neuroreport.
[28] B. Yankner. Mechanisms of Neuronal Degeneration in Alzheimer's Disease , 1996, Neuron.
[29] K. Krause,et al. Overexpression of Calreticulin Increases Intracellular Ca Storage and Decreases Store-operated Ca Influx (*) , 1996, The Journal of Biological Chemistry.
[30] R. Oppenheim,et al. Peptide inhibitors of the ice protease family arrest programmed cell death of motoneurons in vivo and in vitro , 1995, Neuron.
[31] Patrick R. Griffin,et al. Identification and inhibition of the ICE/CED-3 protease necessary for mammalian apoptosis , 1995, Nature.
[32] H. Sorimachi,et al. Calpain: new perspectives in molecular diversity and physiological‐pathological involvement , 1994, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[33] Y. Ihara,et al. Spatial resolution of the primary beta-amyloidogenic process induced in postischemic hippocampus. , 1994, The Journal of biological chemistry.
[34] K. Suzuki,et al. Spatial resolution of fodrin proteolysis in postischemic brain. , 1993, The Journal of biological chemistry.
[35] R. Nixon,et al. Widespread activation of calcium-activated neutral proteinase (calpain) in the brain in Alzheimer disease: a potential molecular basis for neuronal degeneration. , 1993, Proceedings of the National Academy of Sciences of the United States of America.
[36] D. Stephenson,et al. Amyloid precursor protein accumulates in regions of neurodegeneration following focal cerebral ischemia in the rat , 1992, Brain Research.
[37] K. Yoshikawa,et al. Degeneration in vitro of post-mitotic neurons overexpressing the Alzheimer amyloid protein precursor , 1992, Nature.
[38] Brian J Cummings,et al. Aggregation of the amyloid precursor protein within degenerating neurons and dystrophic neurites in alzheimer's disease , 1992, Neuroscience.
[39] V M Lee,et al. Pure, postmitotic, polarized human neurons derived from NTera 2 cells provide a system for expressing exogenous proteins in terminally differentiated neurons , 1992, The Journal of neuroscience : the official journal of the Society for Neuroscience.
[40] G. Demartino,et al. Calcium-activated neutral protease (calpain) system: structure, function, and regulation. , 1991, Physiological reviews.
[41] E. Masliah,et al. Accumulation of amyloid precursor fragment in Alzheimer plaques , 1991, Neurobiology of Aging.
[42] K. Blomgren,et al. Calpain and calpastatin in normal and Alzheimer-degenerated human brain tissue , 1990, Neurobiology of Aging.
[43] R. Neve,et al. The amyloid precursor protein is concentrated in neuronal lysosomes in normal and Alzheimer disease subjects , 1989, Experimental Neurology.
[44] Carl W. Cotman,et al. Protease nexin-II, a potent anti-chymotrypsin, shows identity to amyloid β-protein precursor , 1989, Nature.
[45] P. Andrews. Retinoic acid induces neuronal differentiation of a cloned human embryonal carcinoma cell line in vitro. , 1984, Developmental biology.
[46] G. Glenner,et al. Alzheimer's disease: Initial report of the purification and characterization of a novel cerebrovascular amyloid protein , 1984 .
[47] D. Green,et al. Calpain functions in a caspase-independent manner to promote apoptosis-like events during platelet activation. , 1999, Blood.
[48] D. Selkoe,et al. Normal and abnormal biology of the beta-amyloid precursor protein. , 1994, Annual review of neuroscience.
[49] K. Suzuki,et al. Autolytic transition of mu-calpain upon activation as resolved by antibodies distinguishing between the pre- and post-autolysis forms. , 1992, Journal of biochemistry.