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Subcellular localization of Daxx determines its opposing functions in ischemic cell death.

Authors: Jung, YS  Kim, HY  Lee, YJ  Kim, E 
Citation: Jung YS, etal., FEBS Lett. 2007 Mar 6;581(5):843-52. Epub 2007 Feb 2.
Pubmed: (View Article at PubMed) PMID:17289031
DOI: Full-text: DOI:10.1016/j.febslet.2007.01.055

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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CRRD Object Information
CRRD ID: 9587773
Created: 2014-10-17
Species: All species
Last Modified: 2014-10-17
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.