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1 ataxia type 2 (SCA2), an autosomal dominant polyglutamine disease.
2 reduce lethality in two Drosophila models of polyglutamine disease.
3 nd indicate a novel therapeutic strategy for polyglutamine disease.
4 Drosophila models of Alzheimer's disease and polyglutamine disease.
5 assay that recapitulates several features of polyglutamine disease.
6 d neurodegeneration in a Drosophila model of polyglutamine disease.
7 erones as a potential therapeutic target for polyglutamine diseases.
8 an important role in the pathophysiology of polyglutamine diseases.
9 is thus regarded as the most unstable of the polyglutamine diseases.
10 ons (NIIs), a hallmark of SBMA and the other polyglutamine diseases.
11 ng therapeutic strategies for this and other polyglutamine diseases.
12 clearance might underlie the pathogenesis of polyglutamine diseases.
13 ease, reminiscent of juvenile forms of other polyglutamine diseases.
14 and Parkinson's disease, prion disorders and polyglutamine diseases.
15 o altering the progression of this and other polyglutamine diseases.
16 RAN translation may also contribute to other polyglutamine diseases.
17 spinocerebellar ataxia type 8, and the nine polyglutamine diseases.
18 enerative disorders, such as Alzheimer's and polyglutamine diseases.
19 structure/function and neurodegeneration in polyglutamine diseases.
20 inal and bulbar muscular atrophy and related polyglutamine diseases.
21 r's disease, Spinomuscular Atrophy and other polyglutamine diseases.
22 sregulation is an important early feature of polyglutamine diseases.
23 ations for the pathogenesis and treatment of polyglutamine diseases.
24 mportant for unravelling the pathogenesis of polyglutamine diseases.
25 ction, a mechanism that may apply broadly to polyglutamine diseases.
26 onal dysfunction and/or neurodegeneration in polyglutamine diseases.
27 ecular pathogenesis of SCA1 as well as other polyglutamine diseases.
28 for histone deacetylase (HDAC) inhibitors in polyglutamine diseases.
29 e pathways may be effective for treatment of polyglutamine diseases.
30 n DNA repair genes have wider effects in the polyglutamine diseases.
31 diseases may be much broader than HD or even polyglutamine diseases.
32 mentia, Huntington's disease (HD), and other polyglutamine diseases.
33 l intervention in SBMA and potentially other polyglutamine diseases.
34 rse neurodegenerative diseases including the polyglutamine diseases.
35 plicing may contribute to the progression of polyglutamine diseases.
36 es a new treatment strategy for HD and other polyglutamine diseases.
38 arly, largely independent, manifestations of polyglutamine disease and suggests that additional epige
39 Ggamma is not a viable therapeutic target in polyglutamine disease and that overall proteasome functi
40 s affected in Huntington's disease and other polyglutamine diseases and by discerning whether gene ex
41 etic mechanism modulates age at onset across polyglutamine diseases and could extend to other repeat
42 omparing modifiers isolated in the models of polyglutamine diseases and in a Drosophila model of tauo
43 xpanded protein is a unifying feature of CAG/polyglutamine diseases and may be initiated or catalyzed
44 gest a therapeutic approach for treatment of polyglutamine diseases and provide the potential for yea
46 findings may be relevant to the treatment of polyglutamine diseases and, perhaps, to other neurodegen
56 ease, amyotrophic lateral sclerosis, and the polyglutamine diseases, are characterized by intracellul
57 roteins may also be present in the tissue of polyglutamine diseases as a result of frameshifting of t
58 loss of neurite outgrowth and cell death in polyglutamine diseases, as these phenotypes were partial
59 ew leads for therapeutic development for the polyglutamine diseases based on their efficacy in mammal
60 into the cell specificity of pathology for a polyglutamine disease by relating SCA7-induced retinal d
61 Ggamma could contribute to UPS impairment in polyglutamine diseases by suppressing the proteasomal ca
63 damental unanswered question in the field of polyglutamine diseases concerns the pathophysiology of n
65 Here, we show that, in a mouse model for the polyglutamine disease dentatorubral-pallidoluysian atrop
66 Consistently, the recovery of lifespan in polyglutamine disease fly models by TERA/VCP/p97 corresp
68 ociation with age at onset when grouping all polyglutamine diseases (HD+SCAs; p = 1.43 x 10(-5) ).
69 n the striatum of various knock-in models of polyglutamine diseases highlights the role of trans-acti
74 HSP27 is also found in cell models of other polyglutamine diseases, including Huntington disease as
76 nisms of neurodegeneration in the CAG repeat polyglutamine diseases, including Spinal and Bulbar Musc
79 A key unanswered question in SCA3 and other polyglutamine diseases is the extent to which neurodegen
82 tment exists for the fatal neurodegenerative polyglutamine disease known both as Machado-Joseph disea
83 pendent manner, suggesting that pathology in polyglutamine disease may result from cellular depletion
87 ion for further studies as a therapeutic for polyglutamine diseases, particularly as it is an establi
92 nally blocked versions of one substrate, the polyglutamine disease protein ataxin-3, and showed that
93 regulates the activity of a DUB, ataxin-3, a polyglutamine disease protein implicated in protein qual
97 ations, and reporter assays to show that the polyglutamine disease protein, ataxin-3, interacts with
98 cell-based approaches we establish that the polyglutamine disease protein, ataxin-3, is a poly-ubiqu
102 protein (VCP)/p97 directly binds to multiple polyglutamine disease proteins (huntingtin, ataxin-1, at
103 he mechanisms of pathology for the family of polyglutamine disease proteins are unknown; however, rec
104 ng all conditions studied (DM1, DM2, C9-ALS, polyglutamine diseases), reduction of polyglutamine prot
106 l sclerosis/frontotemporal dementia and with polyglutamine diseases, respectively, localize to neurit
107 sed, the neurodegeneration in SCA1 and other polyglutamine diseases selectively involves a few neuron
108 orders, such as Alzheimer's, Parkinson's and polyglutamine diseases, share a common pathogenic mechan
109 contrast to this view, we show that, in the polyglutamine disease spinal and bulbar muscular atrophy
110 We have developed a transgenic model of the polyglutamine disease spinal and bulbar muscular atrophy
111 loss in the inherited ataxias, including the polyglutamine disease spinocerebellar ataxia type 3 (SCA
112 se pathogenesis to ubiquitin pathways in the polyglutamine disease spinocerebellar ataxia type 3 (SCA
114 ) as a candidate mediator of toxicity in the polyglutamine disease, spinocerebellar ataxia type 1 (SC
115 ns formed in a cell culture model of another polyglutamine disease, spinocerebellar ataxia type 3.
116 may be a common mechanism of pathogenesis in polyglutamine diseases such as Huntington disease and sp
117 a primary cause of cellular pathogenesis in polyglutamine diseases such as Huntington disease; the r
120 ults, together with recent findings in other polyglutamine diseases, suggest that CAG repeat expansio
121 primary site of protein aggregation in many polyglutamine diseases, suggesting a central role in pat
122 de a novel common pathomechanism in multiple polyglutamine diseases that is mediated by DNA repair fu
125 or class of neurodegenerative disorders, the polyglutamine diseases, to show reduced polyglutamine ag
128 Drosophila model for Huntington's and other polyglutamine diseases was used to screen for genetic fa
129 important development in the study of such "polyglutamine" diseases was the realization that merely
130 Using a Drosophila melanogaster model of polyglutamine disease, we show that directed expression
131 as allowed subclassification into translated polyglutamine diseases, which are due to CAG repeat expa
132 erstanding of the role of protein folding in polyglutamine disease with emerging evidence that altera
133 G repeats are often used to create models of polyglutamine diseases yet are very rare in humans where
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