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 Q81, which consists of multiple repeats of a polyglutamine tract.
2 which has a conserved AXH domain but lacks a polyglutamine tract.
3 cleotide (CAG) repeat coding for an extended polyglutamine tract.
4 n that is translated into an abnormally long polyglutamine tract.
5 elix, a leucine zipper, a zinc finger, and a polyglutamine tract.
6 lying mutation is a CAG expansion encoding a polyglutamine tract.
7 expressing a transcript encoding an expanded polyglutamine tract.
8 ne is increased, resulting in expansion of a polyglutamine tract.
9 lying mutation is a CAG expansion encoding a polyglutamine tract.
10 n that is translated into an abnormally long polyglutamine tract.
11 of mutant ataxin-1 that contains an expanded polyglutamine tract.
12 generative diseases caused by expansion of a polyglutamine tract.
13 ot caused by a CAG expansion translated as a polyglutamine tract.
14 n of the androgen receptor gene coding for a polyglutamine tract.
15 iated multimerization involving the ataxin-1 polyglutamine tract.
16 rative disorders caused by an expansion of a polyglutamine tract.
17 appear to be influenced by expansion of the polyglutamine tract.
18 by the expansion of a CAG repeat encoding a polyglutamine tract.
19 o GAPDH does not vary with the length of the polyglutamine tract.
20 actions with other proteins via the expanded polyglutamine tract.
21 n requires expressing ATXN1 with an expanded polyglutamine tract.
22 1-17 domains and possibly with the proximal polyglutamine tract.
23 K6 to F17, i.e., up to the very start of the polyglutamine tract.
24 ease caused by ATXN1[82Q] having an expanded polyglutamine tract.
25 in regions of the protein in addition to the polyglutamine tract.
26 t repeat stretch, which encodes an elongated polyglutamine tract.
27 ion of a CAG trinucleotide repeat encoding a polyglutamine tract.
28 nteraction motifs neighboring the pathogenic polyglutamine tract.
29 t disorders are linked to the expansion of a polyglutamine tract.
30 o suppress aggregation of proteins with long polyglutamine tracts.
31 known result from CAG expansions that encode polyglutamine tracts.
32 e diseases caused by pathogenic expansion of polyglutamine tracts.
33 y expression of proteins containing expanded polyglutamine tracts.
34 er transgenic models overexpressing expanded polyglutamine tracts.
35 aining SBMA or DRPLA with normal or expanded polyglutamine tracts.
36 enerative disorders associated with expanded polyglutamine tracts.
37 ontaining exon 1 of huntingtin with extended polyglutamine tracts.
38 rminal huntingtin fragments with an expanded polyglutamine tract aberrantly localized to intracellula
40 contrast, Drosophila expressing an expanded polyglutamine tract alone, or an expanded polyglutamine
43 the proteins with a process dictated by the polyglutamine tracts, although increasing evidence sugge
44 a putative transcription factor containing a polyglutamine tract and a forkhead DNA-binding domain, i
45 ding for a transcription factor containing a polyglutamine tract and a forkhead DNA-binding domain.
47 scoideum has evolved to normally encode long polyglutamine tracts and express these proteins in a sol
48 ave been reported to cleave only once within polyglutamine tracts and then only after the N-terminal
49 ER; binding is modulated by the size of the polyglutamine tract, and mutating a sequence adjacent to
50 This flexibility is impaired with expanded polyglutamine tracts, and we can detect changes in hunti
51 on of the androgen receptor with an expanded polyglutamine tract (AR-polyQ) has been linked to the de
52 covery that residues in ATXN1 outside of the polyglutamine tract are crucial for pathogenesis hinted
53 rminal fragments of huntingtin with expanded polyglutamine tracts are able to accumulate in the nucle
56 is due to an androgen receptor containing a polyglutamine tract (ARpolyQ) that misfolds and aggregat
57 ceptor sites; human MPI is translated into a polyglutamine tract associated with spinocerebellar atax
58 expansion that results in elongation of the polyglutamine tract at the N terminus of huntingtin (Htt
59 isease (HD) is caused by an expansion of the polyglutamine tract at the N terminus of huntingtin.
64 e show that polypeptides containing expanded polyglutamine tracts, but not normal N-terminal huntingt
65 Our data support the hypothesis that the polyglutamine tract can act as a flexible domain, allowi
66 of toxic function as a result of an expanded polyglutamine tract can cause the protein huntingtin to
69 peats are translated into an abnormally long polyglutamine tract close to the N-terminus of the HD ge
70 of huntingtin (HTT) protein with an expanded polyglutamine tract, could also benefit from this approa
74 a stretch of glutamine amino acid residues (polyglutamine tract) encoded by any of several SCA-causi
77 sive motor neuron disease caused by abnormal polyglutamine tract expansion in the androgen receptor (
78 erebellar ataxia type 17 that is caused by a polyglutamine tract expansion in the TATA box-binding pr
84 gregation diseases is an abnormally expanded polyglutamine tract found in the respective proteins.
85 t viral approach to locally express expanded polyglutamine tracts fused to the green fluorescent prot
88 udy suggested that the glutamine residues in polyglutamine tracts have a significant propensity to ad
90 n's protein exon-1 fragment with an expanded polyglutamine tract (Htt-103Q), which is dependent upon
91 s been suggested that proteins with expanded polyglutamine tracts impair ubiquitin-dependent proteoly
94 ion analysis excluded the involvement of the polyglutamine tract in ataxin-1 self-association, and in
96 ia type 2 (SCA2) is caused by expansion of a polyglutamine tract in ataxin-2, a protein of unknown fu
97 by the expansion of a CAG repeat encoding a polyglutamine tract in ataxin-2, the SCA2 gene product.
99 ansion of a translated CAG repeat encoding a polyglutamine tract in ataxin-7, the SCA7 gene product.
101 used by expansion of a CAG repeat encoding a polyglutamine tract in ATXN7, a component of the SAGA hi
102 ility in Huntington's disease (HD) encodes a polyglutamine tract in full-length huntingtin that is co
107 t causes Huntington's disease (HD) encodes a polyglutamine tract in huntingtin, which first targets t
109 y of expanded HD CAG repeats that encode the polyglutamine tract in mutant huntingtin has been implic
110 the Huntington's disease gene HTT extends a polyglutamine tract in mutant huntingtin that enhances i
118 is associated with anomalous expansion of a polyglutamine tract in the coding region of the correspo
119 ed polyglutamine tract alone, or an expanded polyglutamine tract in the context of the spinocerebella
120 generative diseases caused by expansion of a polyglutamine tract in the disease protein, in this case
123 isorder associated with the expansion of the polyglutamine tract in the exon-1 domain of the huntingt
128 caused by a CAG repeat expansion encoding a polyglutamine tract in the huntingtin (Htt) protein.
129 disorder, is caused by a lengthening of the polyglutamine tract in the huntingtin (Htt) protein.
130 a CAG trinucleotide sequence that encodes a polyglutamine tract in the huntingtin (Htt) protein.
131 n disease derives from a critically expanded polyglutamine tract in the huntingtin (Htt) protein; a s
132 exon 1 of the HTT gene that translates to a polyglutamine tract in the huntingtin protein (HTT).
135 generative disorder caused by expansion of a polyglutamine tract in the huntingtin protein that resul
143 disease (HD) is caused by the expansion of a polyglutamine tract in the N-terminal region of huntingt
147 Mutations resulting in the expansion of a polyglutamine tract in the protein ataxin-2 give rise to
148 generative disorder caused by expansion of a polyglutamine tract in the protein huntingtin (Htt), whi
149 gton's disease (HD) is caused by an expanded polyglutamine tract in the protein huntingtin (htt).
150 In addition, the presence of an expanded polyglutamine tract in the SBMA androgen receptor appear
151 rodegenerative disease caused by an expanded polyglutamine tract in the ubiquitously expressed huntin
154 generative disease caused by an expansion of polyglutamine tracts in the cytosolic protein ataxin-2 (
156 untingtin (amino acids 1-171), including the polyglutamine tract, in the yeast two-hybrid system.
158 act, and mutating a sequence adjacent to the polyglutamine tract inhibits the AT3-VCP interaction and
159 tin is an essential protein that with mutant polyglutamine tracts initiates dominant striatal neurode
160 ence of in vivo recruitment of proteins with polyglutamine tracts into intraneuronal aggregates.
161 function in the context of expansion of the polyglutamine tract is critical for understanding the di
162 y to neuronal dysfunction, while an expanded polyglutamine tract is essential for neuronal death.
167 induced by Htt proteins containing expanded polyglutamine tracts is likely mediated, at least in par
168 gic disorder produced by expansion of an Htt polyglutamine tract, is characterized by neurodegenerati
169 vely worsened with age and was influenced by polyglutamine tract length in mutant huntingtin (mhtt).
170 nd explains the positive correlation between polyglutamine tract length, protein aggregation, and dis
171 ic mice containing pathological alleles with polyglutamine tract lengths of 64, 67, 72, 76 and 84 rep
172 es of disease-specific proteins that contain polyglutamine tracts longer than a critical length.
175 the causative mutation is expansion of a CAG/polyglutamine tract near the 5' end of the androgen rece
176 n's disease (HD) is caused by expansion of a polyglutamine tract near the N-terminal of huntingtin.
177 aggregation is the anomalous expansion of a polyglutamine tract near the protein N-terminus, but the
178 expansion of variable length, which encodes polyglutamine tracts near the amino terminus of the HD p
179 uman huntingtin fragment containing a mutant polyglutamine tract of 103Q fused to green fluorescent p
181 e the molecular basis of HD, we extended the polyglutamine tract of the mouse homologue, Hdh, by targ
183 e mutant huntingtin protein with an expanded polyglutamine tract plays a central role in the patholog
184 s directly located upstream of the protein's polyglutamine tract, plays a decisive role in several im
187 ntifying the mechanism by which the expanded polyglutamine tract renders a protein toxic to a subset
188 actions with other proteins containing short polyglutamine tracts such as the transcriptional coactiv
189 ndary structure accompanies expansion of the polyglutamine tract, suggesting destabilization of the n
190 in the Huntingtin gene, creating an extended polyglutamine tract that makes the Huntingtin protein to
191 ures caused by ATXN1[82Q] having an expanded polyglutamine tract, they fail to manifest the age-relat
192 ssociation is modulated by the length of the polyglutamine tract whereby S4 shows a stronger associat
194 protein of unknown function that contains a polyglutamine tract, which is expanded in patients with
196 ant huntingtin exon 1 containing an expanded polyglutamine tract with 51 residues (mhttQ51), and reso
200 ar ataxia associated with the expansion of a polyglutamine tract within the ataxin-1 (ATXN1) protein.
203 Disease (HD) is caused by an expansion of a polyglutamine tract within the huntingtin (htt) protein.
205 t AR function is reduced by expansion of the polyglutamine tract within the receptor [AR(Gln)(n)]; th
206 rative disorder caused by the expansion of a polyglutamine tract within the SCA1 gene product, ataxin
207 erative disease caused by the expansion of a polyglutamine tract within the SCA1 product, ataxin-1.
208 refore, we hypothesize that wild-type length polyglutamine tracts within huntingtin can form a flexib
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。