Role of calmodulin in the modulation of the MAPK signalling pathway and the transactivation of epidermal growth factor receptor mediated by PKC

FEBS Letters

Tebar, Francesc¹  Lladó, Anna¹  Enrich, Carlos¹ 

[1] Departament de Biologia Cellular, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Facultat de Medicina, Universitat de Barcelona, Casanova 143, 08036 Barcelona, Spain

关键词: Epidermal growth factor receptor;    Calmodulin;    Protein kinase C;    Transactivation;    Calmodulin antagonist;    Mitogen-activated protein kinase;    Shedding;    EGFR;    epidermal growth factor receptor;    HB-EGF;    heparin-binding EGF-like growth factor;    AR;    amphiregulin;    RBD;    Ras-binding domain;    BIM;    bisindolylmaleimide;    AG1478;    tyrphostin;    CaM;    calmodulin;    TPA;    12-O-tetradecanoylphorbol-13-acetate;    PKC;    protein kinase C;    MAPK;    mitogen-activated protein kinase;    TGFα;    transforming growth factor-α;    W-13;    N-(4-aminobutyl)-5-chloro-2-naphthalenesulfonamide;    BB94;    batimastat;   

DOI  :  10.1016/S0014-5793(02)02624-8

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

We have recently shown that calmodulin (CaM) regulates the trafficking of epidermal growth factor receptor (EGFR) as well as the mitogen-activated protein kinase (MAPK) signalling pathway. However, the overall regulation of the MAPK pathway is achieved through a complex interplay of other several upstream effectors including G-proteins, EGF, EGFR, protein kinase C (PKC), phosphatidylinositol-3-kinase and CaM. In order to understand the role of CaM in the PKC-mediated transactivation of EGFR we have analysed the effect of a CaM antagonist, N-(4-aminobutyl)-5-chloro-2-naphthalenesulfonamide, on the 12-O-tetradecanoylphorbol-13-acetate-mediated activation of EGFR and the subsequent MAPK activation. The results show that CaM interferes with MAPK activation and the transactivation of EGFR mediated by PKC.

【 授权许可】

Unknown