戻る
「早戻しボタン」を押すと検索画面に戻ります。

今後説明を表示しない

[OK]

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  same JUNQ-like inclusion whereas the other, polyglutamine (72Q), formed spatially distinct IPOD-like
2 lins by genetic ablation or sequestration in polyglutamine aggregates leads to accumulation of non-in
3 ve disorders and intracerebral deposition of polyglutamine aggregates motivates attempts to better un
4                   Furthermore, we found that polyglutamine aggregates specifically recruit some stres
5 lerance and reduced levels of stress-induced polyglutamine aggregates, likely due to upregulated IPR
6  heart of huntingtin exon1 fibrils and other polyglutamine aggregates, via measurements of long-range
7                They are effective at seeding polyglutamine aggregation and exhibit cytotoxic effects
8 ward genetic screen in a C. elegans model of polyglutamine aggregation and identified the protein MOA
9 periments and in cell models and accelerated polyglutamine aggregation and toxicity in an oxidation-s
10 ify the driving forces for and mechanisms of polyglutamine aggregation as modulated by N17 and C38.
11 s on the one hand known to markedly increase polyglutamine aggregation rates and on the other hand ha
12 a possible pathway for the initial stages of polyglutamine aggregation, in which beta-hairpin-contain
13 hat control the intrinsic heterogeneities of polyglutamine aggregation.
14  mutant mice, placing a dominant HD knock-in polyglutamine allele onto the slow-aging Snell dwarf gen
15                              Internally, the polyglutamine amyloid fibrils are coassembled from diffe
16 er in their flanking domains rather than the polyglutamine amyloid structure.
17 polyglutamine toxicity and prevents purified polyglutamine and Abeta peptides from forming amyloid.
18  Htt17 monomer, as well as the impact of the polyglutamine and proline-rich segments, remains, howeve
19 ormational TR-FRET based immunoassay detects polyglutamine- and temperature-dependent changes on the
20          This suggests a novel mechanism for polyglutamine-associated developmental and cell biologic
21 behavior, huntingtin exon1 fibrils and other polyglutamine-based aggregates contain identical beta-st
22                                              Polyglutamine-binding protein 1 (PQBP1) is a highly cons
23                                              Polyglutamine-binding protein 1 (PQBP1) is an RNA-splici
24                   These results suggest that polyglutamine can induce an aggregation-promoting activi
25                                              Polyglutamine-coding (CAG)n repeat expansions in seven d
26 tability of dimers to assess whether a given polyglutamine conformer can be on the aggregation path.
27     We also find that these temperature- and polyglutamine-dependent conformational changes are sensi
28               Overall, our findings identify polyglutamine-dependent inhibition of nucleocytoplasmic
29 on between aberrant accumulation of expanded polyglutamine-dependent insoluble protein species and pa
30 arly, largely independent, manifestations of polyglutamine disease and suggests that additional epige
31 Here, we show that, in a mouse model for the polyglutamine disease dentatorubral-pallidoluysian atrop
32    Consistently, the recovery of lifespan in polyglutamine disease fly models by TERA/VCP/p97 corresp
33 tment exists for the fatal neurodegenerative polyglutamine disease known both as Machado-Joseph disea
34 ate a direct role of arginine methylation in polyglutamine disease pathogenesis.
35 nally blocked versions of one substrate, the polyglutamine disease protein ataxin-3, and showed that
36 protein (VCP)/p97 directly binds to multiple polyglutamine disease proteins (huntingtin, ataxin-1, at
37  contrast to this view, we show that, in the polyglutamine disease spinal and bulbar muscular atrophy
38  ataxia type 2 (SCA2), an autosomal dominant polyglutamine disease.
39 ociation with age at onset when grouping all polyglutamine diseases (HD+SCAs; p = 1.43 x 10(-5) ).
40 etic mechanism modulates age at onset across polyglutamine diseases and could extend to other repeat
41                                              Polyglutamine diseases are a class of dominantly inherit
42                                              Polyglutamine diseases are caused by CAG expansions in d
43                                              Polyglutamine diseases are dominantly inherited neurodeg
44  A key unanswered question in SCA3 and other polyglutamine diseases is the extent to which neurodegen
45 de a novel common pathomechanism in multiple polyglutamine diseases that is mediated by DNA repair fu
46 ng all conditions studied (DM1, DM2, C9-ALS, polyglutamine diseases), reduction of polyglutamine prot
47                                          The polyglutamine diseases, including Huntington's disease (
48                                              Polyglutamine diseases, including spinocerebellar ataxia
49 l sclerosis/frontotemporal dementia and with polyglutamine diseases, respectively, localize to neurit
50 orders, such as Alzheimer's, Parkinson's and polyglutamine diseases, share a common pathogenic mechan
51 ults, together with recent findings in other polyglutamine diseases, suggest that CAG repeat expansio
52 RAN translation may also contribute to other polyglutamine diseases.
53  spinocerebellar ataxia type 8, and the nine polyglutamine diseases.
54  structure/function and neurodegeneration in polyglutamine diseases.
55 inal and bulbar muscular atrophy and related polyglutamine diseases.
56 r's disease, Spinomuscular Atrophy and other polyglutamine diseases.
57 sregulation is an important early feature of polyglutamine diseases.
58 enerative disorders, such as Alzheimer's and polyglutamine diseases.
59 n DNA repair genes have wider effects in the polyglutamine diseases.
60 l intervention in SBMA and potentially other polyglutamine diseases.
61               Huntington's disease (HD) is a polyglutamine disorder caused by a CAG expansion in the
62                      In a mouse model of the polyglutamine disorder spinocerebellar ataxia type 1 (SC
63 sion of neurodegenerative disease, including polyglutamine disorders such as Huntington's disease and
64 cellular compartment for the pathogenesis of polyglutamine disorders, including Huntington's disease
65 ng to disease pathogenesis in SCA3 and other polyglutamine disorders.
66 ggest a therapeutic potential for LNA-CTG in polyglutamine disorders.
67 a an intramolecular collapse of the expanded polyglutamine domain and discuss the implications of thi
68                                 Removing the polyglutamine domain of Whi3 restored the pheromone sens
69 sease caused by an abnormal expansion in the polyglutamine encoding CAG repeat of the androgen recept
70  is a neurodegenerative disorder caused by a polyglutamine-encoding CAG repeat expansion in the ATXN3
71 ve disorders that are caused by expansion of polyglutamine-encoding CAG repeats.
72  atrophy (SBMA), a repeat disorder caused by polyglutamine-expanded androgen receptor (polyQ-AR).
73                                Expression of polyglutamine-expanded AR causes damage to motor neurons
74 e show that treatment of myotubes expressing polyglutamine-expanded AR with the beta-agonist clenbute
75  found that NLK can phosphorylate the mutant polyglutamine-expanded AR, enhance its aggregation, and
76 R) pathway and decreased the accumulation of polyglutamine-expanded AR.
77                      We investigated whether polyglutamine-expanded ATAXIN-1, the protein that underl
78  role in the pathogenic pathways mediated by polyglutamine-expanded ataxin-3 and that phosphorylation
79  with ATXN1, modulates disease phenotypes of polyglutamine-expanded ATXN1 in a Drosophila model of SC
80 cial effects against the toxicity induced by polyglutamine-expanded ATXN1.
81                                Here we use a polyglutamine-expanded form of human huntingtin (Htt) wi
82 odies in cells expressing aggregation-prone, polyglutamine-expanded fragments of HTT.
83 t tracking of individual cells enriched with polyglutamine-expanded Htt exon 1 (Httex1) monomers, oli
84 RK) 1/2 activation was not altered by either polyglutamine-expanded Htt or MKP-1.
85 gs suggest new mechanisms for the effects of polyglutamine-expanded HTT.
86 neurons exposed to an N-terminal fragment of polyglutamine-expanded huntingtin (Htt171-82Q), blocking
87 sp70 system in spatial organization of toxic polyglutamine-expanded Huntingtin (Huntingtin with 103Q
88 disorder Huntington's disease (HD), in which polyglutamine-expanded huntingtin (polyQ-htt) is predomi
89 as the capacity to suppress aggregation of a polyglutamine-expanded Huntingtin construct that aggrega
90 s the viability of neuronal cells expressing polyglutamine-expanded huntingtin exon 1 protein fragmen
91 euronal aggregates and inclusions containing polyglutamine-expanded huntingtin protein and peptide fr
92        Overexpression of MKP-1 prevented the polyglutamine-expanded huntingtin-induced activation of
93 2/LIR-3 can also catalyze the aggregation of polyglutamine-expanded huntingtin.
94 rmal Htt and gain of a toxic function by the polyglutamine-expanded mutant Htt protein have been prop
95 tics aimed at correcting the conformation of polyglutamine-expanded proteins as well as the pharmacod
96                               Proteolysis of polyglutamine-expanded proteins is thought to be a requi
97 ssociated protein huntingtin with a 103 copy-polyglutamine expansion (HTT gene; htt-103Q).
98 misfolded huntingtin exon I containing a 103-polyglutamine expansion (Htt103QP) as a model substrate
99 or a floxed exon 1 containing the pathogenic polyglutamine expansion (Q97).
100                                     Although polyglutamine expansion accelerates protein aggregation,
101                       In Huntington disease, polyglutamine expansion causes N-terminal huntingtin (Ht
102 Spinocerebellar ataxia type 1 is one of nine polyglutamine expansion diseases and is characterized by
103 n in HD, and may have implications for other polyglutamine expansion diseases in which mutant protein
104                            HD is one of nine polyglutamine expansion diseases.
105  disease (HD) is the most commonly inherited polyglutamine expansion disorder, but how mutant Hunting
106 sight, down to the molecular level, into how polyglutamine expansion drives aggregation and explains
107                    The clinical threshold of polyglutamine expansion for HD is near 37 repeats, but t
108                                              Polyglutamine expansion in androgen receptor (AR) is res
109                                 For example, polyglutamine expansion in ataxin-3 allosterically trigg
110 neurodegenerative disease caused by abnormal polyglutamine expansion in huntingtin (Exp-HTT) leading
111                                            A polyglutamine expansion in huntingtin (HTT) causes the s
112 rodegenerative disease caused by an abnormal polyglutamine expansion in huntingtin (Htt).
113 untington's disease (HD), which is caused by polyglutamine expansion in huntingtin.
114          Huntington's disease is caused by a polyglutamine expansion in huntingtin.
115 s, we and others have recently reported that polyglutamine expansion in purified or recombinantly exp
116 eurodegenerative disorder caused by abnormal polyglutamine expansion in the amino-terminal end of the
117                                              Polyglutamine expansion in the androgen receptor (AR) ca
118  progressive neuromuscular disease caused by polyglutamine expansion in the androgen receptor (AR) pr
119                                              Polyglutamine expansion in the androgen receptor causes
120                                              Polyglutamine expansion in the androgen receptor, causin
121  fatal neurodegenerative disease caused by a polyglutamine expansion in the coding region of ATXN1.
122 neurodegenerative disease caused by abnormal polyglutamine expansion in the huntingtin protein (Htt).
123                                              Polyglutamine expansion in the huntingtin protein is the
124 tive disorder caused by an aggregation-prone polyglutamine expansion in the huntingtin protein.
125 erited neurodegenerative disease caused by a polyglutamine expansion in the huntington protein (htt).
126 erited neurodegenerative condition caused by polyglutamine expansion in the N terminus of the hunting
127 th Huntington disease (HD) is triggered by a polyglutamine expansion in the N-terminal region of the
128 se is neurodegenerative disorder caused by a polyglutamine expansion in the N-terminal region of the
129  ataxia type 1 (SCA1), a disease caused by a polyglutamine expansion in the protein ATAXIN1 (ATXN1).
130                      Here, we establish that polyglutamine expansion increases the molecular mobility
131                                              Polyglutamine expansion is a hallmark of nine neurodegen
132 neurodegenerative disorder that results from polyglutamine expansion of the ataxin-7 (ATXN7) protein.
133   Tat-beclin 1 decreases the accumulation of polyglutamine expansion protein aggregates and the repli
134                                              Polyglutamine expansion within the exon1 of huntingtin l
135     Huntington's disease (HD) is caused by a polyglutamine expansion within the huntingtin (Htt) prot
136 's disease (HD) is caused in large part by a polyglutamine expansion within the huntingtin (Htt) prot
137  a fatal neurodegenerative disease caused by polyglutamine-expansion in huntingtin (HTT).
138 n expression of the highly aggregation-prone polyglutamine-expansion proteins and Abeta-peptide.
139 se (HD) is a neurological disorder caused by polyglutamine expansions in mutated Huntingtin (mHtt) pr
140 ominant neurodegenerative disorder caused by polyglutamine expansions in the amino-terminal region of
141 cts males, results from a CAG triplet repeat/polyglutamine expansions in the androgen receptor (AR) g
142  in yeast and flies, and intermediate-length polyglutamine expansions in the ataxin-2 gene increase r
143  an indirect and poorly understood manner by polyglutamine expansions in the huntingtin (HTT) protein
144  the huntingtin protein (mHTT) with aberrant polyglutamine expansions.
145 dence for beta-arch-containing structures in polyglutamine fibrils and open future possibilities for
146 s the driving force, vis-a-vis homopolymeric polyglutamine, for forming insoluble aggregates.
147                                Homopolymeric polyglutamine forms a mixture of amorphous aggregates an
148  neurodegenerative disease-related proteins (polyglutamine, huntingtin, ataxin-1, and superoxide dism
149  Abeta aggregation mechanism that uses Abeta-polyglutamine hybrid peptides designed to retard amyloid
150                            Huntingtin-linked polyglutamine initially accumulates in nuclei, leading t
151  mice, accumulation of RanGAP1 together with polyglutamine is shifted to perinuclear and cytoplasmic
152 that although the alpha-helical conformer of polyglutamine is very stable, dimers of alpha-helices la
153 t onset of disease decreases with increasing polyglutamine length in these proteins and the normal le
154 ino acids 171, 463, 536, 552, and 586 with a polyglutamine length of 148.
155 1 aggregation in cells with respect to time, polyglutamine length, expression levels, cell survival,
156 d that HDAC4 associates with huntingtin in a polyglutamine-length-dependent manner and co-localises w
157                   We identified two variable polyglutamine microsatellites in chimpanzees and orangut
158                            In the absence of polyglutamine, MOAG-2/LIR-3 regulates the RNA polymerase
159 ay impair FOXO protective activity in mutant polyglutamine neurons, suggesting that neurons are unabl
160                            The similarity to polyglutamine nucleation suggests that monomeric nuclei
161                     We report that synthetic polyglutamine oligomers and cerebrospinal fluid (CSF) fr
162 l fragment delays aggregation onset by Abeta-polyglutamine peptides and redirects assembly of Abeta42
163 nhibit the formation of amyloid fibrils from polyglutamine peptides associated with neurodegenerative
164 ogy calls for understanding the structure of polyglutamine peptides in the early stages of aggregatio
165  to simultaneously probe fibril formation in polyglutamine peptides, the aggregating subunit associat
166 ington disease (HD) is caused by an expanded polyglutamine (poly(Q)) repeat near the N terminus of th
167 otein (mHTT) with an expanded amino-terminal polyglutamine (poly(Q)) stretch.
168 egenerative disease caused by expansion of a polyglutamine [poly(Q)] tract in ATXN7, a subunit of the
169                                              Polyglutamine (polyQ) amyloid fibrils are observed in di
170 AT yeast homologs, NMA1 and NMA2, suppresses polyglutamine (PolyQ) and alpha-synuclein-induced cytoto
171  ubiquitinated inclusions immunoreactive for polyglutamine (polyQ) antibodies.
172               Huntington's disease (HD) is a polyglutamine (polyQ) disease caused by aberrant expansi
173 further show that PML deficiency exacerbates polyglutamine (polyQ) disease in a mouse model of spinoc
174 odegenerative disorder caused by an expanded polyglutamine (polyQ) domain near the N-terminus of the
175 ington's disease is caused by expansion of a polyglutamine (polyQ) domain within exon 1 of the huntin
176 ith an increased aggregation propensity of a polyglutamine (polyQ) expansion in exon 1 of mutant hunt
177                            It is caused by a polyglutamine (polyQ) expansion in the androgen receptor
178 rebellar ataxia type 7 (SCA7) is caused by a polyglutamine (polyQ) expansion in the ataxin-7 protein,
179 -onset neurodegenerative disease caused by a polyglutamine (polyQ) expansion in the N-terminal region
180                                              Polyglutamine (polyQ) expansion of the androgen receptor
181 n an encoded region of the gene resulting in polyglutamine (polyQ) expansion which has been assumed t
182 A7) is a neurodegenerative disease caused by polyglutamine (polyQ) expansion within the N-terminal re
183 nerative disorder caused by the expansion of Polyglutamine (polyQ) in exon 1 of the Huntingtin protei
184                                              Polyglutamine (polyQ) peptides are a useful model system
185  the toxic molecular species in the expanded polyglutamine (polyQ) repeat diseases range from various
186 neurodegenerative disorder caused by a CAG - polyglutamine (polyQ) repeat expansion in the ataxin-7 g
187                                              Polyglutamine (polyQ) repeat expansion in the deubiquiti
188                        SBMA is caused by CAG-polyglutamine (polyQ) repeat expansions in the androgen
189 ington's disease is caused by expansion of a polyglutamine (polyQ) repeat in the huntingtin protein.
190 odegenerative disorder caused by an expanded polyglutamine (polyQ) repeat in the TATA-box-binding pro
191 odegenerative disorder caused by an expanded polyglutamine (polyQ) repeat within the protein huntingt
192            Aggregates of proteins containing polyglutamine (polyQ) repeats are strongly associated wi
193 esulting mutant protein (mHtt) with extended polyglutamine (polyQ) sequence at the N terminus leads t
194 rongly dependent on the repeat length of the polyglutamine (polyQ) sequence in the disease protein.
195                                              Polyglutamine (polyQ) sequences are found in a variety o
196            The conformational preferences of polyglutamine (polyQ) sequences are of major interest be
197  of huntingtin protein arising from expanded polyglutamine (polyQ) sequences in the exon-1 region of
198 generative disorder caused by expansion of a polyglutamine (polyQ) stretch within the Huntingtin (Htt
199 sease caused by an abnormal expansion in the polyglutamine (polyQ) track of the Huntingtin (HTT) prot
200 are enhanced in the presence of the expanded polyglutamine (polyQ) tract and are stronger in the nucl
201 Fragments of proteins containing an expanded polyglutamine (polyQ) tract are thought to initiate aggr
202  gene, which is translated into an elongated polyglutamine (polyQ) tract in AR protein (ARpolyQ).
203 h is caused by a pathological expansion of a polyglutamine (polyQ) tract in the coding region of the
204 gton's disease (HD) is caused by an expanded polyglutamine (polyQ) tract in the huntingtin (htt) prot
205 ng catalytic activity or bearing an expanded polyglutamine (polyQ) tract led to partially overlapping
206  is unusual in that it includes a C-terminal polyglutamine (polyQ) tract that is absent in nonrodent
207                  alpha1ACT also contains the polyglutamine (polyQ) tract that, when expanded, causes
208                             Expansion of the polyglutamine (polyQ) tract within the androgen receptor
209  of huntingtin (HTT) fragments with expanded polyglutamine (polyQ) tracts are a pathological hallmark
210  genes, TR copy number mutations that expand polyglutamine (polyQ) tracts beyond a certain threshold
211                    Expansions of preexisting polyglutamine (polyQ) tracts in at least nine different
212 degenerative diseases are caused by expanded polyglutamine (polyQ) tracts in different proteins, such
213                                Expansions of polyglutamine (polyQ) tracts in nine different proteins
214    The aggregation of proteins with expanded polyglutamine (polyQ) tracts is directly relevant to the
215  caused by cell death after the expansion of polyglutamine (polyQ) tracts longer than approximately 4
216 zed by aggregation of proteins with expanded polyglutamine (polyQ) tracts.
217                           The aggregation of polyglutamine (polyQ)-containing proteins is at the orig
218 a type 6 (SCA6) belongs to the family of CAG/polyglutamine (polyQ)-dependent neurodegenerative disord
219 xpansion of CAG repeats encoding consecutive polyglutamines (polyQ) in the corresponding disease prot
220 ists strong correlation between the extended polyglutamines (polyQ) within exon-1 of Huntingtin prote
221                Changes caused by an expanded polyglutamine protein are possibly influenced by endogen
222 ll-length protein, challenging the notion of polyglutamine protein fragment-associated toxicity by re
223 elated decline in chaperone activity affects polyglutamine protein function that is important for the
224 9-ALS, polyglutamine diseases), reduction of polyglutamine protein products, relocalization of repeat
225 y and involved in the clearance of misfolded polyglutamine protein, is strongly recruited to the muta
226 oratory and wild strains and disease-related polyglutamine proteins expressed in both yeast and mamma
227                                       Mutant polyglutamine proteins impair accumulation of TERA/VCP/p
228                   Although normal and mutant polyglutamine proteins interact with TERA/VCP/p97, only
229                   The accepted view for many polyglutamine proteins is that proteolysis of the mutant
230  cell lines that expressed aggregation-prone polyglutamine proteins over several months.
231 f the aggregation pathway for toxic expanded polyglutamine proteins.
232 he expression of TDP-43, alpha-synuclein, or polyglutamine proteins.
233                                          The polyglutamine-proximal portions of these domains are imm
234  diseases, namely at early stages of another polyglutamine-related disorder such as Huntington's dise
235                                              Polyglutamine repeat expansion in ataxin-3 causes neurod
236  at residue T3) of a protein associated with polyglutamine repeat expansion, namely Huntingtin, and c
237  neurodegenerative disorder, caused by a CAG/polyglutamine repeat expansion, which is associated with
238 ative disorder caused by an expansion of the polyglutamine repeat in the first exon in the androgen r
239 odegenerative disorder caused by an extended polyglutamine repeat in the N terminus of the Huntingtin
240            This DNA sequence translates to a polyglutamine repeat in the protein product, leading to
241 nal properties in a manner dependent on both polyglutamine repeat length and temperature but independ
242 ng the aggregation free energy profile for a polyglutamine repeat with site-specific PG mutations tha
243 ng a mutant huntingtin protein (mHTT) with a polyglutamine-repeat expansion.
244 cular atrophy mice that carry 100 pathogenic polyglutamine repeats in the androgen receptor, and deve
245 degenerative disease, caused by expansion of polyglutamine repeats in the Huntingtin gene, with longe
246 is a rare genetic disease caused by expanded polyglutamine repeats in the huntingtin protein resultin
247  disorder caused by an abnormal expansion of polyglutamine repeats in the N-terminal of huntingtin.
248           HD is triggered by an expansion of polyglutamine repeats in the protein huntingtin (Htt), i
249 ncoding huntingtin (Htt) leading to expanded polyglutamine repeats of mutant Htt (mHtt) that elicit o
250 pendent cohort of 1,462 subjects with HD and polyglutamine SCAs, and genotyped single-nucleotide poly
251  relevant to pathogenic amyloid formation by polyglutamine segments in human proteins.
252 taxin-1, ataxin-7 and androgen receptor) via polyglutamine sequence.
253                                 A stochastic polyglutamine-specific aggregation mechanism is introduc
254               The protein ataxin-3 carries a polyglutamine stretch close to the C-terminus that trigg
255 CAG repeat expansion leading to an elongated polyglutamine stretch in huntingtin.
256 cleotide CAG repeat expansion that encodes a polyglutamine stretch in the huntingtin (HTT) protein.
257 of an RNA-binding protein, and deletion of a polyglutamine stretch in this protein results in random
258 on's disease (HD) results from expansions of polyglutamine stretches (polyQ) in the huntingtin protei
259 re we find DnaJB6-protected yeast cells from polyglutamine toxicity and cured yeast of both [URE3] pr
260 efects cause myopathies, protects cells from polyglutamine toxicity and prevents purified polyglutami
261  is due to an androgen receptor containing a polyglutamine tract (ARpolyQ) that misfolds and aggregat
262 by misfolding and aggregation of an expanded polyglutamine tract (polyQ).
263 ceptor sites; human MPI is translated into a polyglutamine tract associated with spinocerebellar atax
264     Our data support the hypothesis that the polyglutamine tract can act as a flexible domain, allowi
265 sis derives, at least in part, from the long polyglutamine tract encoded by mutant HTT.
266     Huntington's disease (HD) is caused by a polyglutamine tract expansion in huntingtin (HTT).
267                   NTFs typically encompass a polyglutamine tract flanked by an N-terminal 17-residue
268 gregation diseases is an abnormally expanded polyglutamine tract found in the respective proteins.
269 1 (SCA1), a disease caused by expansion of a polyglutamine tract in ataxin 1 (ATXN1).
270                  It is caused by an expanded polyglutamine tract in huntingtin (Htt).
271  the Huntington's disease gene HTT extends a polyglutamine tract in mutant huntingtin that enhances i
272 isorder associated with the expansion of the polyglutamine tract in the exon-1 domain of the huntingt
273            SBMA is caused by expansions of a polyglutamine tract in the gene coding for androgen rece
274 n the huntingtin (HTT) gene, which encodes a polyglutamine tract in the HTT protein.
275           It is caused by the expansion of a polyglutamine tract in the huntingtin (HTT) protein, whi
276  caused by a CAG repeat expansion encoding a polyglutamine tract in the huntingtin (Htt) protein.
277  exon 1 of the HTT gene that translates to a polyglutamine tract in the huntingtin protein (HTT).
278 vely worsened with age and was influenced by polyglutamine tract length in mutant huntingtin (mhtt).
279 nd explains the positive correlation between polyglutamine tract length, protein aggregation, and dis
280  aggregation is the anomalous expansion of a polyglutamine tract near the protein N-terminus, but the
281 ownstream polyproline region that flanks the polyglutamine tract of huntingtin.
282 ant huntingtin exon 1 containing an expanded polyglutamine tract with 51 residues (mhttQ51), and reso
283 expansion, which translates into an expanded polyglutamine tract within ataxin-3.
284 ar ataxia associated with the expansion of a polyglutamine tract within the ataxin-1 (ATXN1) protein.
285 riplet in the ATXN3 gene, translating into a polyglutamine tract within the ataxin-3 protein.
286 of huntingtin (HTT) protein with an expanded polyglutamine tract, could also benefit from this approa
287 s directly located upstream of the protein's polyglutamine tract, plays a decisive role in several im
288 ures caused by ATXN1[82Q] having an expanded polyglutamine tract, they fail to manifest the age-relat
289                   The WW domain belonging to polyglutamine tract-binding protein 1 (PQBP1) is of part
290 n requires expressing ATXN1 with an expanded polyglutamine tract.
291  1-17 domains and possibly with the proximal polyglutamine tract.
292 K6 to F17, i.e., up to the very start of the polyglutamine tract.
293 scoideum has evolved to normally encode long polyglutamine tracts and express these proteins in a sol
294 s been suggested that proteins with expanded polyglutamine tracts impair ubiquitin-dependent proteoly
295                    In addition, we find that polyglutamine tracts of increasing length are associated
296 refore, we hypothesize that wild-type length polyglutamine tracts within huntingtin can form a flexib
297   This flexibility is impaired with expanded polyglutamine tracts, and we can detect changes in hunti
298 o suppress aggregation of proteins with long polyglutamine tracts.
299   This regulation is lost in the presence of polyglutamine, which mislocalizes MOAG-2/LIR-3 from the
300                                  We designed polyglutamines with a few lysines inserted to overcome t

WebLSDに未収録の専門用語(用法)は "新規対訳" から投稿できます。
 
Page Top