4.8 Article

Ezrin is a negative regulator of death receptor-induced apoptosis

Journal

ONCOGENE
Volume 29, Issue 9, Pages 1374-1383

Publisher

NATURE PUBLISHING GROUP
DOI: 10.1038/onc.2009.417

Keywords

Fas; ezrin; apoptosis; moesin; DISC

Funding

  1. National Health Research Institute [NHRI-EX96-9527NI]
  2. National Science Council [NSC 95-2320-B001-023]
  3. Academia Sinica, Taiwan, ROC.

Ask authors/readers for more resources

Ezrin links cortical actin filaments with the cell membrane, and has a critical role in many membrane-initiated events. Fas is directly associated with ezrin, but conflicting results have been reported for the involvement of ezrin in Fas-induced cell death. In this study we show that ezrin was associated with Fas in T cells before stimulation and was released shortly after Fas ligand (FasL) engagement. The knockdown of ezrin moderately increased Fas-triggered or tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-triggered cell death in normal T lymphocytes and in H9 cells, but had no effect on death receptor-induced apoptosis in type II cells, such as Jurkat and CEM. Expression of a dominant-negative form of ezrin also led to an increased Fas-induced apoptosis in H9 cells. Ezrin deficiency did not affect the internalization of Fas after Fas ligation. Instead, an enhanced formation of death-inducing signaling complex (DISC) was observed in H9 cells with ezrin knockdown, leading to accelerated caspase-8 activation. Together, our results suggest that ezrin has a negative role in the recruitment of Fas into signaling complexes in type I T cells. Loss of ezrin likely removes the constraint imposed by ezrin and facilitates the assembly of death receptor complex in T cells. Oncogene (2010) 29, 1374-1383; doi:10.1038/onc.2009.417; published online 23 November 2009

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.8
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available