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Proc Natl Acad Sci U S A. 2008 Mar 18;105(11):4459-64. doi: 10.1073/pnas.0800958105. Epub 2008 Mar 11.

A brain-specific SGK1 splice isoform regulates expression of ASIC1 in neurons.

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  • 1Department of Cellular and Molecular Physiology, Yale University, 333 Cedar Street, New Haven, CT 06520, USA.

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.

PMID:
18334630
PMCID:
PMC2393749
DOI:
10.1073/pnas.0800958105
[PubMed - indexed for MEDLINE]
Free PMC Article
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