Direct interaction of Smac with NADE promotes TRAIL-induced apoptosis

Kwiyeom Yoon, Hyun Duk Jang, Soo Young Lee

Research output: Contribution to journalArticlepeer-review

21 Scopus citations

Abstract

Second mitochondria-derived activator of caspase (Smac) has been implicated in the activation of apoptosis in response to cell stress. We screened for Smac/DIABLO-binding protein for further understanding of Smac-mediated apoptosis. We identified NADE, previously known as p75NTR-associated cell death executor, as a Smac-binding protein. Smac-NADE interaction was mapped to the N-terminal region of Samc and the C-terminal region of NADE. Co-expression of NADE and Smac promotes TRAIL-induced apoptosis in MCF-7 cells. Interestingly, the co-presence of Smac and NADE inhibits XIAP-mediated Smac ubiquitination. In conclusion, our results provide the first evidence that the interaction between Smac and NADE regulates apoptosis through the inhibition of Smac ubiquitination.

Original languageEnglish
Pages (from-to)649-654
Number of pages6
JournalBiochemical and Biophysical Research Communications
Volume319
Issue number2
DOIs
StatePublished - 25 Jun 2004

Bibliographical note

Funding Information:
We thank Dr. T. Sato (Columbia University, USA) for NADE expression vectors and Dr. J. Ashwell (NIH, USA) for XIAP expression vectors. This work was supported by Korea Research Foundation Grant (KRF-2000-015-FS0006) (to S.Y.L). K.Y. and H.J. were supported by BK21 fellowship.

Keywords

  • Apoptosis
  • NADE
  • Smac
  • TRAIL
  • Ubiquitination
  • XIAP

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