Huntingtin Spheroids and Protofibrils as Precursors in Polyglutamine Fibrilization*
暂无分享,去创建一个
Christopher A. Ross | Huilin Li | Shuowei Cai | C. Ross | Huilin Li | J. Macosko | S. Cai | Michelle A. Poirier | Jed Macosko | Mario Amzel | M. Amzel
[1] 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.
[2] C. Bustamante,et al. Wrapping of DNA around the E.coli RNA polymerase open promoter complex , 1999, The EMBO journal.
[3] B. Singh,et al. Infrared analysis of peptides and proteins : principles and applications , 1999 .
[4] Hans Lehrach,et al. Huntingtin-Encoded Polyglutamine Expansions Form Amyloid-like Protein Aggregates In Vitro and In Vivo , 1997, Cell.
[5] Mark Turmaine,et al. Formation of Neuronal Intranuclear Inclusions Underlies the Neurological Dysfunction in Mice Transgenic for the HD Mutation , 1997, Cell.
[6] E. Altschuler,et al. Random coil conformation for extended polyglutamine stretches in aqueous soluble monomeric peptides. , 2009, The journal of peptide research : official journal of the American Peptide Society.
[7] C. Finch,et al. Targeting small Aβ oligomers: the solution to an Alzheimer's disease conundrum? , 2001, Trends in Neurosciences.
[8] P. Patterson,et al. Effects of intracellular expression of anti-huntingtin antibodies of various specificities on mutant huntingtin aggregation and toxicity , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[9] G P Bates,et al. Self-assembly of polyglutamine-containing huntingtin fragments into amyloid-like fibrils: implications for Huntington's disease pathology. , 1999, Proceedings of the National Academy of Sciences of the United States of America.
[10] S. Hersch,et al. Huntingtin aggregates may not predict neuronal death in Huntington's disease , 1999 .
[11] S. W. Davies,et al. Intranuclear Neuronal Inclusions in Huntington's Disease and Dentatorubral and Pallidoluysian Atrophy: Correlation between the Density of Inclusions andIT15CAG Triplet Repeat Length , 1998, Neurobiology of Disease.
[12] S. W. Davies,et al. Aggregation of huntingtin in neuronal intranuclear inclusions and dystrophic neurites in brain. , 1997, Science.
[13] F. Fu,et al. Role of zinc in the structure and toxic activity of botulinum neurotoxin. , 1998, Biochemistry.
[14] H. Zoghbi,et al. Glutamine repeats and neurodegeneration. , 2000, Annual review of neuroscience.
[15] P S Harper,et al. Phenotypic characterization of individuals with 30-40 CAG repeats in the Huntington disease (HD) gene reveals HD cases with 36 repeats and apparently normal elderly individuals with 36-39 repeats. , 1996, American journal of human genetics.
[16] C. Ross,et al. Preparation of human cDNAs encoding expanded polyglutamine repeats , 1999, Neuroscience Letters.
[17] James F. Gusella,et al. Molecular genetics: Unmasking polyglutamine triggers in neurodegenerative disease , 2000, Nature Reviews Neuroscience.
[18] J. Penney,et al. Trinucleotide repeat length instability and age of onset in Huntington's disease , 1993, Nature Genetics.
[19] C. Ross,et al. Isolation of a 40-kDa Huntingtin-associated Protein* , 2001, The Journal of Biological Chemistry.
[20] H. Paulson. Toward an Understanding of Polyglutamine Neurodegeneration , 2000, Brain pathology.
[21] H. Lehrach,et al. Inhibition of huntingtin fibrillogenesis by specific antibodies and small molecules: implications for Huntington's disease therapy. , 2000, Proceedings of the National Academy of Sciences of the United States of America.
[22] Peter T. Lansbury,et al. Assembly of Aβ Amyloid Protofibrils: An in Vitro Model for a Possible Early Event in Alzheimer's Disease† , 1999 .
[23] R. Wetzel,et al. Polyglutamine aggregation behavior in vitro supports a recruitment mechanism of cytotoxicity. , 2001, Journal of molecular biology.
[24] R. Wetzel,et al. Conformational Abs recognizing a generic amyloid fibril epitope , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[25] P. Lansbury,et al. Inhibition of fibrillization and accumulation of prefibrillar oligomers in mixtures of human and mouse alpha-synuclein. , 2000, Biochemistry.
[26] S. Lindquist,et al. Nucleated conformational conversion and the replication of conformational information by a prion determinant. , 2000, Science.
[27] Peter T. Lansbury,et al. Kinetic Stabilization of the α-Synuclein Protofibril by a Dopamine-α-Synuclein Adduct , 2001, Science.
[28] Claire-Anne Gutekunst,et al. Nuclear and Neuropil Aggregates in Huntington’s Disease: Relationship to Neuropathology , 1999, The Journal of Neuroscience.
[29] W. K. Cullen,et al. Naturally secreted oligomers of amyloid β protein potently inhibit hippocampal long-term potentiation in vivo , 2002, Nature.
[30] S. Sisodia. Nuclear Inclusions in Glutamine Repeat Disorders Are They Pernicious, Coincidental, or Beneficial? , 1998, Cell.
[31] Annalisa Pastore,et al. Solution structure of polyglutamine tracts in GST‐polyglutamine fusion proteins , 2002, FEBS letters.
[32] C. Dobson,et al. Inherent toxicity of aggregates implies a common mechanism for protein misfolding diseases , 2002, Nature.
[33] D. Housman,et al. A bivalent Huntingtin binding peptide suppresses polyglutamine aggregation and pathogenesis in Drosophila , 2002, Nature Genetics.