Reversing neurodegeneration: A promise unfolds

[1] Ubiquitin, cellular inclusions and their role in neurodegeneration [J]. TRENDS IN NEUROSCIENCES, 1998, 21 (12) : 516 - 520

[2] Degradation of α-synuclein by proteasome [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (48) : 33855 - 33858

[3] Up-regulation of protein chaperones preserves viability of cells expressing toxic Cu/Zn-superoxide dismutase mutants associated with amyotrophic lateral sclerosis [J]. JOURNAL OF NEUROCHEMISTRY, 1999, 72 (02) : 693 - 699

[4] Chai YH, 1999, J NEUROSCI, V19, P10338

[5] Acceleration of oligomerization, not fibrillization, is a shared property of both α-synuclein mutations linked to early-onset Parkinson's disease:: Implications for pathogenesis and therapy [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2000, 97 (02) : 571 - 576

[6] Mutation of the E6-AP ubiquitin ligase reduces nuclear inclusion frequency while accelerating polyglutamine-induced pathology in SCA1 mice [J]. NEURON, 1999, 24 (04) : 879 - 892

[7] Chaperone suppression of aggregation and altered subcellular proteasome localization imply protein misfolding in SCA1 [J]. NATURE GENETICS, 1998, 19 (02) : 148 - 154

[8] A YAC mouse model for Huntington's disease with full-length mutant huntingtin, cytoplasmic toxicity, and selective striatal neurodegeneration [J]. NEURON, 1999, 23 (01) : 181 - 192

[9] The tyrosine kinase negative regulator c-Cbl as a RING-type, E2-dependent ubiquitin-protein ligase [J]. SCIENCE, 1999, 286 (5438) : 309 - 312

[10] Aberrant protein deposition and neurological disease [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (53) : 37507 - 37510

[1] Ubiquitin, cellular inclusions and their role in neurodegeneration [J]. TRENDS IN NEUROSCIENCES, 1998, 21 (12) : 516 - 520

[2] Degradation of α-synuclein by proteasome [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (48) : 33855 - 33858

[3] Up-regulation of protein chaperones preserves viability of cells expressing toxic Cu/Zn-superoxide dismutase mutants associated with amyotrophic lateral sclerosis [J]. JOURNAL OF NEUROCHEMISTRY, 1999, 72 (02) : 693 - 699

[4] Chai YH, 1999, J NEUROSCI, V19, P10338

[5] Acceleration of oligomerization, not fibrillization, is a shared property of both α-synuclein mutations linked to early-onset Parkinson's disease:: Implications for pathogenesis and therapy [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2000, 97 (02) : 571 - 576

[6] Mutation of the E6-AP ubiquitin ligase reduces nuclear inclusion frequency while accelerating polyglutamine-induced pathology in SCA1 mice [J]. NEURON, 1999, 24 (04) : 879 - 892

[7] Chaperone suppression of aggregation and altered subcellular proteasome localization imply protein misfolding in SCA1 [J]. NATURE GENETICS, 1998, 19 (02) : 148 - 154

[8] A YAC mouse model for Huntington's disease with full-length mutant huntingtin, cytoplasmic toxicity, and selective striatal neurodegeneration [J]. NEURON, 1999, 23 (01) : 181 - 192

[9] The tyrosine kinase negative regulator c-Cbl as a RING-type, E2-dependent ubiquitin-protein ligase [J]. SCIENCE, 1999, 286 (5438) : 309 - 312

[10] Aberrant protein deposition and neurological disease [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (53) : 37507 - 37510