The activation of p38 MAPK by the β‐adrenergic agonist isoproterenol in rat epididymal fat cells

FEBS Letters

Denton, Richard M.¹  Moule, S.Kelly¹ 

[1] Department of Biochemistry, School of Medical Sciences, University Walk, Bristol, BS8 1TD, UK

关键词: p38 MAPK;    Isoproterenol;    Adipocyte;    AMP-activated protein kinase;    Cyclic AMP;    AICAR;    5-amino-4-imidazolecarboxamide ribonucleoside;    AMPK;    AMP-activated protein kinase;    ATF2;    activating transcription factor 2;    cpt-cAMP;    chlorophenylthio-cyclic AMP;    CREB;    cyclic AMP response element binding protein;    GST;    glutathione S-transferase;    HSP27;    heat shock protein 27;    JNK;    c-Jun N-terminal kinase;    p38 MAPK;    p38 mitogen activated protein kinase;    MAPKAP-K;    mitogen activated protein kinase activated protein kinase;   

DOI  :  10.1016/S0014-5793(98)01392-1

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Here we report that the β-adrenergic agonist isoproterenol increases the activity of the stress-activated kinase p38 MAPK over 10-fold in freshly isolated rat epididymal fat cells. Stimulation of the kinase was rapid, sustained for at least 60 min and sensitive to the specific p38 MAPK inhibitor, SB 203580. Half-maximal stimulation of p38 MAPK by isoproterenol occurred at 13 nM isoproterenol. The cell permeable cyclic AMP analogue, chlorophenylthio-cyclic AMP increased p38 MAPK activity to a similar extent to isoproterenol, suggesting that the effect of the β-adrenergic agonist is mediated via increases in the activity of cyclic-AMP dependent protein kinase. Although it had little or no effect on the activity of c-Jun N-terminal kinase, isoproterenol and a number of other treatments which activated p38 MAPK were found to stimulate AMP-activated protein kinase in fat cells. Activation of AMPK and p38 MAPK were not, however, found to be directly linked.

【 授权许可】

Unknown