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. 1997 Mar;90(3):383–387. doi: 10.1111/j.1365-2567.1997.00383.x

Apoptosis in a Fas-resistant, T-cell receptor-sensitive human leukaemic T-cell clone.

L L Delehanty 1, J A Payne 1, S N Farrow 1, R Brown 1, B R Champion 1
PMCID: PMC1456596  PMID: 9155645

Abstract

The Fas (CD95) antigen plays a key role in regulating T-cell activation and survival. We have generated a Fas-resistant subclone of the human T-cell leukaemia line, H9, which is still able to undergo apoptosis in response to T-cell receptor ligation. Molecular analyses revealed that resistance to Fas-mediated apoptosis was due to a heterozygous mutation in the death domain of the Fas gene which generates a stop codon, and thus encodes a truncated Fas molecule. Fas ligation was able to induce apoptosis in the presence of cycloheximide, indicating that the mutant Fas molecule retained some signalling capability, which is death-domain independent. These cells will provide a useful tool for dissecting the complexities of Fas signalling pathways.

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Selected References

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