戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (１語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1 f many neurodegenerative disorders caused by polyglutamine expansion.
2 erived ataxin-7, which contains a pathogenic polyglutamine expansion.
3 bberant protein interactions mediated by the polyglutamine expansion.
4  C terminal to amino acid 221 to include the polyglutamine expansion.
5 enerative disorder caused by ataxin-3 with a polyglutamine expansion.
6  Huntingtin (Htt), that contains an abnormal polyglutamine expansion.
7 uclear factor or process is disrupted by the polyglutamine expansion.
8 to sites of DNA damage, which is impaired by polyglutamine expansion.
9 s, and inclusion bodies caused by huntingtin polyglutamine expansion.
10 dels of tauopathy, amyloid beta-peptide, and polyglutamine expansion.
11 ease (HD) is expression of huntingtin with a polyglutamine expansion.
12 e epitope of human huntingtin is enhanced by polyglutamine expansion.
13 ited neurodegenerative disorders result from polyglutamine expansions.
14 1 hereditary neurological diseases involving polyglutamine expansions.
15  the huntingtin protein (mHTT) with aberrant polyglutamine expansions.
16                                     Although polyglutamine expansion accelerates protein aggregation,
17 yglutamine disease proteins, indicating that polyglutamine expansion alone is insufficient to promote
18                    Our findings suggest that polyglutamine expansion alters androgen receptor functio
19  N-terminus of mutant huntingtin (htt) has a polyglutamine expansion and forms neuronal aggregates in
20 cytoplasmic inclusions, which increased with polyglutamine expansion and with time after transfection
21  chromatin remodeling complex, is subject to polyglutamine expansion at the amino terminus, causing s
22 ne, we demonstrate that, while determined by polyglutamine expansion, ataxin-1 aggregation is noticea
23                               Concomitantly, polyglutamine expansion attenuates the formation and fun
24 itors inhibit oxidative death independent of polyglutamine expansions by activating an Sp1-dependent
25          In at least nine inherited diseases polyglutamine expansions cause neurodegeneration associa
26                                          The polyglutamine expansion causes huntingtin to interact ab
27                                              Polyglutamine expansion causes Huntington disease (HD) a
28                       In Huntington disease, polyglutamine expansion causes N-terminal huntingtin (Ht
29              While the mechanism(s) by which polyglutamine expansion causes neurodegeneration in each
30                             To elucidate how polyglutamine expansion causes neuronal dysfunction, we
31                  In Huntington disease (HD), polyglutamine expansion causes the disease protein hunti
32 s are decreased in disease suggests that the polyglutamine expansion contributes to disease by both a
33                                We found that polyglutamine expansion decreased ATXN7 occupancy, which
34 onsible for Spinocerebellar ataxia type 3, a polyglutamine expansion disease, represents one of such
35 se data support a CBP-sequestration model of polyglutamine expansion disease.
36 ms in SCA1 and Huntington's Disease, another polyglutamine expansion disease.
37 Spinocerebellar ataxia type 1 is one of nine polyglutamine expansion diseases and is characterized by
38                       This disease and other polyglutamine expansion diseases are characterized by la
39  Divergent protein context helps explain why polyglutamine expansion diseases differ clinically and p
40 n in HD, and may have implications for other polyglutamine expansion diseases in which mutant protein
41 tly proposed mechanisms of neuronal death in polyglutamine expansion diseases include activation of c
42 o its role in the molecular pathology of the polyglutamine expansion diseases, mutations of the prote
43                                 The dominant polyglutamine expansion diseases, which include spinocer
44 nesis and selective neuronal degeneration of polyglutamine expansion diseases.
45 regates that have been identified in the CAG/polyglutamine expansion diseases.
46 elationship between this disease and the CAG/polyglutamine expansion diseases.
47 upport for a shared pathogenic mechanism for polyglutamine expansion diseases.
48                            HD is one of nine polyglutamine expansion diseases.
49 nce AR SUMOylation may be of clinical use in polyglutamine expansion diseases.
50 e therapy for Huntington's disease and other polyglutamine-expansion diseases.
51 e those seen in models of Kennedy disease, a polyglutamine expansion disorder caused by a CAG repeat
52 se Spinocerebellar ataxia type 1 (SCA1) is a polyglutamine expansion disorder characterized by the de
53  disease (HD) is the most commonly inherited polyglutamine expansion disorder, but how mutant Hunting
54                        Here, we focus on the polyglutamine-expansion disorder HD and employ mechanist
55 ntington disease patients (and perhaps other polyglutamine expansion disorders).
56 nd neurodegenerative diseases, including the polyglutamine expansion disorders, because of its abilit
57 is increasingly implicated in the biology of polyglutamine expansion disorders, Parkinson's disease a
58 therapeutic target for treating HD and other polyglutamine expansion disorders.
59                           Here, we find that polyglutamine expansions disrupted the global balance of
60 Data from the present study demonstrate that polyglutamine expansion does not dramatically impair pro
61 sight, down to the molecular level, into how polyglutamine expansion drives aggregation and explains
62 nd genetic studies provide evidence that the polyglutamine expansion enhances interactions that are n
63 ing and immunoprecipitation assays show that polyglutamine expansion enhances the interaction of N-te
64       Huntington's disease (HD) is caused by polyglutamine expansion (exp) in huntingtin (Htt).
65       Huntington's disease (HD) is caused by polyglutamine expansion (exp) in huntingtin.
66 c features, we have examined the behavior of polyglutamine expansions expressed in Caenorhabditis ele
67 hology of expanded CAG repeat disorders with polyglutamine expansions expressed within the affected p
68                                      Whereas polyglutamine expansion-expressing animals with WT therm
69                    The clinical threshold of polyglutamine expansion for HD is near 37 repeats, but t
70                                          CAG/polyglutamine expansion has been shown to form the molec
71  intracellular consequences of expression of polyglutamine expansion have been the object of intensiv
72 lthough the AR N/C-interaction is reduced by polyglutamine-expansion, homodimers of 5alpha-dihydrotes
73 ssociated protein huntingtin with a 103 copy-polyglutamine expansion (HTT gene; htt-103Q).
74 misfolded huntingtin exon I containing a 103-polyglutamine expansion (Htt103QP) as a model substrate
75                 Our results demonstrate that polyglutamine expansion impairs the ability of huntingti
76                                              Polyglutamine expansion in androgen receptor (AR) is res
77 inant neurodegenerative disorder caused by a polyglutamine expansion in ataxin-3 (ATX3; MJD1) protein
78                                 For example, polyglutamine expansion in ataxin-3 allosterically trigg
79                            SCA3 is caused by polyglutamine expansion in ataxin-3.
80 SCA3, a neurodegenerative disorder caused by polyglutamine expansion in ataxin-3.
81                                              Polyglutamine expansion in ATXN1 favours the formation o
82                            SCA7 is caused by polyglutamine expansion in ATXN7, a subunit of the trans
83                                              Polyglutamine expansion in certain proteins causes neuro
84 (HD), which is a movement disorder caused by polyglutamine expansion in Htt.
85 neurodegenerative disease caused by abnormal polyglutamine expansion in huntingtin (Exp-HTT) leading
86                                            A polyglutamine expansion in huntingtin (HTT) causes the s
87 rodegenerative disease caused by an abnormal polyglutamine expansion in huntingtin (Htt).
88                                 However, how polyglutamine expansion in huntingtin promotes glutamate
89  corepressor C-terminal binding protein, and polyglutamine expansion in huntingtin reduced this inter
90              Huntington disease is caused by polyglutamine expansion in huntingtin, a 350 kD protein
91 used by a genetic mutation that results in a polyglutamine expansion in huntingtin.
92 untington's disease (HD), which is caused by polyglutamine expansion in huntingtin.
93          Huntington's disease is caused by a polyglutamine expansion in huntingtin.
94 minant neurodegenerative disease caused by a polyglutamine expansion in huntingtin.
95                       The mechanism by which polyglutamine expansion in Huntington's disease (HD) res
96             Huntingtin, a protein altered by polyglutamine expansion in Huntington's disease (Httexp)
97                                              Polyglutamine expansion in proteins can cause selective
98 s, we and others have recently reported that polyglutamine expansion in purified or recombinantly exp
99 erized by cerebellar degeneration because of polyglutamine expansion in specific proteins.
100 herited neurodegenerative diseases caused by polyglutamine expansion in the affected proteins.
101 eurodegenerative disorder caused by abnormal polyglutamine expansion in the amino-terminal end of the
102 t in the huntingtin (Htt) protein; a similar polyglutamine expansion in the androgen receptor (AR) ca
103                                              Polyglutamine expansion in the androgen receptor (AR) ca
104                                              Polyglutamine expansion in the androgen receptor (AR) ca
105  bulbar muscular atrophy) is caused by a CAG/polyglutamine expansion in the androgen receptor (AR) ge
106  progressive neuromuscular disease caused by polyglutamine expansion in the androgen receptor (AR) pr
107 y progressive motor neuron disease caused by polyglutamine expansion in the androgen receptor (AR).
108  is a neurodegenerative disorder caused by a polyglutamine expansion in the androgen receptor (AR).
109 uromuscular degenerative disease caused by a polyglutamine expansion in the androgen receptor (AR).
110 rophy and Huntington's disease are caused by polyglutamine expansion in the androgen receptor and hun
111                                              Polyglutamine expansion in the androgen receptor causes
112                                              Polyglutamine expansion in the androgen receptor, causin
113  bulbar muscular atrophy (SBMA) is caused by polyglutamine expansion in the androgen receptor, which
114 inant neurodegenerative disorder caused by a polyglutamine expansion in the ataxin-1 protein.
115 -onset neurodegenerative disease caused by a polyglutamine expansion in the ataxin-3 (ATXN3) gene.
116 D), an autosomal dominant ataxia caused by a polyglutamine expansion in the ataxin-3 protein.
117  fatal neurodegenerative disease caused by a polyglutamine expansion in the coding region of ATXN1.
118     Huntington's disease (HD) is caused by a polyglutamine expansion in the disease protein huntingti
119                                              Polyglutamine expansion in the exon 1 domain of huntingt
120 gene huntingtin (HTT) that is reflected by a polyglutamine expansion in the Htt protein.
121                     We conclude that a small polyglutamine expansion in the human alpha 1A calcium ch
122                                          The polyglutamine expansion in the huntingtin (htt) protein
123 lmark of HD is neurodegeneration caused by a polyglutamine expansion in the huntingtin (htt) protein
124 a neurodegenerative disorder associated with polyglutamine expansion in the huntingtin (htt) protein.
125     Huntington's disease (HD) is caused by a polyglutamine expansion in the Huntingtin (Htt) protein.
126  The disease is characterized by an abnormal polyglutamine expansion in the huntingtin gene, which dr
127 ) is a neurodegenerative disease caused by a polyglutamine expansion in the huntingtin gene.
128 neurodegenerative disease caused by abnormal polyglutamine expansion in the huntingtin protein (Htt).
129 nant neurodegenerative disorder, caused by a polyglutamine expansion in the huntingtin protein (htt).
130                                              Polyglutamine expansion in the huntingtin protein is the
131 tive disorder caused by an aggregation-prone polyglutamine expansion in the huntingtin protein.
132 on in exon 1 of the HTT gene, resulting in a polyglutamine expansion in the huntingtin protein.
133 erited neurodegenerative disease caused by a polyglutamine expansion in the huntington protein (htt).
134                                              Polyglutamine expansion in the N terminus of huntingtin
135         Huntington disease (HD) is caused by polyglutamine expansion in the N terminus of huntingtin
136 erited neurodegenerative condition caused by polyglutamine expansion in the N terminus of the hunting
137  The Huntington's disease (HD) mutation is a polyglutamine expansion in the N-terminal region of hunt
138 se is neurodegenerative disorder caused by a polyglutamine expansion in the N-terminal region of the
139 th Huntington disease (HD) is triggered by a polyglutamine expansion in the N-terminal region of the
140  ataxia type 1 (SCA1), a disease caused by a polyglutamine expansion in the protein ATAXIN1 (ATXN1).
141 erited neurodegenerative disease caused by a polyglutamine expansion in the protein huntingtin (Htt).
142 odegenerative disorder caused by an abnormal polyglutamine expansion in the protein Huntingtin (Htt).
143  inherited neurological disorder caused by a polyglutamine expansion in the protein huntingtin and is
144 se, a neurodegenerative disorder caused by a polyglutamine expansion in the protein huntingtin.
145  (SCA17), a neurological disease caused by a polyglutamine expansion in the TATA-binding protein (TBP
146 inherited neurodegenerative diseases share a polyglutamine expansion in their respective disease prot
147                                              Polyglutamine expansions in huntingtin, which causes Hun
148 se (HD) is a neurological disorder caused by polyglutamine expansions in mutated Huntingtin (mHtt) pr
149                                              Polyglutamine expansions in specific proteins are also r
150 ominant neurodegenerative disorder caused by polyglutamine expansions in the amino-terminal region of
151 cts males, results from a CAG triplet repeat/polyglutamine expansions in the androgen receptor (AR) g
152  in yeast and flies, and intermediate-length polyglutamine expansions in the ataxin-2 gene increase r
153                              HD is caused by polyglutamine expansions in the huntingtin (htt) protein
154  an indirect and poorly understood manner by polyglutamine expansions in the huntingtin (HTT) protein
155                                              Polyglutamine expansions in the transcriptional co-repre
156                 SCA2 results from a poly(Q) (polyglutamine) expansion in the cytosolic protein ataxin
157 neurodegenerative disease linked to a polyQ (polyglutamine) expansion in the huntingtin protein.
158  a fatal neurodegenerative disease caused by polyglutamine-expansion in huntingtin (HTT).
159 urodegenerative diseases are caused by a CAG/polyglutamine expansion, including spinal and bulbar mus
160                      Here, we establish that polyglutamine expansion increases the molecular mobility
161 gain further insights into the mechanisms of polyglutamine expansion-induced cell death, the Affymetr
162   Knowledge regarding the pathophysiology of polyglutamine-expansion-induced protein dysfunction is a
163 ediates its binding to huntingtin, and (iii) polyglutamine expansion interferes with the ability of h
164  huntingtin interacts with MLK2, whereas the polyglutamine expansion interferes with this interaction
165                                              Polyglutamine expansion is a hallmark of nine neurodegen
166 erturbation in a target protein induced by a polyglutamine expansion is also discussed.
167                                              Polyglutamine expansion is central for determining solub
168                                              Polyglutamine expansion is the cause of several neurodeg
169 nerative diseases, including those caused by polyglutamine expansion, is the formation of ubiquitin (
170 t is dependent on mutant huntingtin dose and polyglutamine expansion; many neurons die without formin
171 y (SBMA) is a motor neuron disease caused by polyglutamine expansion mutation in the androgen recepto
172     Huntington's disease (HD) is caused by a polyglutamine expansion mutation in the huntingtin prote
173 ssive neurodegenerative disorder caused by a polyglutamine expansion near the N-terminus of huntingti
174 ynamics and is a candidate disease sensor in polyglutamine expansion neurodegeneration.
175 , has been implicated in the pathogenesis of polyglutamine expansion neurodegenerative disease.
176 ction of ataxin-2 and the mechanism by which polyglutamine expansion of ataxin-2 causes neurodegenera
177 ction of ataxin-2 and the mechanism by which polyglutamine expansion of ataxin-2 causes neurodegenera
178                                          The polyglutamine expansion of huntingtin (mHTT) causes Hunt
179 neurodegenerative disorder that results from polyglutamine expansion of the ataxin-7 (ATXN7) protein.
180     Huntington's disease (HD) is caused by a polyglutamine expansion of the huntingtin protein, resul
181 protein constructs to examine the effects of polyglutamine expansion on protein aggregation, proteaso
182  growth properties of mutant huntingtin with polyglutamine expansions or mutant SOD1 (G85R/G93A) to e
183                     Our results suggest that polyglutamine expansions perturb transcription of CREB/C
184 n, is affected by the mutant huntingtin with polyglutamine expansion (polyQ-htt).
185   Tat-beclin 1 decreases the accumulation of polyglutamine expansion protein aggregates and the repli
186  heat-shock proteins also delay the onset of polyglutamine-expansion protein aggregation, suggesting
187          Here we show, in animals expressing polyglutamine expansion proteins and mutant SOD-1(G93A)
188 the accumulation of SCA8 polyalanine and DM1 polyglutamine expansion proteins in previously establish
189 erminal mutant Huntingtin fragment or simple polyglutamine expansion proteins.
190 n expression of the highly aggregation-prone polyglutamine-expansion proteins and Abeta-peptide.
191 or a floxed exon 1 containing the pathogenic polyglutamine expansion (Q97).
192                                          How polyglutamine expansions render the resulting proteins t
193                               In addition to polyglutamine expansion, requirements for development of
194                                              Polyglutamine expansion results in an aggregation-prone
195 ted with decreased clearance of protein with polyglutamine expansion, the accumulation of p62 in neur
196 l-length HD gene expression and differential polyglutamine expansion with possible pathophysiological
197                                              Polyglutamine expansion within the androgen receptor (AR
198                                              Polyglutamine expansion within the exon1 of huntingtin l
199 's disease (HD) is caused in large part by a polyglutamine expansion within the huntingtin (Htt) prot
200     Huntington's disease (HD) is caused by a polyglutamine expansion within the huntingtin (Htt) prot
201  is a neurodegenerative disorder caused by a polyglutamine expansion within the huntingtin protein.
202                                              Polyglutamine expansion within the N-terminal region of
203 untington's disease is caused by an abnormal polyglutamine expansion within the protein huntingtin an
204       Our results raise the possibility that polyglutamine expansions within ataxin-2 cause neurodege
205                                              Polyglutamine expansions within different proteins are a

 
Page Top