PKC‐β and PKC‐ζ mediate opposing effects on proximal tubule Na+,K+‐ATPase activity

FEBS Letters

Bertorello, Alejandro M²  Efendiev, Riad¹  Pedemonte, Carlos H¹ 

[1] College of Pharmacy, University of Houston, 4800 Calhoun Blvd., Houston, TX 77204-5515, USA;Dept. of Molecular Medicine, Karolinska Institutet, Karolinska Hospital, S-171 76 Stockholm, Sweden

关键词: Na+;    K+-ATPase;    Na-pump;    Sodium-pump;    PKC isoform;    Proximal tubule sodium transport;    PKC;    protein kinase C;    PMA;    phorbol 12-myristate 13-acetate;    DA;    dopamine;    OK cells;    opossum kidney cells;   

DOI  :  10.1016/S0014-5793(99)00925-4

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Dopamine (DA) inhibits rodent proximal tubule Na⁺,K⁺-ATPase via stimulation of protein kinase C (PKC). However, direct stimulation of PKC by phorbol 12-myristate 13-acetate (PMA) results in increased Na⁺,K⁺-ATPase. LY333531, a specific inhibitor of the PKC-β isoform, prevents PMA-dependent activation of Na⁺,K⁺-ATPase, but has no effect on DA inhibition of this activity. A similar result was obtained with a PKC-β inhibitor peptide. Concentrations of staurosporine, that inhibits PKC-ζ, prevent DA-dependent inhibition of Na⁺,K⁺-ATPase and a similar effect was obtained with a PKC-ζ inhibitor peptide. Thus, PMA-dependent stimulation of Na⁺,K⁺-ATPase is mediated by activation of PKC-β, whereas inhibition by DA requires activation of PKC-ζ.

【 授权许可】

Unknown