Please use this identifier to cite or link to this item:
|Title:||Reactive oxygen species-mediated regulation of the Na+- H+ exchanger 1 gene expression connects intracellular redox status with cells' sensitivity to death triggers|
Na+/H+ exchanger NHE-1
|Source:||Akram, S., Teong, H.F.C., Fliegel, L., Pervaiz, S., Clément, M.V. (2006-04). Reactive oxygen species-mediated regulation of the Na+- H+ exchanger 1 gene expression connects intracellular redox status with cells' sensitivity to death triggers. Cell Death and Differentiation 13 (4) : 628-641. ScholarBank@NUS Repository. https://doi.org/10.1038/sj.cdd.4401775|
|Abstract:||We have previously demonstrated that a slight increase in intracellular superoxide (O2 •-) anion confers resistance to death stimuli. Using pharmacological and molecular approaches to manipulate intracellular O2 •-, here we report that an increase in intracellular O2 •- anion induces Na+/H+ exchanger 1 (NHE-1) gene promoter activity resulting in increased NHE-1 protein expression, which strongly correlates with the resistance of cells to death stimuli. In contrast, exposure to exogenous hydrogen peroxide suppressed NHE-1 promoter activity and gene expression, and increased cell sensitivity to death triggers. Furthermore, the increase in cell sensitivity to death upon downregulation of NHE-1 gene expression correlates with reduced capacity of cells to recover from an acid load, while survival upon overexpression of NHE-1 appears independent of its pump activity. These findings indicate that NHE-1 is a redox-regulated gene, and provide a novel intracellular target for the redox control of cell death sensitivity. © 2006 Nature Publishing Group. All rights reserved.|
|Source Title:||Cell Death and Differentiation|
|Appears in Collections:||Staff Publications|
Show full item record
Files in This Item:
There are no files associated with this item.
checked on Feb 27, 2018
WEB OF SCIENCETM
checked on Feb 14, 2018
checked on Mar 12, 2018
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.