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

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