Cell Cycle Effects by C-FADD Depend on its C-terminal Phosphorylation Site

Elizabeth C. Alappat, Jörg Volkland, Marcus E. Peter*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

48 Scopus citations


Expression of a truncated form of the death receptor adaptor FADD (C-FADD) as a transgene in mice blocks T cell proliferation. Here we provide evidence that the C-terminal phosphorylation site Ser194 in C-FADD affects the cell cycle in nonlymphoid cells as well. High expression of wild type C-FADD but not C-FADD with a S194A point mutation arrested the nontumor cell line MCF10A in G2/M but not the tumor cell line MCF7. BJAB as well as MCF10A cells expressing moderate levels of C-FADD with a S194E mutation mimicking phosphorylated C-FADD were more susceptible to a Taxol®-induced G2/M arrest than cells expressing C-FADD S194A suggesting that C-FADD S194E lowers the threshold for G2/M arrest. Our data suggest that C-FADD may affect apoptosis sensitivity of cells by interfering with cell cycle progression and not only by binding to death receptors.

Original languageEnglish (US)
Pages (from-to)41585-41588
Number of pages4
JournalJournal of Biological Chemistry
Issue number43
StatePublished - Oct 24 2003

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology


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