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Kidney Int. 2008 Aug;74(3):310-8. doi: 10.1038/ki.2008.192. Epub 2008 May 14.

Induction of proapoptotic Daxx following ischemic acute kidney injury.

Author information

1
Nephrology and Hypertension, Cincinnati Children's Hospital Medical Center, University of Cincinnati, Cincinnati, Ohio, USA.

Abstract

Transcriptome profiling has shown that the pro-apoptotic death-domain-associated protein Daxx is rapidly induced in the kidney of animals following ischemic injury. Here we found that Daxx protein was increased 5-fold in tubule cells in both animal and human models of ischemic acute kidney injury. Further there was upregulation of its primary interacting partner, Fas and phosphorylation of its primary downstream activator (JNK) in parallel to Daxx induction. In cultured tubule cells, partial ATP depletion resulted in a rapid induction of Daxx, Fas, JNK phosphorylation and apoptosis. Antisense oligonucleotides to Daxx and specific JNK inhibitors blunted the apoptotic response to ATP depletion. These studies indicate that Daxx may play an unrecognized role in the early apoptotic response to ischemic renal injury.

PMID:
18480747
DOI:
10.1038/ki.2008.192
[Indexed for MEDLINE]
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