ライフサイエンスコーパス: SCA6

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1 anded, causes spinocerebellar ataxia type 6 (SCA6).

2 inocerebellar ataxias: SCA1, SCA2, SCA3, and SCA6.

3 There are few animal models of SCA6.

4 .01] per additional SARA point; p=0.0195) in SCA6.

5 ential predictor of future motor deficits in SCA6.

6 DnaJ-1 as a potential therapeutic target for SCA6.

7 with SCA3, and 0.80 (0.09) in patients with SCA6.

8 potential mechanism for the pathogenesis of SCA6.

9 adjacent to the genes for Cayman ataxia and SCA6.

10 e CACNA1A protein lead to PC degeneration in SCA6.

11 reached or exceeded the pathogenic range for SCA6.

12 motor dysfunction at a pre-clinical stage of SCA6.

13 d autosomal dominant spinocerebellar ataxia, SCA6.

14 ive oculomotor studies in four kindreds with SCA6.

15 etic ataxias were Friedreich's ataxia (22%), SCA6 (14%), EA2 (13%), SPG7 (10%) and mitochondrial dise

16 ing the more prevalent SCA1, SCA2, SCA3, and SCA6 along with SCA7 and SCA17 are caused by expansion o

17 Spinocerebellar ataxia type 6 (SCA6), an autosomal dominant, progressive disease, arise

18 cal stages of spinocerebellar ataxia type 6 (SCA6), an inherited neurodegenerative disease.

19 Spinocerebellar ataxias 6 and 7 (SCA6 and SCA7) are neurodegenerative disorders caused by

20 n about the steps leading to degeneration in SCA6 and the means to protect neurons in this disease ar

21 ive genetic testing for SCA1, SCA2, SCA3, or SCA6 and with progressive, otherwise unexplained ataxia

22 1A, five with spinocerebellar ataxia type 6 (SCA6) and one with episodic ataxia type 2 (EA-2).

23 enes have been identified: SCA1, SCA2, SCA3, SCA6, and SCA7.

24 Spinocerebellar ataxia type 6 (SCA6) belongs to the family of CAG/polyglutamine (polyQ)

25 Invertebrate animal models of SCA6 can expand our understanding of molecular sequelae

26 One hypothesis regarding SCA6 disease is that a CT fragment of the Cav2.1 channel

27 can be a potential therapeutic strategy for SCA6, here we created knockin mice that exclusively expr

28 SCA6 is caused by abnormal expansion in a CAG trinucleot

29 Spinocerebellar ataxia type 6 (SCA6) is linked to poly-glutamine (polyQ) within the C t

30 d (Q33) as in spinocerebellar ataxia type 6 (SCA6), is toxic to cells.

31 PCs in mice reveals that only CT-long causes SCA6-like symptoms, i.e., deficits in eyeblink condition

32 Suppression of CACNA1A IRES function in SCA6 may be a potential therapeutic strategy.

33 the P/Q-type channel is sufficient to cause SCA6 pathogenesis in mice and identifies EBC as a new di

34 ons in SCA6 patients, is associated with the SCA6 pathogenesis.

35 Our results showed that Ca(2+) channels from SCA6 patients display near-normal biophysical properties

36 human CT splice variants, as predicted from SCA6 patients, in PCs of mice using viral and transgenic

37 ically in cytosolic and nuclear fractions in SCA6 patients, is associated with the SCA6 pathogenesis.

38 In patients with SCA6, the number of non-ataxia symptoms increased linear

39 Spinocerebellar ataxia type 6 (SCA6) was recently identified as a form of autosomal dom

40 us, in this large study of motor features in SCA6, we provide novel evidence for the existence of sub

41 2006, 526 patients with SCA1, SCA2, SCA3, or SCA6 were enrolled.

42 tes the progressively degenerative nature of SCA6 when expressed in various fly tissues and the prese

43 sociated with spinocerebellar ataxia type 6 (SCA6), whereas MPc splices to an immediate stop codon, r

44 the first Drosophila melanogaster models of SCA6, which express the entire human alpha1ACT protein w

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