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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.
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-
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
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
30 autophagic pathways, rapamycin may alleviate polyQ disease pathology via its effect on global protein
32 similar phenomenon was also seen with other polyQ disease proteins, including mutant ataxin 3 itself
36 Drosophila model for the CAG/polyglutamine (polyQ) disease spinocerebellar ataxia type 3 recapitulat
39 r ataxia type 3 is one of the polyglutamine (polyQ) diseases, which are caused by a CAG-repeat expans
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