Modulated kinase activities in cells undergoing tumour necrosis factor‐induced apoptotic cell death

FEBS Letters

MacEwan, David J¹  Helms, Matt J¹  Mohamed, Ahmed A.A¹ 

[1] Department of Biomedical Sciences, Institute of Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen AB25 2ZD, UK

关键词: Cytokine;    Receptor;    Subtype;    Signal transduction;    Kinase;    Tumor;    ERK;    extracellular signal-regulated kinase;    JNK;    c-Jun N-terminal kinase;    MAPK;    mitogen-activated protein kinase;    PI;    propidium iodide;    TNF;    tumour necrosis factor-α;    TNFR;    TNF receptor;    TNFR1;    type I 55 kDa TNFR;    TNFR2;    type II 75 kDa TNFR;    TRAF;    TNFR-associating factor;   

DOI  :  10.1016/S0014-5793(01)02779-X

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

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.

【 授权许可】

Unknown