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X-linked inhibitor of apoptosis protein increases mitochondrial antioxidants through NF-kappaB activation
(Lindholm)
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience. (Lindholm)
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience. (Lindholm)
2007 (English)In: Biochemical and Biophysical Research Communications - BBRC, ISSN 0006-291X, E-ISSN 1090-2104, Vol. 364, no 1, 138-144 p.Article in journal (Refereed) Published
Abstract [en]

X chromosome-linked inhibitor of apoptosis protein is an endogenous inhibitor of caspases and is an important regulator of cell death. XIAP can also influence cell signaling, but downstream proteins affected are largely unknown. We show here using neuronal PC6.3 cells that XIAP increases the levels of antioxidants, particularly superoxide dismutase-2 that is localized to mitochondria. Studies using reporter constructs and NF-κB Rel-A deficient mouse embryonic fibroblasts showed that NF-κB signaling is required for the induction of Sod2 by XIAP. XIAP also reduced oxidative stress in the PC6.3 cells as shown by decreased production of reactive oxygen species. These findings disclose a novel role for XIAP in control of oxidative stress and mitochondrial antioxidants that may contribute to cell protection after various injuries.

Place, publisher, year, edition, pages
2007. Vol. 364, no 1, 138-144 p.
Keyword [en]
Mitochondria, NF-κB, Oxidative stress, Sod2, XIAP
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:uu:diva-12878DOI: 10.1016/j.bbrc.2007.09.115ISI: 000250661500022PubMedID: 17936246OAI: oai:DiVA.org:uu-12878DiVA: diva2:40648
Available from: 2008-01-18 Created: 2008-01-18 Last updated: 2017-12-11Bibliographically approved

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Korhonen, LauraLindholm, Dan

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