期刊论文详细信息
FEBS Letters
Activation of mitogen‐activated protein kinase by the bradykinin B2 receptor is independent of receptor phosphorylation and phosphorylation‐triggered internalization
Pizard, Anne1  Dikic, Ivan2  Blaukat, Andree2  Alhenc-Gelas, François1  Rajerison, Rabary M.1  Müller-Esterl, Werner3 
[1] INSERM U367, 17 rue du Fer à Moulin, 75005 Paris, France;Ludwig Institute for Cancer Research, Box 595, S-75124 Uppsala, Sweden;Institute of Physiological Chemistry and Pathobiochemistry, Johannes Gutenberg University at Mainz, Duesbergweg 6, D-55099 Mainz, Germany
关键词: Bradykinin B2 receptor;    Mitogenic signalling;    Mitogen-activated protein kinase;    Internalization;    Phosphorylation;    B2R;    bradykinin B2 receptor;    EGF;    epidermal growth factor;    ERK2;    extracellular-regulated kinase 2;    GPCR;    G protein-coupled receptor;    HA;    hemagglutinin;    MAP kinase;    mitogen-activated protein kinase;    MBP;    myelin basic protein;    PMA;    phorbol-12-myristate-13-acetate;   
DOI  :  10.1016/S0014-5793(99)00613-4
学科分类:生物化学/生物物理
来源: John Wiley & Sons Ltd.
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【 摘 要 】

Recent evidence suggests that serine/threonine phosphorylation and internalization of β2-adrenergic receptors play critical roles in signalling to the mitogen-activated protein kinase cascade. To investigate whether this represents a general mechanism employed by G protein-coupled receptors, we studied the requirement of these processes in the activation of mitogen-activated protein kinase by Gαq-coupled bradykinin B2 receptors. Mutant B2 receptors impaired in receptor phosphorylation and internalization are fully capable to activate mitogen-activated protein kinase. Bradykinin-induced long-term effects on mitogenic signalling monitored by measuring the transcriptional activity of Elk1 were identical in cells expressing the wild-type or mutant B2 receptors. Therefore, G protein-coupled bradykinin receptors activate the mitogen-activated protein kinase pathway independently of receptor phosphorylation and internalization.

【 授权许可】

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