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1  with disease caused by ATXN1[82Q] having an expanded polyglutamine tract.
2 plasmids expressing a transcript encoding an expanded polyglutamine tract.
3 pression of mutant ataxin-1 that contains an expanded polyglutamine tract.
4 lve interactions with other proteins via the expanded polyglutamine tract.
5  gene, yielding a Huntingtin protein with an expanded polyglutamine tract.
6 generation requires expressing ATXN1 with an expanded polyglutamine tract.
7  neurodegenerative disorders associated with expanded polyglutamine tracts.
8  caused by expression of proteins containing expanded polyglutamine tracts.
9 ed in other transgenic models overexpressing expanded polyglutamine tracts.
10 ucts containing SBMA or DRPLA with normal or expanded polyglutamine tracts.
11      N-terminal huntingtin fragments with an expanded polyglutamine tract aberrantly localized to int
12        In contrast, Drosophila expressing an expanded polyglutamine tract alone, or an expanded polyg
13                Previous studies suggest that expanded polyglutamine tracts alter transcription by seq
14            This flexibility is impaired with expanded polyglutamine tracts, and we can detect changes
15 aggregation of the androgen receptor with an expanded polyglutamine tract (AR-polyQ) has been linked
16 asm, N-terminal fragments of huntingtin with expanded polyglutamine tracts are able to accumulate in
17                                              Expanded polyglutamine tracts are responsible for at lea
18  ataxin-1 SUMOylation in the presence of the expanded polyglutamine tract, ataxin-1[82Q].
19    Here we show that polypeptides containing expanded polyglutamine tracts, but not normal N-terminal
20   A gain of toxic function as a result of an expanded polyglutamine tract can cause the protein hunti
21                                              Expanded polyglutamine tracts cause huntingtin and other
22 sfolding of huntingtin (HTT) protein with an expanded polyglutamine tract, could also benefit from th
23                        Here we show that the expanded polyglutamine tract differentially affects the
24  by exon 1 of the htt gene and containing an expanded polyglutamine tract, form fibrils that accumula
25 coded by exon-1 (htt(ex1)) and containing an expanded polyglutamine tract, forms fibrils that accumul
26 rotein aggregation diseases is an abnormally expanded polyglutamine tract found in the respective pro
27 d a direct viral approach to locally express expanded polyglutamine tracts fused to the green fluores
28                                           An expanded polyglutamine tract (>37 glutamines) in the N-t
29 pressing a human huntingtin fragment with an expanded polyglutamine tract (Htn-Q150).
30 huntingtin's protein exon-1 fragment with an expanded polyglutamine tract (Htt-103Q), which is depend
31     It has been suggested that proteins with expanded polyglutamine tracts impair ubiquitin-dependent
32 ington's disease (HD), which is caused by an expanded polyglutamine tract in huntingtin (htt).
33                           It is caused by an expanded polyglutamine tract in huntingtin (Htt).
34 ssive neurodegenerative disease caused by an expanded polyglutamine tract in huntingtin protein (Htt)
35 an expanded polyglutamine tract alone, or an expanded polyglutamine tract in the context of the spino
36 the Huntingtin (HTT) gene, translating to an expanded polyglutamine tract in the HTT protein.
37 is a neurodegenerative disorder caused by an expanded polyglutamine tract in the huntingtin (HTT) pro
38 Huntington disease derives from a critically expanded polyglutamine tract in the huntingtin (Htt) pro
39 etic neurodegenerative disorder caused by an expanded polyglutamine tract in the huntingtin protein.
40    Huntington's disease (HD) is caused by an expanded polyglutamine tract in the huntingtin protein.
41 on in the huntingtin gene that results in an expanded polyglutamine tract in the huntingtin protein.
42                                The resulting expanded polyglutamine tract in the N-terminal region of
43    Huntington's disease (HD) is caused by an expanded polyglutamine tract in the protein huntingtin (
44              In addition, the presence of an expanded polyglutamine tract in the SBMA androgen recept
45 inant neurodegenerative disease caused by an expanded polyglutamine tract in the ubiquitously express
46 f CHIP to protect against toxicity caused by expanded polyglutamine tracts in different protein conte
47 he pathway to neuronal dysfunction, while an expanded polyglutamine tract is essential for neuronal d
48                                 In SCA1, the expanded polyglutamine tract is in the ataxin-1 (ATXN1)
49                               Aggregation of expanded polyglutamine tracts is associated with nine di
50 otoxicity induced by Htt proteins containing expanded polyglutamine tracts is likely mediated, at lea
51 ion of the mutant huntingtin protein with an expanded polyglutamine tract plays a central role in the
52 cterized by misfolding and aggregation of an expanded polyglutamine tract (polyQ).
53 ed on identifying the mechanism by which the expanded polyglutamine tract renders a protein toxic to
54 ical features caused by ATXN1[82Q] having an expanded polyglutamine tract, they fail to manifest the
55                  The expansion results in an expanded polyglutamine tract, which likely confers a nov
56 es of mutant huntingtin exon 1 containing an expanded polyglutamine tract with 51 residues (mhttQ51),
57 rmal CAG expansion, which translates into an expanded polyglutamine tract within ataxin-3.