MAP kinase activation by mu opioid receptor involves phosphatidylinositol 3‐kinase but not the cAMP/PKA pathway

FEBS Letters

Ai, Wandong¹  Gong, Jianhua¹  Yu, Lei¹ 

[1] Department of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, IN 46202-5251, USA

关键词: Mu opioid receptor;    Mitogen-activated protein kinase;    Protein kinase A;    Phosphatidylinositol 3-kinase;    AC;    adenylyl cyclase;    CHO;    Chinese hamster ovary;    MAP;    mitogen-activated protein;    PKA;    protein kinase A;    PKC;    protein kinase C;    PTK;    protein tyrosine kinase;    8-CPT-cAMP;    8-chlorophenylthio-cAMP;    PI;    phosphatidylinositol;   

DOI  :  10.1016/S0014-5793(99)00949-7

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

The involvement of protein kinases was studied in mu opioid receptor activation of mitogen-activated protein (MAP) kinase using cells transfected with the receptor clone. The cAMP/protein kinase A (PKA) pathway is known to be the major biochemical pathway for mu opioid receptor signaling. However, our data showed that stimulating adenylyl cyclase or activating PKA had no effect on mu receptor enhancement of MAP kinase activity, suggesting that the cAMP/PKA pathway is not involved in mediating the mu receptor activation of MAP kinase. Inhibition of phosphatidylinositol (PI) 3-kinase reduced mu receptor enhancement of MAP kinase activity, suggesting PI 3-kinase involvement. Together, these results show that cross-talk between the mu opioid receptor and the MAP kinase cascade is not mediated by the cAMP/PKA pathway, but involves PI 3-kinase.

【 授权许可】

Unknown