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1 gh, particularly for Machado-Joseph disease (spinocerebellar ataxia type 3).
2 The difference missed significance in spinocerebellar ataxia type 3.
3 in Friedreich's ataxia, and mildy reduced in spinocerebellar ataxia type 3.
4 he polyglutamine neurodegenerative disorder, Spinocerebellar Ataxia Type 3.
5 essed in myotonic dystrophy type 1 (DM1) and spinocerebellar ataxia type 3.
6 le therapeutic strategy for the treatment of spinocerebellar ataxia type 3.
7 r performance in a transgenic mouse model of spinocerebellar ataxia type 3.
8 at might be important in the pathogenesis of spinocerebellar ataxia type 3.
9 ase known both as Machado-Joseph disease and spinocerebellar ataxia type 3.
10 gives rise to the neurodegenerative disease spinocerebellar ataxia type 3.
11 ture model of another polyglutamine disease, spinocerebellar ataxia type 3.
12 lei in patients with Friedreich's ataxia and spinocerebellar ataxia type 3.
13 phy of the nuclei in Friedreich's ataxia and spinocerebellar ataxia type 3.
15 y silenced the mutant Machado-Joseph disease/spinocerebellar ataxia type 3 allele while sparing expre
16 show that ataxin-3, the protein involved in spinocerebellar ataxia type 3, also known as Machado-Jos
19 n in the protein ataxin-3 is associated with spinocerebellar ataxia type 3, an inherited neurodegener
20 bellar ataxia type 2; ATXN2, ATN1 and HTT in spinocerebellar ataxia type 3; ATXN1 and ATXN3 in spinoc
23 implicated in the neurodegenerative disease spinocerebellar ataxia type 3, in a bioinformatics searc
26 ed that pathology in Friedreich's ataxia and spinocerebellar ataxia type 3 is not restricted to the c
28 ther mutant ataxin-3, the disease protein in spinocerebellar ataxia type 3/Machado-Joseph disease (SC
29 glutamine tract in ataxin-3 (AT3) results in spinocerebellar ataxia type 3/Machado-Joseph disease, on
30 = 12, age range 21-55 years, seven female), spinocerebellar ataxia type 3 (n = 10, age range 34-67 y
31 uitinating enzyme, is the disease protein in spinocerebellar ataxia type 3, one of many neurodegenera
34 ed polyglutamine tract in the context of the spinocerebellar ataxia type 3 protein, display only nucl
35 el for the CAG/polyglutamine (polyQ) disease spinocerebellar ataxia type 3 recapitulates key features
37 ogenic ataxin-3 protein of the human disease spinocerebellar ataxia type 3 (SCA3) and the yeast prion
39 difiers of polyQ degeneration induced by the spinocerebellar ataxia type 3 (SCA3) protein ataxin-3, w
43 itinase ataxin-3 causes neurodegeneration in Spinocerebellar Ataxia Type 3 (SCA3), one of nine inheri
44 ataxias, including the polyglutamine disease spinocerebellar ataxia type 3 (SCA3), remains poorly und
50 expanded polyglutamine (polyQ) repeat causes spinocerebellar ataxia type-3 (SCA3), also called Machad
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