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dc.contributor.authorPradoldej Sompolen_US
dc.contributor.authorYong Xuen_US
dc.contributor.authorWanida Ittaraten_US
dc.contributor.authorChotiros Daosukhoen_US
dc.contributor.authorDaret St. Clairen_US
dc.contributor.otherUniversity of Kentucky College of Medicineen_US
dc.contributor.otherMahidol Universityen_US
dc.identifier.citationJournal of Molecular Neuroscience. Vol.29, No.3 (2006), 279-288en_US
dc.description.abstractExpression of manganese superoxide dismutase (MnSOD), a nuclear-encoded mitochondrial primary antioxidant enzyme, is protective against various paradigms of oxidative stress-induced brain injury. We have shown previously that the presence of an intronic nuclear factor site, κB (NF-κB), in the MnSOD gene is essential for the induction of MnSOD by tumor necrosis factor α (TNF-α). However, whether activation of NF-κB is protective against oxidative stress-induced neuronal injury is unclear. In the present study, we demonstrate that TNF-α activates NF-κB activity in neuronal, SH-SY5Y, cells and preferentially enhances the binding of p50 and p65 to the promoter/enhancer regions of the MnSOD gene. Binding of NF-κB members to the MnSOD gene leads to the induction of MnSOD mRNA and protein levels. Consequently, induction of MnSOD by TNF-α primes neuronal cells to develop resistance against subsequent exposure to β-amyloid and FeSO4. Taken together, these results suggest that NF-κB might exert its protective function by induction of MnSOD leading to subsequent protection against oxidative stress-induced neuronal injury. Copyright © 2006 Humana Press Inc.en_US
dc.rightsMahidol Universityen_US
dc.titleNF-κB-associated MnSOD induction protects against β-amyloid-induced neuronal apoptosisen_US
Appears in Collections:Scopus 2006-2010

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