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Differential regulation of cell cycle‐related proteins by CD95 engagement in thymocytes and T cell leukemic cell line, Jurkat
Author(s) -
Bae Youngmee,
Crispe I. Nicholas
Publication year - 2000
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/1097-4644(20010301)80:3<328::aid-jcb50>3.0.co;2-4
Subject(s) - jurkat cells , fas receptor , apoptosis , cell cycle , microbiology and biotechnology , cyclin e , downregulation and upregulation , cell , programmed cell death , biology , t cell , cancer research , cyclin , immunology , immune system , biochemistry , gene
CD95 engagement results in apoptosis in thymocytes and in the Jurkat human leukemic T cell line. Biochemical analyses in CD95‐engaged thymocytes and Jurkat cells revealed dysregulation of the G1/S cell cycle control point. Cyclin E was upregulated upon CD95 engagement, suggesting G1‐to‐S progression, but there was no upregulation of cyclin A. Instead, cyclin E was degraded by caspases. In addition, c‐myc that normally acts on S‐phase progression through the activation of cdc25A appeared to be involved in the inhibition of S‐phase progression after CD95 ligation. This implies that G1→S progression and apoptosis are intimately linked in cells undergoing CD95 ligation. Furthermore, our data suggest that CD95‐induced apoptosis occurs at the G1/S phase transition. We therefore suggest that CD95 engagement not only triggers death signals but also affects the G1/S checkpoint. J. Cell. Biochem. 80:328–338, 2001. © 2001 Wiley‐Liss, Inc.