RETRACTED: G protein-induced trafficking of voltage-dependent calcium channels (Retracted Article)

被引：40

作者：

Tombler, E ^{[1
]}

Cabanilla, NJ ^{[1
]}

Carman, P ^{[1
]}

Permaul, N ^{[1
]}

Hall, JJ ^{[1
]}

Richman, RW ^{[1
]}

Lee, J ^{[1
]}

Rodriguez, J ^{[1
]}

Felsenfeld, DP ^{[1
]}

Hennigan, RF ^{[1
]}

Diversé-Pierluissi, MA ^{[1
]}

机构：

[1] Mt Sinai Sch Med, Dept Pharmacol & Biol Chem, New York, NY 10029 USA

来源：

JOURNAL OF BIOLOGICAL CHEMISTRY | 2006年 / 281卷 / 03期

关键词：

D O I：

10.1074/jbc.M508829200

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Calcium channels are well known targets for inhibition by G protein-coupled receptors, and multiple forms of inhibition have been described. Here we report a novel mechanism for G protein-mediated modulation of neuronal voltage-dependent calcium channels that involves the destabilization and subsequent removal of calcium channels from the plasma membrane. Imaging experiments in living sensory neurons show that, within seconds of receptor activation, calcium channels are cleared from the membrane and sequestered in clathrin-coated vesicles. Disruption of the L1-CAM-ankyrin B complex with the calcium channel mimics transmitter-induced trafficking of the channels, reduces calcium influx, and decreases exocytosis. Our results suggest that G protein-induced removal of plasma membrane calcium channels is a consequence of disrupting channel-cytoskeleton interactions and might represent a novel mechanism of presynaptic inhibition.

引用

页码：1827 / 1839

页数：13

共 36 条

[1] NEUROTRANSMITTER INHIBITION OF NEURONAL CALCIUM CURRENTS BY CHANGES IN CHANNEL VOLTAGE DEPENDENCE [J].

BEAN, BP .

NATURE, 1989, 340 (6229) :153-156

[2] ALTERED PREVALENCE OF GATING MODES IN NEUROTRANSMITTER INHIBITION OF N-TYPE CALCIUM CHANNELS [J].

DELCOUR, AH ;

TSIEN, RW .

SCIENCE, 1993, 259 (5097) :980-984

[3] G protein-coupled receptor kinase mediates desensitization of norepinephrine-induced Ca2+ channel inhibition [J].

DiversePierluissi, M ;

Inglese, J ;

Stoffel, RH ;

Lefkowitz, RJ ;

Dunlap, K .

NEURON, 1996, 16 (03) :579-585

[4] Novel form of crosstalk between G protein and tyrosine kinase pathways [J].

DiversePierluissi, M ;

Remmers, AE ;

Neubig, RR ;

Dunlap, K .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1997, 94 (10) :5417-5421

[5] G protein modulation of voltage-gated calcium channels [J].

Dolphin, AC .

PHARMACOLOGICAL REVIEWS, 2003, 55 (04) :607-627

[6] NEUROTRANSMITTERS DECREASE THE CALCIUM CONDUCTANCE ACTIVATED BY DEPOLARIZATION OF EMBRYONIC CHICK SENSORY NEURONS [J].

DUNLAP, K ;

FISCHBACH, GD .

JOURNAL OF PHYSIOLOGY-LONDON, 1981, 317 (AUG) :519-535

[7] Tyrosine phosphorylation at a site highly conserved in the L1 family of cell adhesion molecules abolishes ankyrin binding and increases lateral mobility of neurofascin [J].

Garver, TD ;

Ren, Q ;

Tuvia, S ;

Bennett, V .

JOURNAL OF CELL BIOLOGY, 1997, 137 (03) :703-714

[8] Ankyrin binding mediates L1CAM interactions with static components of the cytoskeleton and inhibits retrograde movement of L1CAM on the cell surface [J].

Gil, OD ;

Sakurai, T ;

Bradley, AE ;

Fink, MY ;

Cassella, MR ;

Kuo, JA ;

Felsenfeld, DP .

JOURNAL OF CELL BIOLOGY, 2003, 162 (04) :719-730

[9]

GRUNER W, 1994, J NEUROSCI, V14, P2800

[10] Modulation of Ca2+ channels by G-protein beta gamma subunits [J].

Herlitze, S ;

Garcia, DE ;

Mackie, K ;

Hille, B ;

Scheuer, T ;

Catterall, WA .

NATURE, 1996, 380 (6571) :258-262

← 1 2 3 4 →