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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Bhattacharjee, Arin Gancarz-kausch, Amy M. Tomasello, Danielle L. Dietz, David M. |
| Description | Author Affiliation: Tomasello DL ( From the Program in Neuroscience and.); Gancarz-Kausch AM ( Department of Pharmacology and Toxicology, The State University of New York at Buffalo, Buffalo, New York 14214.); Dietz DM ( From the Program in Neuroscience and Department of Pharmacology and Toxicology, The State University of New York at Buffalo, Buffalo, New York 14214.); Bhattacharjee A ( From the Program in Neuroscience and Department of Pharmacology and Toxicology, The State University of New York at Buffalo, Buffalo, New York 14214 ab68@buffalo.edu.) |
| Abstract | Although recent studies have shown the sodium-activated potassium channel SLACK (KCNT1) can contribute to neuronal excitability, there remains little information on the physiological role of the closely related SLICK (KCNT2) channel. Activation of SLICK channels may be important during pathological states such as ischemia, in which an increase in intracellular sodium and chloride can perturb membrane potential and ion homeostasis. We have identified two NFκB-binding sites within the promoter region of the human SLICK (KCNT2) and orthologous rat Slick (Kcnt2) genes, suggesting that conditions in which NFκB transcriptional activity is elevated promote expression of this channel. NFκB binding to the rat Slick promoter was confirmed in vivo by ChIP analyses, and NFκB was found differentially bound to the two sites. We verified NFκB transcriptional regulation of SLICK/Slick by mutational analyses and studying gene expression by luciferase assay in P19 cells, where NFκB is constitutively active. For the rat gene, activation of the Slick promoter was found to be additive in single NFκB mutations and synergistic in double mutations. Unexpectedly, for the human gene, NFκB exhibited cooperativity in activating the SLICK promoter. The human SLICK promoter constructs were then tested under hypoxic conditions in PC-12 cells, where NFκB is not active. Only under hypoxic conditions could luciferase activity be detected; the double NFκB mutant construct failed to exhibit activity. Transcriptional regulation of Slick by NFκB was verified in primary neurons. The Slick transcript decreased 24 h after NFκB inhibition. Our data show SLICK expression is predominantly under the control of NFκB. Because neuronal NFκB activation occurs during stressful stimuli such as hypoxia and injury, our findings suggest that SLICK is a neuroprotective gene. |
| ISSN | 00219258 |
| e-ISSN | 1083351X |
| Journal | Journal of Biological Chemistry |
| Issue Number | 30 |
| Volume Number | 290 |
| Language | English |
| Publisher | American Society for Biochemistry and Molecular Biology (United States) |
| Publisher Date | 2015-07-24 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | NF-kappa B Metabolism Neurons Potassium Channels Transcription, Genetic Animals Cell Hypoxia Genetics Ganglia, Spinal Gene Expression Regulation PC12 Cells Biosynthesis Promoter Regions, Genetic Signal Transduction Sodium Research Support, N.I.H., Extramural Biochemistry Molecular Biology |
| Content Type | Text |
| Resource Type | Article |
| Subject | Cell Biology Biochemistry Molecular Biology |
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