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.

authors

Arteaga MF,Coric T,Straub C,Canessa CM

doi

10.1073/pnas.0800958105

subject

Has Abstract

pub_date

2008-03-18 00:00:00

pages

4459-64

issue

11

eissn

0027-8424

issn

1091-6490

pii

0800958105

journal_volume

105

pub_type

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