ライフサイエンスコーパス: polyQ disease

1 nsights into the pathogenicity of the RNA in polyQ disease.

2 HAT) whose decreased activity contributes to polyQ disease.

3 ation in distinct brain regions in different polyQ diseases.

4 considered a possible therapeutic agent for polyQ diseases.

5 its activity may influence susceptibility to polyQ diseases.

6 t be a novel therapeutic target for treating polyQ diseases.

7 or the development of therapeutics for human polyQ diseases.

8 for unraveling early events in the onset of polyQ diseases.

9 ative disorder that belongs to the family of polyQ diseases.

10 may contribute to selective neurotoxicity in polyQ diseases.

11 family of neurodegenerative disorders called polyQ diseases.

12 findings elucidate the molecular etiology of polyQ diseases.

13 structurally related compounds for treating polyQ diseases.

14 ed protein is provided by the polyglutamine (polyQ) diseases.

15 Polyglutamine (polyQ) diseases are a class of dominantly inherited neur

16 of neurological disorders and polyglutamine (polyQ) diseases are caused by misfolded proteins.

17 Polyglutamine (polyQ) diseases are devastating, slowly progressing neur

18 , collectively referred to as polyglutamine (polyQ) diseases, are caused by expansion of a coding CAG

19 cerebellar ataxia type 2 is a polyglutamine (polyQ) disease associated with an expanded polyQ domain

20 lts have implications for drug discovery for polyQ diseases because they suggest that the residues fl

21 untington's disease (HD) is a polyglutamine (polyQ) disease caused by aberrant expansion of the polyQ

22 Polyglutamine (polyQ) diseases, caused by a CAG repeat expansion encodi

23 (polyQ) neurodegenerative diseases, yet each polyQ disease displays a unique pattern of neuronal dege

24 ized that long normal alleles in the other 8 polyQ disease genes were associated with premature disea

25 of-function toxicity found in polyglutamine (polyQ) diseases has been the subject of considerable deb

26 ation associated with various polyglutamine (polyQ) diseases has prompted extensive studies of polyQ-

27 SBMA is one of nine polyQ diseases in which polyQ expansion is believed to i

28 at PML deficiency exacerbates polyglutamine (polyQ) disease in a mouse model of spinocerebellar ataxi

29 SBMA; Kennedy's disease) is a polyglutamine (polyQ) disease in which the affected males suffer progre

30 polyQ diseases, including Huntington's disease (HD), pre

31 In contrast to other polyQ diseases, intranuclear inclusions are not prominen

32 studies have focused on protein toxicity in polyQ disease mechanisms.

33 n of mutant gene expression by only 50% in a polyQ disease model can have a significant impact on dis

34 However, conditional expression studies of polyQ disease models demonstrate that suppression of gen

35 transport defects may be a common feature of polyQ disease pathogenesis.

36 autophagic pathways, rapamycin may alleviate polyQ disease pathology via its effect on global protein

37 The polyQ disease protein, ataxin-3, has predicted ubiquitin

38 similar phenomenon was also seen with other polyQ disease proteins, including mutant ataxin 3 itself

39 t neurons from the toxic effects of expanded polyQ disease proteins.

40 that influence misfolding and aggregation of polyQ disease proteins.

41 PolyQ diseases show a strong inverse correlation between

42 Drosophila model for the CAG/polyglutamine (polyQ) disease spinocerebellar ataxia type 3 recapitulat

43 In polyQ diseases, such polyQ sequences (38-300Qs) exceed t

44 In polyQ diseases, the pathology and death of affected neur

45 r ataxia type 3 is one of the polyglutamine (polyQ) diseases, which are caused by a CAG-repeat expans