Abstract
Abstract The process of apoptosis is a critical component of normal immune system development and homeostasis, and in many cells this involves signaling through the c-Jun amino terminal kinase (JNK) pathway. In Jurkat T cells, Fas-induced JNK activity is dependent upon activation of the caspase cascades known to be central components of the apoptotic program. We show in Jurkat cell lines expressing a dominant negative PAK construct that PAK signaling is necessary for JNK activation in response to Fas receptor cross-linking. Inhibition of JNK activation induced by Fas does not impair cell death as assessed by DNA fragmentation. However, expression of the catalytically active C terminus of PAK2, which is generated through caspase action during Fas-mediated apoptosis, induces Jurkat cell apoptosis. We conclude that PAK activity resulting from caspase-mediated cleavage is a necessary component of JNK activation induced by Fas receptor signaling and that PAK2 can contribute to the induction of cell death.
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Dates
Type | When |
---|---|
Created | 2 years, 8 months ago (Jan. 1, 2023, 7:29 p.m.) |
Deposited | 5 months ago (March 30, 2025, 10:09 p.m.) |
Indexed | 2 months, 3 weeks ago (June 10, 2025, 3:05 p.m.) |
Issued | 27 years, 8 months ago (Jan. 1, 1998) |
Published | 27 years, 8 months ago (Jan. 1, 1998) |
Published Online | 27 years, 8 months ago (Jan. 1, 1998) |
Published Print | 27 years, 8 months ago (Jan. 1, 1998) |
@article{Rudel_1998, title={Cutting Edge: p21-Activated Kinase (PAK) Is Required for Fas-Induced JNK Activation in Jurkat Cells}, volume={160}, ISSN={1550-6606}, url={http://dx.doi.org/10.4049/jimmunol.160.1.7}, DOI={10.4049/jimmunol.160.1.7}, number={1}, journal={The Journal of Immunology}, publisher={Oxford University Press (OUP)}, author={Rudel, Thomas and Zenke, Frank T and Chuang, Tsung-Hsien and Bokoch, Gary M}, year={1998}, month=jan, pages={7–11} }