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1 erived ataxin-7, which contains a pathogenic polyglutamine expansion.
2 bberant protein interactions mediated by the polyglutamine expansion.
3 C terminal to amino acid 221 to include the polyglutamine expansion.
4 enerative disorder caused by ataxin-3 with a polyglutamine expansion.
5 Huntingtin (Htt), that contains an abnormal polyglutamine expansion.
6 uclear factor or process is disrupted by the polyglutamine expansion.
7 dels of tauopathy, amyloid beta-peptide, and polyglutamine expansion.
8 ease (HD) is expression of huntingtin with a polyglutamine expansion.
9 e epitope of human huntingtin is enhanced by polyglutamine expansion.
10 f many neurodegenerative disorders caused by polyglutamine expansion.
11 ited neurodegenerative disorders result from polyglutamine expansions.
12 1 hereditary neurological diseases involving polyglutamine expansions.
13 the huntingtin protein (mHTT) with aberrant polyglutamine expansions.
16 N-terminus of mutant huntingtin (htt) has a polyglutamine expansion and forms neuronal aggregates in
17 cytoplasmic inclusions, which increased with polyglutamine expansion and with time after transfection
18 ne, we demonstrate that, while determined by polyglutamine expansion, ataxin-1 aggregation is noticea
20 itors inhibit oxidative death independent of polyglutamine expansions by activating an Sp1-dependent
28 s are decreased in disease suggests that the polyglutamine expansion contributes to disease by both a
30 onsible for Spinocerebellar ataxia type 3, a polyglutamine expansion disease, represents one of such
32 Spinocerebellar ataxia type 1 is one of nine polyglutamine expansion diseases and is characterized by
34 n in HD, and may have implications for other polyglutamine expansion diseases in which mutant protein
35 tly proposed mechanisms of neuronal death in polyglutamine expansion diseases include activation of c
36 o its role in the molecular pathology of the polyglutamine expansion diseases, mutations of the prote
44 e those seen in models of Kennedy disease, a polyglutamine expansion disorder caused by a CAG repeat
45 se Spinocerebellar ataxia type 1 (SCA1) is a polyglutamine expansion disorder characterized by the de
46 disease (HD) is the most commonly inherited polyglutamine expansion disorder, but how mutant Hunting
48 nd neurodegenerative diseases, including the polyglutamine expansion disorders, because of its abilit
49 is increasingly implicated in the biology of polyglutamine expansion disorders, Parkinson's disease a
52 Data from the present study demonstrate that polyglutamine expansion does not dramatically impair pro
53 sight, down to the molecular level, into how polyglutamine expansion drives aggregation and explains
54 nd genetic studies provide evidence that the polyglutamine expansion enhances interactions that are n
55 ing and immunoprecipitation assays show that polyglutamine expansion enhances the interaction of N-te
58 c features, we have examined the behavior of polyglutamine expansions expressed in Caenorhabditis ele
59 hology of expanded CAG repeat disorders with polyglutamine expansions expressed within the affected p
63 intracellular consequences of expression of polyglutamine expansion have been the object of intensiv
65 misfolded huntingtin exon I containing a 103-polyglutamine expansion (Htt103QP) as a model substrate
68 inant neurodegenerative disorder caused by a polyglutamine expansion in ataxin-3 (ATX3; MJD1) protein
74 neurodegenerative disease caused by abnormal polyglutamine expansion in huntingtin (Exp-HTT) leading
78 corepressor C-terminal binding protein, and polyglutamine expansion in huntingtin reduced this inter
86 s, we and others have recently reported that polyglutamine expansion in purified or recombinantly exp
88 eurodegenerative disorder caused by abnormal polyglutamine expansion in the amino-terminal end of the
90 t in the huntingtin (Htt) protein; a similar polyglutamine expansion in the androgen receptor (AR) ca
91 bulbar muscular atrophy) is caused by a CAG/polyglutamine expansion in the androgen receptor (AR) ge
92 progressive neuromuscular disease caused by polyglutamine expansion in the androgen receptor (AR) pr
93 y progressive motor neuron disease caused by polyglutamine expansion in the androgen receptor (AR).
94 is a neurodegenerative disorder caused by a polyglutamine expansion in the androgen receptor (AR).
95 rophy and Huntington's disease are caused by polyglutamine expansion in the androgen receptor and hun
98 bulbar muscular atrophy (SBMA) is caused by polyglutamine expansion in the androgen receptor, which
99 fatal neurodegenerative disease caused by a polyglutamine expansion in the coding region of ATXN1.
100 Huntington's disease (HD) is caused by a polyglutamine expansion in the disease protein huntingti
105 lmark of HD is neurodegeneration caused by a polyglutamine expansion in the huntingtin (htt) protein
106 a neurodegenerative disorder associated with polyglutamine expansion in the huntingtin (htt) protein.
107 Huntington's disease (HD) is caused by a polyglutamine expansion in the Huntingtin (Htt) protein.
108 neurodegenerative disease caused by abnormal polyglutamine expansion in the huntingtin protein (Htt).
109 nant neurodegenerative disorder, caused by a polyglutamine expansion in the huntingtin protein (htt).
112 erited neurodegenerative disease caused by a polyglutamine expansion in the huntington protein (htt).
115 erited neurodegenerative condition caused by polyglutamine expansion in the N terminus of the hunting
116 The Huntington's disease (HD) mutation is a polyglutamine expansion in the N-terminal region of hunt
117 se is neurodegenerative disorder caused by a polyglutamine expansion in the N-terminal region of the
118 th Huntington disease (HD) is triggered by a polyglutamine expansion in the N-terminal region of the
119 ataxia type 1 (SCA1), a disease caused by a polyglutamine expansion in the protein ATAXIN1 (ATXN1).
120 erited neurodegenerative disease caused by a polyglutamine expansion in the protein huntingtin (Htt).
121 odegenerative disorder caused by an abnormal polyglutamine expansion in the protein Huntingtin (Htt).
122 inherited neurological disorder caused by a polyglutamine expansion in the protein huntingtin and is
124 (SCA17), a neurological disease caused by a polyglutamine expansion in the TATA-binding protein (TBP
125 inherited neurodegenerative diseases share a polyglutamine expansion in their respective disease prot
127 se (HD) is a neurological disorder caused by polyglutamine expansions in mutated Huntingtin (mHtt) pr
128 ominant neurodegenerative disorder caused by polyglutamine expansions in the amino-terminal region of
129 cts males, results from a CAG triplet repeat/polyglutamine expansions in the androgen receptor (AR) g
130 in yeast and flies, and intermediate-length polyglutamine expansions in the ataxin-2 gene increase r
132 an indirect and poorly understood manner by polyglutamine expansions in the huntingtin (HTT) protein
134 neurodegenerative disease linked to a polyQ (polyglutamine) expansion in the huntingtin protein.
136 urodegenerative diseases are caused by a CAG/polyglutamine expansion, including spinal and bulbar mus
138 gain further insights into the mechanisms of polyglutamine expansion-induced cell death, the Affymetr
139 Knowledge regarding the pathophysiology of polyglutamine-expansion-induced protein dysfunction is a
140 ediates its binding to huntingtin, and (iii) polyglutamine expansion interferes with the ability of h
141 huntingtin interacts with MLK2, whereas the polyglutamine expansion interferes with this interaction
146 nerative diseases, including those caused by polyglutamine expansion, is the formation of ubiquitin (
147 t is dependent on mutant huntingtin dose and polyglutamine expansion; many neurons die without formin
148 y (SBMA) is a motor neuron disease caused by polyglutamine expansion mutation in the androgen recepto
149 Huntington's disease (HD) is caused by a polyglutamine expansion mutation in the huntingtin prote
150 ssive neurodegenerative disorder caused by a polyglutamine expansion near the N-terminus of huntingti
153 ction of ataxin-2 and the mechanism by which polyglutamine expansion of ataxin-2 causes neurodegenera
154 ction of ataxin-2 and the mechanism by which polyglutamine expansion of ataxin-2 causes neurodegenera
155 neurodegenerative disorder that results from polyglutamine expansion of the ataxin-7 (ATXN7) protein.
156 protein constructs to examine the effects of polyglutamine expansion on protein aggregation, proteaso
157 growth properties of mutant huntingtin with polyglutamine expansions or mutant SOD1 (G85R/G93A) to e
160 Tat-beclin 1 decreases the accumulation of polyglutamine expansion protein aggregates and the repli
161 heat-shock proteins also delay the onset of polyglutamine-expansion protein aggregation, suggesting
163 the accumulation of SCA8 polyalanine and DM1 polyglutamine expansion proteins in previously establish
165 n expression of the highly aggregation-prone polyglutamine-expansion proteins and Abeta-peptide.
169 ted with decreased clearance of protein with polyglutamine expansion, the accumulation of p62 in neur
170 l-length HD gene expression and differential polyglutamine expansion with possible pathophysiological
173 's disease (HD) is caused in large part by a polyglutamine expansion within the huntingtin (Htt) prot
174 Huntington's disease (HD) is caused by a polyglutamine expansion within the huntingtin (Htt) prot
175 is a neurodegenerative disorder caused by a polyglutamine expansion within the huntingtin protein.
176 untington's disease is caused by an abnormal polyglutamine expansion within the protein huntingtin an
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