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Role of nuclear PKC δ in mediating caspase‐3‐upregulation in Jurkat T leukemic cells exposed to ionizing radiation
Author(s) -
Cataldi Amelia,
Miscia Sebastiano,
Centurione Lucia,
Rapino Monica,
Bosco Domenico,
Grifone Giovanna,
Valerio Valentina Di,
Garaci Francesco,
Rana Rosalba
Publication year - 2002
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/jcb.10251
Subject(s) - jurkat cells , microbiology and biotechnology , apoptosis , protein kinase c , intracellular , programmed cell death , downregulation and upregulation , dna damage , biology , effector , signal transduction , chemistry , t cell , genetics , dna , gene , immune system
The response of Jurkat T cells to ionizing radiation (IR) includes cell cycle arrest and DNA damage, which lead to the occurrence of apoptosis. Here, we try to elucidate some of the early intracellular signals which control the induction of such a process upon IR exposure, addressing to examine the specific role of several PKC isoforms (δ, ε, ζ) and their subcellular distribution. Attention has been focused on the connections between nuclear PKC δ activation and the expression of cell death regulators (Bcl‐2 family proteins Bad, Bax and Bcl‐2) and cell death effector caspase‐3 (CPP32) which lead to the cleavage of cytoskeletal and nuclear proteins and induction of apoptosis. Altogether these results let us to conclude that PKC δ, potentiating the pro‐apoptotic effect of caspase 3, plays a key role in the cellular response to IR and thus can be considered a molecular target for therapy. © 2002 Wiley‐Liss, Inc.