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Modulated kinase activities in cells undergoing tumour necrosis factor‐induced apoptotic cell death
Author(s) -
Helms Matt J,
Mohamed Ahmed A.A,
MacEwan David J
Publication year - 2001
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(01)02779-x
Subject(s) - apoptosis , tumor necrosis factor alpha , p38 mitogen activated protein kinases , kinase , programmed cell death , protein kinase a , protein kinase r , microbiology and biotechnology , cytotoxic t cell , mapk/erk pathway , hela , necrosis , biology , chemistry , cancer research , mitogen activated protein kinase kinase , cell , immunology , biochemistry , in vitro , genetics
Tumour necrosis factor‐α (TNF) has a variety of cellular effects including apoptotic and necrotic cytotoxicity. TNF activates a range of kinases, but their role in cytotoxic mechanisms is unclear. HeLa cells expressing elevated type II 75 kDa TNF receptor (TNFR2) protein, analysed by flow cytometry and Western analysis, showed altered c‐Jun N‐terminal kinase (JNK) and p38 mitogen‐activated protein kinase (p38MAPK; but not MAPK) protein content and activation. There was greater JNK activation, but reduced p38MAPK activation in dying cells compared to those still to enter TNF‐induced apoptosis. Moreover, cells displaying more rapid apoptosis possess higher levels of type I 55 kDa TNFR1 receptor isoform, but less TNFR2. These findings reveal differential kinase activation in TNF‐induced apoptotic death.