Abstract:
:Early onset generalized dystonia is a dominantly inherited movement disorder caused by neuronal dysfunction without an apparent loss of neurons. The same single mutation (GAG deletion) causes most cases and results in loss of a glutamic acid (E) in the carboxy terminal region of torsinA (Delta302/303). To model the neuronal involvement, adult rat primary sensory dorsal root ganglion neurons in culture were infected with lentivirus vectors expressing human wild-type or mutant torsinA. Expression of the mutant protein resulted in formation of torsinA-positive perinuclear inclusions. When the cells were co-infected with lentivirus vectors expressing the mutant torsinA message and a shRNA selectively targeting this message, inclusion formation was blocked. Vector-delivered siRNAs have the potential to decrease the adverse effects of this mutant protein in neurons without affecting wild-type protein.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Kock N,Allchorne AJ,Sena-Esteves M,Woolf CJ,Breakefield XOdoi
10.1016/j.neulet.2005.10.098keywords:
subject
Has Abstractpub_date
2006-03-13 00:00:00pages
201-5issue
3eissn
0304-3940issn
1872-7972pii
S0304-3940(05)01259-0journal_volume
395pub_type
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journal_title:Neuroscience letters
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journal_title:Neuroscience letters
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journal_title:Neuroscience letters
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journal_title:Neuroscience letters
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journal_title:Neuroscience letters
pub_type: 杂志文章
doi:10.1016/0304-3940(90)90092-n
更新日期:1990-08-24 00:00:00
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