Suppression of basal autophagy in neural cells causes neurodegenerative disease in mice
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Hideyuki Okano | Kenji Nakamura | Ichiro Saito | H. Okano | Taichi Hara | K. Mishima | I. Saito | Kenji Nakamura | M. Matsui | A. Yamamoto | Yohko Nakahara | Rika Suzuki-Migishima | M. Yokoyama | N. Mizushima | Noboru Mizushima | Akitsugu Yamamoto | Taichi Hara | Makoto Matsui | Yohko Nakahara | Rika Suzuki-Migishima | Minesuke Yokoyama | Kenji Mishima
[1] Terje Johansen,et al. p62/SQSTM1 forms protein aggregates degraded by autophagy and has a protective effect on huntingtin-induced cell death , 2005, The Journal of cell biology.
[2] N. Mizushima. The pleiotropic role of autophagy: from protein metabolism to bactericide , 2005, Cell Death and Differentiation.
[3] Atsushi Iwata,et al. Increased susceptibility of cytoplasmic over nuclear polyglutamine aggregates to autophagic degradation. , 2005, Proceedings of the National Academy of Sciences of the United States of America.
[4] Masaaki Komatsu,et al. Impairment of starvation-induced and constitutive autophagy in Atg7-deficient mice , 2005, The Journal of cell biology.
[5] N. Heintz,et al. Autophagy and Its Possible Roles in Nervous System Diseases, Damage and Repair , 2005, Autophagy.
[6] D. Klionsky. The molecular machinery of autophagy: unanswered questions , 2005, Journal of Cell Science.
[7] Takeshi Tokuhisa,et al. The role of autophagy during the early neonatal starvation period , 2004, Nature.
[8] Mark R. Segal,et al. Inclusion body formation reduces levels of mutant huntingtin and the risk of neuronal death , 2004, Nature.
[9] A. Yoshimura,et al. Socs3 deficiency in the brain elevates leptin sensitivity and confers resistance to diet-induced obesity , 2004, Nature Medicine.
[10] Francesco Scaravilli,et al. Inhibition of mTOR induces autophagy and reduces toxicity of polyglutamine expansions in fly and mouse models of Huntington disease , 2004, Nature Genetics.
[11] Daniel J Klionsky,et al. Development by self-digestion: molecular mechanisms and biological functions of autophagy. , 2004, Developmental cell.
[12] Takeshi Iwatsubo,et al. Aggresomes Formed by α-Synuclein and Synphilin-1 Are Cytoprotective* , 2004, Journal of Biological Chemistry.
[13] A. Cuervo. Autophagy: in sickness and in health. , 2004, Trends in cell biology.
[14] T. Kikuchi,et al. Axonal degeneration of ascending sensory neurons in gracile axonal dystrophy mutant mouse , 2004, Acta Neuropathologica.
[15] L. Notterpek,et al. Emerging Role for Autophagy in the Removal of Aggresomes in Schwann Cells , 2003, The Journal of Neuroscience.
[16] Fumiaki Tanaka,et al. Aggresomes protect cells by enhancing the degradation of toxic polyglutamine-containing protein. , 2003, Human molecular genetics.
[17] L. Lossi,et al. Synapse-independent and synapse-dependent apoptosis of cerebellar granule cells in postnatal rabbits occur at two subsequent but partly overlapping developmental stages , 2002, Neuroscience.
[18] Rainer Duden,et al. Aggregate-prone proteins with polyglutamine and polyalanine expansions are degraded by autophagy. , 2002, Human molecular genetics.
[19] Takeshi Tokuhisa,et al. Dissection of Autophagosome Formation Using Apg5-Deficient Mouse Embryonic Stem Cells , 2001, The Journal of cell biology.
[20] R. Kopito,et al. Aggresomes, inclusion bodies and protein aggregation. , 2000, Trends in cell biology.
[21] Takeshi Noda,et al. LC3, a mammalian homologue of yeast Apg8p, is localized in autophagosome membranes after processing , 2000, The EMBO journal.
[22] S. Hersch,et al. Huntingtin aggregates may not predict neuronal death in Huntington's disease , 1999 .
[23] S. Hersch,et al. Huntington aggregates may not predict neuronal death in Huntington's disease. , 1999, Annals of neurology.
[24] Steven Finkbeiner,et al. Huntingtin Acts in the Nucleus to Induce Apoptosis but Death Does Not Correlate with the Formation of Intranuclear Inclusions , 1998, Cell.
[25] J. Miyazaki,et al. A transgenic mouse line that retains Cre recombinase activity in mature oocytes irrespective of the cre transgene transmission. , 1997, Biochemical and biophysical research communications.
[26] S. W. Davies,et al. Exon 1 of the HD Gene with an Expanded CAG Repeat Is Sufficient to Cause a Progressive Neurological Phenotype in Transgenic Mice , 1996, Cell.
[27] Werner Müller,et al. Bypass of lethality with mosaic mice generated by Cre–loxP-mediated recombination , 1996, Current Biology.
[28] M Aguet,et al. Inducible gene targeting in mice , 1995, Science.
[29] J. Julien,et al. Progressive neuronopathy in transgenic mice expressing the human neurofilament heavy gene: A mouse model of amyotrophic lateral sclerosis , 1993, Cell.
[30] K. Mikoshiba,et al. Stacks of flattened smooth endoplasmic reticulum highly enriched in inositol 1,4,5-trisphosphate (InsP3) receptor in mouse cerebellar Purkinje cells. , 1991, Cell structure and function.
[31] C. Sotelo. Axonal abnormalities in cerebellar Purkinje cells of the ‘hyperspiny Purkinje cell’ mutant mouse , 1990, Journal of neurocytology.
[32] A. Vinokur,et al. "In Sickness and in Health" , 1990 .