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Published on: November 27, 2016
Subcellular localization of Daxx determines its opposing functions in ischemic cell death
Yong-Sam Jung1, Hye-Young Kim, Yong J Lee
1Department of Bioscience and Biotechnology, Chungnam National University, 220 Gung-dong, Yuseong-gu, Daejeon 305-764, Republic of Korea.
Abstract:
This study examined the role of Daxx in ischemic stress. Upon ischemic stress, nuclear export of Daxx to the cytoplasm was observed in primary myocytes as well as in various cell lines. Daxx silencing using siRNAs was detrimental in tethering PML-nuclear body (PML-NB) constituents together. Overexpression of Daxx (W621A) caused nuclear export of p53 independently of PML and promoted ischemic cell death via activation of JNK. Conversely, overexpression of Daxx (S667A) prevented dissociation of PML-NB constituents and protected cells from ischemic death. Collectively, our results demonstrate that the subcellular localization of Daxx determines its role in ischemic cell death.
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