RAIDD aggregation facilitates apoptotic death of PC12 cells and sympathetic neurons.

Autor: Jabado, O., Wang, Q., Rideout, H. J., Yeasmin, M., Guo, K. X., Vekrellis, K., Papantonis, S., Angelastro, J. M., Troy, C. M., Stefanis, L.
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Zdroj: Cell Death & Differentiation; Jun2004, Vol. 11 Issue 6, p618-630, 13p
Abstrakt: In human cell lines, the caspase 2 adaptor RAIDD interacts selectively with caspase 2 through its caspase recruitment domain (CARD) and leads to caspase 2-dependent death. Whether RAIDD induces such effects in neuronal cells is unknown. We have previously shown that caspase 2 is essential for apoptosis of trophic factor-deprived PC12 cells and rat sympathetic neurons. We report here that rat RAIDD, cloned from PC12 cells, interacts with rat caspase 2 CARD. RAIDD overexpression induced caspase 2 CARD- and caspase 9-dependent apoptosis of PC12 cells and sympathetic neurons. Apoptosis correlated with the formation of discrete perinuclear aggregates. Both death and aggregates required the expression of full-length RAIDD. Such aggregates may enable more effective activation of caspase 2 through close proximity. Following trophic deprivation, RAIDD overexpression increased death and aggregate formation. Therefore, RAIDD aggregation is important for its death-promoting effects and may play a role in trophic factor withdrawal-induced neuronal apoptosis.Cell Death and Differentiation (2004) 11, 618-630. doi:10.1038/sj.cdd.4401397 Published online 6 February 2004 [ABSTRACT FROM AUTHOR]
Databáze: Complementary Index