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 nsights into the pathogenicity of the RNA in polyQ disease.
2 HAT) whose decreased activity contributes to polyQ disease.
3  for unraveling early events in the onset of polyQ diseases.
4 its activity may influence susceptibility to polyQ diseases.
5 t be a novel therapeutic target for treating polyQ diseases.
6 or the development of therapeutics for human polyQ diseases.
7 family of neurodegenerative disorders called polyQ diseases.
8 ative disorder that belongs to the family of polyQ diseases.
9 may contribute to selective neurotoxicity in polyQ diseases.
10  considered a possible therapeutic agent for polyQ diseases.
11 ed protein is provided by the polyglutamine (polyQ) diseases.
12                               Polyglutamine (polyQ) diseases are a class of dominantly inherited neur
13 of neurological disorders and polyglutamine (polyQ) diseases are caused by misfolded proteins.
14 , collectively referred to as polyglutamine (polyQ) diseases, are caused by expansion of a coding CAG
15 lts have implications for drug discovery for polyQ diseases because they suggest that the residues fl
16 untington's disease (HD) is a polyglutamine (polyQ) disease caused by aberrant expansion of the polyQ
17 (polyQ) neurodegenerative diseases, yet each polyQ disease displays a unique pattern of neuronal dege
18 ized that long normal alleles in the other 8 polyQ disease genes were associated with premature disea
19 of-function toxicity found in polyglutamine (polyQ) diseases has been the subject of considerable deb
20 ation associated with various polyglutamine (polyQ) diseases has prompted extensive studies of polyQ-
21                          SBMA is one of nine polyQ diseases in which polyQ expansion is believed to i
22 at PML deficiency exacerbates polyglutamine (polyQ) disease in a mouse model of spinocerebellar ataxi
23 SBMA; Kennedy's disease) is a polyglutamine (polyQ) disease in which the affected males suffer progre
24                                              polyQ diseases, including Huntington's disease (HD), pre
25                         In contrast to other polyQ diseases, intranuclear inclusions are not prominen
26  studies have focused on protein toxicity in polyQ disease mechanisms.
27 n of mutant gene expression by only 50% in a polyQ disease model can have a significant impact on dis
28   However, conditional expression studies of polyQ disease models demonstrate that suppression of gen
29 transport defects may be a common feature of polyQ disease pathogenesis.
30 autophagic pathways, rapamycin may alleviate polyQ disease pathology via its effect on global protein
31                                          The polyQ disease protein, ataxin-3, has predicted ubiquitin
32  similar phenomenon was also seen with other polyQ disease proteins, including mutant ataxin 3 itself
33 t neurons from the toxic effects of expanded polyQ disease proteins.
34 that influence misfolding and aggregation of polyQ disease proteins.
35                                              PolyQ diseases show a strong inverse correlation between
36  Drosophila model for the CAG/polyglutamine (polyQ) disease spinocerebellar ataxia type 3 recapitulat
37                                           In polyQ diseases, such polyQ sequences (38-300Qs) exceed t
38                                           In polyQ diseases, the pathology and death of affected neur
39 r ataxia type 3 is one of the polyglutamine (polyQ) diseases, which are caused by a CAG-repeat expans

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。