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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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

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.[1]


  1. RAIDD aggregation facilitates apoptotic death of PC12 cells and sympathetic neurons. Jabado, O., Wang, Q., Rideout, H.J., Yeasmin, M., Guo, K.X., Vekrellis, K., Papantonis, S., Angelastro, J.M., Troy, C.M., Stefanis, L. Cell Death Differ. (2004) [Pubmed]
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