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This cell line can be used to study the role of FADD in apoptotic signaling pathways in the absence of overxpression.

Juo P, et al. Essential requirement for caspase-8/FLICE in the initiation of the Fas-induced apoptotic cascade. Curr. Biol. 8: 1001-1008, 1998. PubMed: 9740801
ICR-191 treated clones were serially diluted in 96-well plates in the presence of Fas Antibody for 3 to 5 weeks. Ref
Juo P, et al. FADD is required for multiple signaling events downstream of the receptor Fas. Cell Growth Differ. 10: 797-804, 1999. PubMed: 10616904 Two of these ICR-191 treated clones have been deposited at the ATCC . They are I 9.2 (ATCC CRL-2571), a clone with a mutation in the cysteine protease caspase-8/FLICE and I 2.1 (ATCC CRL-2572), a clone with a mutation in the adaptor FADD.
Unlike the parental line A3 that does express FADD, the I 2.1 cell line does not express FADD protein by immunoblot analysis and is completely resistant to Fas-induced death. Complementation of the I 2.1 cell lines with wild-type FADD restores Fas-mediated apoptosis. Fas activation of caspase-2, caspase-3, caspase-7, and caspase-8 is completely defective in the FADD mutant cell line I 2.1. Ref
Juo P, et al. FADD is required for multiple signaling events downstream of the receptor Fas. Cell Growth Differ. 10: 797-804, 1999. PubMed: 10616904
This cell line can be used to study the role of FADD in apoptotic signaling pathways in the absence of overxpression.
Juo P, et al. Essential requirement for caspase-8/FLICE in the initiation of the Fas-induced apoptotic cascade. Curr. Biol. 8: 1001-1008, 1998. PubMed: 9740801
Juo P, et al. FADD is required for multiple signaling events downstream of the receptor Fas. Cell Growth Differ. 10: 797-804, 1999. PubMed: 10616904
Juo P, et al. Fas activation of the p38 mitogen-activated protein kinase signalling pathway requires ICE/CED-3 family proteases. Mol. Cell. Biol. 17: 24-35, 1997. PubMed: 8972182
