Abstract:
:Gamma-aminobutyric acid type A (GABAA) receptor beta1 (gabrb1), a subunit of GABAA receptors involved in inhibitory effects on neurotransmission, was found to associate with the formation of protease-resistant prion protein in prion-infected neuroblastoma cells. Silencing of gabrb1 gene expression significantly decreased the abnormal prion protein level but paradoxically increased the normal prion protein level. Treatment with a gabrb1-specific inhibitor, salicylidene salicylhydrazide, dose-dependently decreased the abnormal prion protein level, but silencing of other GABAA receptor subunits' gene expression and treatments with the receptor antagonists and agonists did not. Therefore, gabrb1 involvement in abnormal prion protein formation is independent of GABAA receptors.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Kimura T,Ishikawa K,Sakasegawa Y,Teruya K,Sata T,Schätzl H,Doh-ura Kdoi
10.1016/j.febslet.2010.02.029subject
Has Abstractpub_date
2010-03-19 00:00:00pages
1193-8issue
6eissn
0014-5793issn
1873-3468pii
S0014-5793(10)00133-Xjournal_volume
584pub_type
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