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Elsevier, Biochemical and Biophysical Research Communications, 1(375), p. 156-161, 2008

DOI: 10.1016/j.bbrc.2008.07.142

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XIAP regulates intracellular ROS by enhancing antioxidant gene expression

Journal article published in 2008 by Ulrike Resch, Yvonne M. Schichl, Susanne Sattler ORCID, Rainer de Martin
This paper is available in a repository.
This paper is available in a repository.

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Abstract

XIAP (X chromosome-linked inhibitor of apoptosis) is a member of the anti-apoptotic IAP gene family and an inhibitor of caspase-3. We show here that loss of XIAP renders cells highly sensitive to oxidative stress. Stimulation of XIAP(-/-) MEF with hydrogen peroxide, or other agents that generate reactive oxygen species (ROS) results in increased apoptosis assessed by caspase-3 activity and PARP cleavage. Furthermore, we observed increased levels of ROS and diminished expression of antioxidative genes, e.g., SOD1, -2, NQO1, HO-1, and Txn2 in XIAP(-/-) cells. In addition, stimulation of XIAP(-/-) MEF with hydrogen peroxide resulted in enhanced phosphorylation of JNK. Our findings reveal that XIAP, in addition to its well described caspase-inhibitory function, prevents prolonged JNK activation and is critically involved in modulating ROS levels through regulation of antioxidative genes, thereby inhibiting ROS-induced apoptosis.