The lipid connection-regulation of voltage-gated Ca2+ channels by phosphoinositides

Ioannis E. Michailidis; Yun Zhang; Jian Yang

doi:10.1007/s00424-007-0272-9

The lipid connection-regulation of voltage-gated Ca²⁺ channels by phosphoinositides

Ioannis E. Michailidis, Yun Zhang, Jian Yang

Genetics

Research output: Contribution to journal › Review article › peer-review

43 Scopus citations

Abstract

Recent findings have revealed a pivotal role for phospholipids phosphatidylinositol -4,5-biphosphate (PIP₂) and phosphatidylinositol -3,4,5-trisphosphate (PIP₃) in the regulation of high voltage-activated (HVA) Ca²⁺ channels. PIP₂ exerts two opposing actions on HVA Ca²⁺ channels: It stabilizes their activity but also produces a voltage-dependent inhibition that can be antagonized by protein kinase A (PKA) phosphorylation. PIP₂ depletion and arachidonic acid together mediate the slow, voltage-independent inhibition of HVA Ca²⁺ channels by G_q/11 -coupled receptors in neurons. A sufficient level of plasma membrane PIP₂ also appears to be necessary for G_βγ -mediated inhibition. On the other hand, increased production of PIP₃ by PI-3 kinases promotes trafficking of HVA Ca²⁺ channels to the plasma membrane. This review discusses these findings and their implications.

Original language	English (US)
Pages (from-to)	147-155
Number of pages	9
Journal	Pflugers Archiv European Journal of Physiology
Volume	455
Issue number	1
DOIs	https://doi.org/10.1007/s00424-007-0272-9
State	Published - Oct 2007

Keywords

Calcium channel
GTP binding protein
Phospholipid
Regulation
Signal transduction

ASJC Scopus subject areas

Physiology
Clinical Biochemistry
Physiology (medical)

Access to Document

10.1007/s00424-007-0272-9

Cite this

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title = "The lipid connection-regulation of voltage-gated Ca2+ channels by phosphoinositides",

abstract = "Recent findings have revealed a pivotal role for phospholipids phosphatidylinositol -4,5-biphosphate (PIP2) and phosphatidylinositol -3,4,5-trisphosphate (PIP3) in the regulation of high voltage-activated (HVA) Ca2+ channels. PIP2 exerts two opposing actions on HVA Ca2+ channels: It stabilizes their activity but also produces a voltage-dependent inhibition that can be antagonized by protein kinase A (PKA) phosphorylation. PIP2 depletion and arachidonic acid together mediate the slow, voltage-independent inhibition of HVA Ca2+ channels by Gq/11 -coupled receptors in neurons. A sufficient level of plasma membrane PIP2 also appears to be necessary for Gβγ -mediated inhibition. On the other hand, increased production of PIP3 by PI-3 kinases promotes trafficking of HVA Ca2+ channels to the plasma membrane. This review discusses these findings and their implications.",

keywords = "Calcium channel, GTP binding protein, Phospholipid, Regulation, Signal transduction",

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AU - Michailidis, Ioannis E.

AU - Zhang, Yun

AU - Yang, Jian

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N2 - Recent findings have revealed a pivotal role for phospholipids phosphatidylinositol -4,5-biphosphate (PIP2) and phosphatidylinositol -3,4,5-trisphosphate (PIP3) in the regulation of high voltage-activated (HVA) Ca2+ channels. PIP2 exerts two opposing actions on HVA Ca2+ channels: It stabilizes their activity but also produces a voltage-dependent inhibition that can be antagonized by protein kinase A (PKA) phosphorylation. PIP2 depletion and arachidonic acid together mediate the slow, voltage-independent inhibition of HVA Ca2+ channels by Gq/11 -coupled receptors in neurons. A sufficient level of plasma membrane PIP2 also appears to be necessary for Gβγ -mediated inhibition. On the other hand, increased production of PIP3 by PI-3 kinases promotes trafficking of HVA Ca2+ channels to the plasma membrane. This review discusses these findings and their implications.

AB - Recent findings have revealed a pivotal role for phospholipids phosphatidylinositol -4,5-biphosphate (PIP2) and phosphatidylinositol -3,4,5-trisphosphate (PIP3) in the regulation of high voltage-activated (HVA) Ca2+ channels. PIP2 exerts two opposing actions on HVA Ca2+ channels: It stabilizes their activity but also produces a voltage-dependent inhibition that can be antagonized by protein kinase A (PKA) phosphorylation. PIP2 depletion and arachidonic acid together mediate the slow, voltage-independent inhibition of HVA Ca2+ channels by Gq/11 -coupled receptors in neurons. A sufficient level of plasma membrane PIP2 also appears to be necessary for Gβγ -mediated inhibition. On the other hand, increased production of PIP3 by PI-3 kinases promotes trafficking of HVA Ca2+ channels to the plasma membrane. This review discusses these findings and their implications.

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KW - Regulation

KW - Signal transduction

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