ライフサイエンスコーパス: repeat disease

1 to the diagnosis of late-onset trinucleotide repeat disease.

2 ested in a Drosophila model of polyglutamine-repeat disease.

3 pecificity is achieved in this polyglutamine repeat disease.

4 pment and onset of DNA expansion and triplet repeat diseases.

5 common theme in the pathogenesis of triplet-repeat diseases.

6 Huntington's disease and other expanded CAG repeat diseases.

7 encing and hence severity in several triplet-repeat diseases.

8 erved in Huntington's and other expanded CAG repeat diseases.

9 molecular etiology of expanded trinucleotide repeat diseases.

10 Huntington's disease and other expanded CAG-repeat diseases.

11 ington's disease (HD) and other expanded CAG-repeat diseases.

12 xpansion that may be common to other triplet repeat diseases.

13 for slowing progression of the polyglutamine repeat diseases.

14 n and understanding the mechanism of triplet repeat diseases.

15 ological mechanism in HD and other glutamine repeat diseases.

16 nature of the toxic species in expanded CAG repeat diseases.

17 untington's Disease and related expanded CAG repeat diseases, a polyglutamine [poly(Gln)] sequence co

18 Trinucleotide repeat disease alleles can undergo 'dynamic' mutations i

19 the latest additions to the list of triplet repeat diseases and is distinct from the other SCAs in t

20 mer's disease, polyQ inclusions in expansion repeat diseases and various proteinopathies associated w

21 that cellular mechanisms of human glutamine-repeat disease are conserved in invertebrates.

22 Huntington's disease and other expanded CAG repeat diseases are associated with the expression of pr

23 Among the CAG/polyQ repeat diseases are Huntington's disease (HD) and spinoc

24 of this latter group, also known as triplet repeat diseases, are caused by the expansion of unstable

25 abnormal number of repeats found in triplet repeat diseases arises from 'repeat instability', in whi

26 clude that in MJD, as in other polyglutamine repeat diseases, cellular expression of the disease gene

27 owever, approximately 5% subsequently have a repeat disease episode, usually within 2 years of succes

28 To eliminate interference by repeated disease episodes and antidepressant treatment,

29 Huntington's disease and other polyglutamine-repeat diseases, even after the onset of symptoms.

30 In contrast to other triplet repeat diseases, expanded alleles found in affected SCA8

31 A3/MJD) is a member of the CAG/polyglutamine repeat disease family.

32 We have recreated glutamine-repeat disease in Drosophila using a segment of the SCA3

33 There are now 10 expanded CAG repeat diseases in which both disease risk and age of on

34 The dominant gain-of-function polyglutamine repeat diseases, in which the initiating mutation is kno

35 ed in the neurological symptoms of glutamine repeat diseases is unknown.

36 As the common thread in expanded polyQ repeat diseases, it is important to understand the struc

37 A7), one of the most unstable of all CAG/CTG repeat disease loci.

38 n spinocerebellar ataxias (SCAs) are triplet repeat diseases, many SCAs are not caused by repeat expa

39 seases resulting from extension of glutamine repeats, disease occurs when the number of repeats excee

40 0 for tracking disease progression in this 4-repeat disease population.

41 fragment or by a second unrelated glutamine-repeat disease protein, ataxin-1.

42 pecies in the expanded polyglutamine (polyQ) repeat diseases range from various types of aggregates t

43 -copy genes, nucleotide-binding-leucine-rich repeat disease resistance gene clusters have undergone d

44 mber of nucleotide-binding site-leucine-rich repeat disease resistance genes were annotated, suggesti

45 ed coil-nucleotide binding site-leucine rich repeat disease resistance genes.

46 's disease, prion diseases and trinucleotide repeat diseases, result from a gain of deleterious prope

47 ecific characteristics of each trinucleotide repeat disease, review their shared clinical and genetic

48 s and might determine when treatment for CAG repeat diseases should start.

49 In expanded CAG repeat diseases such as Huntington's disease, proteins c

50 a promising therapy for human trinucleotide repeat diseases such as Huntington's disease.

51 otoxicity of these sequences in expanded CAG repeat diseases such as Huntington's disease.

52 nsible for neurodegeneration in expanded CAG repeat diseases such as Huntington's disease.

53 Trinucleotide repeat diseases such as myotonic dystrophy type 1 (DM1)

54 In many repeat diseases, such as Huntington's disease (HD), ongo

55 Trinucleotide repeat diseases, such as Huntington's disease, are cause

56 Here, we describe polyglutamine repeat diseases that have been modeled in a variety of o

57 their central importance in the expanded CAG repeat diseases that include Huntington's disease.

58 In this article, we will discuss the CAG repeat diseases, the tauopathies and Parkinson disease,

59 n learned about the pathogenesis of "triplet repeat" diseases through mouse models for spinocerebella

60 Triplet repeat diseases (TRDs) are caused by pathogenic expansio

61 Using a Drosophila model for polyQ repeat disease, we observed that ITSN enhanced polyQ-med

62 cated in repeat instability in other triplet-repeat diseases, were highly expressed in pluripotent st