A microtiter plate assay for polyglutamine aggregate extension

Analytical Biochemistry

Volumn 295, Issue 2, 2001, Pages 227-236

  Berthelier, Valerie ^a   Hamilton, J Bradley ^a   Chen, Songming ^a   Wetzel, Ronald ^a  

^a UNIVERSITY OF TENNESSEE MEDICAL CENTER   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

BIOLOGICAL MATERIALS; DIAGNOSIS; EUROPIUM COMPOUNDS; PEPTIDES;

AGGREGATION KINETICS; ASSEMBLY MECHANISM; CRITICAL FEATURES; LENGTH DEPENDENCE; LOW CONCENTRATIONS; MICROTITER PLATES; POLYGLUTAMINE; TIME-RESOLVED FLUORESCENCE;

AGGREGATES;

BIOTIN; EUROPIUM; POLYGLUTAMINE; STREPTAVIDIN;

AMINO ACID ANALYSIS; ARTICLE; ASSAY; CALCULATION; COMPLEX FORMATION; CONCENTRATION (PARAMETERS); DEGENERATIVE DISEASE; DEVICE; DIAGNOSTIC VALUE; FLUORESCENCE; HUMAN; IMMOBILIZATION; KINETICS; MICROTITER PLATE ASSAY; NEUROPATHOLOGY; PRIORITY JOURNAL; QUANTITATIVE ASSAY; REACTION TIME; REPRODUCIBILITY; SENSITIVITY AND SPECIFICITY; TRINUCLEOTIDE REPEAT;

EID: 0035881211     PISSN: 00032697     EISSN: None     Source Type: Journal    
DOI: 10.1006/abio.2001.5217     Document Type: Article

References (43)

1. Cell death in polyglutamine diseases
2. Fourteen and counting: Unraveling trinucleotide repeat diseases
3. Huntington's disease: Translating a CAG repeat into a pathogenic mechanism
4. Trinucleotide repeats in neurogenetic disorders
5. The influence of huntingtin protein size on nuclear localization and cellular toxicity
6. Aggregation of huntingtin in neuronal intranuclear inclusions and dystrophic neurites in brain
7. Intranuclear inclusions of expanded polyglutamine protein in spinocerebellar ataxia type 3
8. From neuronal inclusions to neurodegeneration: Neuropathological investigation of a transgenic mouse model of Huntington's disease
9. Expanded polyglutamine in the Machado-Joseph disease protein induces cell death in vitro and in vivo
10. Exon 1 of the HD gene with an expanded CAG repeat is sufficient to cause a progressive neurological phenotype in transgenic mice
11. Formation of neuronal intranuclear inclusions underlies the neurological dysfunction in mice transgenic for the HD mutation
12. Ectopically expressed CAG repeats cause intranuclear inclusions and a progressive late onset neurological phenotype in the mouse
13. Behavioural abnormalities and selective neuronal loss in HD transgenic mice expressing mutated full-length HD cDNA
14. Ultrastructural localization and progressive formation of neuropil aggregates in Huntington's disease transgenic mice
15. Polyglutamine aggregates alter protein folding homeostasis in Caenorhabditis elegans
16. Huntingtin acts in the nucleus to induce apoptosis but death does not correlate with the formation of intranuclear inclusions
17. Evidence for both the nucleus and cytoplasm as subcellular sites of pathogenesis in Huntington's disease in cell culture and in transgenic mice expressing mutant huntingtin
18. Intraneuronal aggregate formation and cell death after viral expression of expanded polyglutamine tracts in the adult rat brain
19. The Huntington's disease protein interacts with p53 and CREB-binding protein and represses transcription
20. CREB-binding protein sequestration by expanded polyglutamine
21. Interference by huntingtin and atrophin-1 with cbp-mediated transcription leading to cellular toxicity
22. Self-assembly of polyglutamine-containing huntingtin fragments into amyloid-like fibrils: Implications for Huntington's disease pathology
23. Solubilization and disaggregation of polyglutamine peptides
24. Europium as a label in time-resolved immunofluorometric assays
25. Immunoassays with time-resolved fluorescence spectroscopy: Principles and applications
26. Machado-Joseph disease gene product is a cytoplasmic protein widely expressed in brain
27. Molecular and clinical correlations in spinocerebellar ataxia type 3 and Machado-Joseph disease
28. Huntingtin-encoded polyglutamine expansions form amyloid-like protein aggregates in vitro and in vivo
29. Selective inhibition of βA4 fibril formation
30. Alzheimer's disease amyloid propagation by a template-dependent dock-lock mechanism
31. Amyloid-like inclusions in Huntington's disease
32. Seeding of A beta fibril formation is inhibited by all three isotypes of apolipoprotein E
33. Transglutaminase aggregates huntingtin into nonamyloidogenic polymers, and its enzymatic activity increases in Huntington's disease brain nuclei
34. Tissue transglutaminase is increased in Huntington's disease brain
35. Tissue transglutaminase: A possible role in neurodegenerative diseases
36. Tissue transglutaminase does not contribute to the formation of mutant huntingtin aggregates
37. Aggregation of huntingtin in yeast varies with the length of the polyglutamine expansion and the expression of chaperone proteins
38. Bacterial and yeast chaperones reduce both aggregate formation and cell death in mammalian cell models of Huntington's disease
39. Recruitment and the role of nuclear localization in polyglutamine-mediated aggregation
40. Evidence for proteasome involvement in polyglutamine disease: Localization to nuclear inclusions in SCA3/MJD and suppression of polyglutamine aggregation in vitro
41. Molecular basis of the neurodegenerative disorders
42. Polyglutamine aggregation behavior in vitro supports a recruitment mechanism of cytotoxicity