Abstract:
:Neurodegenerative diseases and noxious stimuli to the brain enhance transcription of serum- and glucocorticoid-induced kinase-1 (SGK1). Here, we report that the SGK1 gene encodes a brain-specific additional isoform, SGK1.1, which exhibits distinct regulation, properties, and functional effects. SGK1.1 decreases expression of the acid-sensing ion channel-1 (ASIC1); thereby, SGK1.1 may limit neuronal injury associated to activation of ASIC1 in ischemia. Given that neurons express at least two splice isoforms, SGK1 and SGK1.1, driven by distinct promoters, any changes in SGK1 transcript level must be examined to define the isoform induced by each stimulus or neurological disorder.
journal_name
Proc Natl Acad Sci U S Aauthors
Arteaga MF,Coric T,Straub C,Canessa CMdoi
10.1073/pnas.0800958105subject
Has Abstractpub_date
2008-03-18 00:00:00pages
4459-64issue
11eissn
0027-8424issn
1091-6490pii
0800958105journal_volume
105pub_type
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