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

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.

SUBMITTER: Arteaga MF

PROVIDER: S-EPMC2393749 | biostudies-literature | 2008 Mar

REPOSITORIES: biostudies-literature

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

Arteaga Maria F MF Coric Tatjana T Straub Christoph C Canessa Cecilia M CM

Proceedings of the National Academy of Sciences of the United States of America 20080311 11

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 spli ...[more]

PMID: 18334630

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