Unknown

Dataset Information

0

Caspase-10 is an initiator caspase in death receptor signaling.


ABSTRACT: A role for caspase-10, previously implicated in the autoimmune lymphoproliferative syndrome, in death receptor signaling has not been directly shown. Here we show that caspase-10 can function independently of caspase-8 in initiating Fas- and tumor necrosis factor-related apoptosis-inducing ligand-receptor-mediated apoptosis. Moreover, Fas crosslinking in primary human T cells leads to the recruitment and activation of caspase-10. Fluorescent resonance energy transfer analysis indicates that the death-effector domains of caspase-8 and -10 both interact with the death-effector domain of FADD. Nonetheless, we find that caspase-8 and -10 may have different apoptosis substrates and therefore potentially distinct roles in death receptor signaling or other cellular processes.

SUBMITTER: Wang J 

PROVIDER: S-EPMC61136 | biostudies-literature | 2001 Nov

REPOSITORIES: biostudies-literature

altmetric image

Publications

Caspase-10 is an initiator caspase in death receptor signaling.

Wang J J   Chun H J HJ   Wong W W   Spencer D M DM   Lenardo M J MJ  

Proceedings of the National Academy of Sciences of the United States of America 20011101 24


A role for caspase-10, previously implicated in the autoimmune lymphoproliferative syndrome, in death receptor signaling has not been directly shown. Here we show that caspase-10 can function independently of caspase-8 in initiating Fas- and tumor necrosis factor-related apoptosis-inducing ligand-receptor-mediated apoptosis. Moreover, Fas crosslinking in primary human T cells leads to the recruitment and activation of caspase-10. Fluorescent resonance energy transfer analysis indicates that the  ...[more]

Similar Datasets

| S-EPMC6727177 | biostudies-literature
| S-EPMC4111576 | biostudies-literature
2013-03-13 | E-GEOD-43878 | biostudies-arrayexpress
2013-03-13 | GSE43878 | GEO
2016-04-20 | GSE75365 | GEO
| S-EPMC4059832 | biostudies-literature
| S-EPMC6288387 | biostudies-literature
| S-EPMC3365430 | biostudies-literature
| S-EPMC4792459 | biostudies-literature
| S-EPMC3122213 | biostudies-literature