RAIDD aggregation facilitates apoptotic death of PC12 cells and sympathetic neurons

O. Jabado, Q. Wang, H. J. Rideout, M. Yeasmin, K. X. Guo, K. Vekrellis, S. Papantonis, James M Angelastro, C. M. Troy, L. Stefanis

Research output: Contribution to journalArticlepeer-review

16 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)618-630
Number of pages13
JournalCell Death and Differentiation
Issue number6
StatePublished - Jun 2004
Externally publishedYes


  • Aggregate
  • Caspase
  • Caspase recruitment domain
  • Neuronal death
  • PC12 cells
  • Sympathetic neurons

ASJC Scopus subject areas

  • Cell Biology


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