Membrane depolarization increases membrane PtdIns(4,5)P2 levels through mechanisms involving PKC ßII and PI4 kinase.
J Biol Chem
; 286(46): 39760-7, 2011 Nov 18.
Article
em En
| MEDLINE
| ID: mdl-21953466
ABSTRACT
In a previous study, we showed that membrane depolarization induced elevation of membrane phosphatidylinositol 4,5-bisphosphates (PtdIns(4,5)P(2), also known as PIP(2)) and subsequently increased the KCNQ2/Q3 currents expressed in Xenopus oocytes through increased PI4 kinase activity. In this study, the underlying mechanism for this depolarization-induced enhancement of PIP(2) synthesis was further investigated. Our results indicate that activation of protein kinase C (PKC) isozyme ßII was responsible for the enhanced PIP(2) synthesis. We found that phorbol-12-myristate, 13-acetate (PMA), an activator of PKC, mimicked the effects of the membrane depolarization by increasing KCNQ2/Q3 activity, elevating membrane PIP(2) levels and increasing activity of PI4 kinase ß. Furthermore, membrane depolarization enhanced PKC activity. The effects of both depolarization and PMA were blocked by a PKC inhibitor or PI4 kinase ß RNA interference. Further results demonstrate that the depolarization selectively activated the PKC ßII isoform and enhanced its interaction with PI4 kinase ß. These results reveal that the depolarization-induced elevation of membrane PIP(2) is through activation of PKC and the subsequent increased activity of PI4 kinase ß.
Texto completo:
1
Bases de dados:
MEDLINE
Assunto principal:
Proteína Quinase C
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Fosfotransferases (Aceptor do Grupo Álcool)
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Fosfatidilinositol 4,5-Difosfato
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Proteínas de Xenopus
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Potenciais da Membrana
Limite:
Animals
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Humans
Idioma:
En
Revista:
J Biol Chem
Ano de publicação:
2011
Tipo de documento:
Article
País de afiliação:
China