scholarly journals Cdk5/p35 Regulates Neurotransmitter Release through Phosphorylation and Downregulation of P/Q-Type Voltage-Dependent Calcium Channel Activity

2002 ◽  
Vol 22 (7) ◽  
pp. 2590-2597 ◽  
Author(s):  
Kazuhito Tomizawa ◽  
Jun Ohta ◽  
Masayuki Matsushita ◽  
Akiyoshi Moriwaki ◽  
Sheng-Tian Li ◽  
...  
Keyword(s):  
Calcium Channel ◽  
Neurotransmitter Release ◽  
Channel Activity ◽  
Voltage Dependent Calcium Channel ◽  
Voltage Dependent

Synexin: Molecular Mechanism of Calcium-Dependent Membrane Fusion and Voltage-Dependent Calcium-Channel Activity.

1991 ◽  
Vol 635 (1 Calcium Entry) ◽  
pp. 328-351 ◽  
Author(s):  
HARVEY B. POLLARD ◽  
EDUARDO ROJAS ◽  
RICHARD W. PASTOR ◽  
EDUARDO M. ROJAS ◽  
H. ROBERT GUY ◽  
...  
Keyword(s):  
Calcium Channel ◽  
Membrane Fusion ◽  
Molecular Mechanism ◽  
Channel Activity ◽  
Calcium Dependent ◽  
Voltage Dependent Calcium Channel ◽  
Voltage Dependent

Scanning Mutagenesis Reveals a Role for Serine 189 of the Heterotrimeric G-Protein Beta 1 Subunit in the Inhibition of N-Type Calcium Channels

2006 ◽  
Vol 96 (1) ◽  
pp. 465-470 ◽  
Author(s):  
H. William Tedford ◽  
Alexandra E. Kisilevsky ◽  
Jean B. Peloquin ◽  
Gerald W. Zamponi
Keyword(s):  
Calcium Channel ◽  
G Protein ◽  
Neurotransmitter Release ◽  
Direct Contact ◽  
Channel Activity ◽  
Heterotrimeric G Protein ◽  
Channel Modulation ◽  
Opioid Drugs ◽  
Voltage Dependent ◽  
Dependent Inhibition

Direct interactions between the presynaptic N-type calcium channel and the β subunit of the heterotrimeric G-protein complex cause voltage-dependent inhibition of N-type channel activity, crucially influencing neurotransmitter release and contributing to analgesia caused by opioid drugs. Previous work using chimeras of the G-protein β subtypes Gβ1 and Gβ5 identified two 20–amino acid stretches of structurally contiguous residues on the Gβ1 subunit as critical for inhibition of the N-type channel. To identify key modulation determinants within these two structural regions, we performed scanning mutagenesis in which individual residues of the Gβ1 subunit were replaced by corresponding Gβ5 residues. Our results show that Gβ1 residue Ser189 is critical for N-type calcium channel modulation, whereas none of the other Gβ1 mutations caused statistically significant effects on the ability of Gβ1 to inhibit N-type channels. Structural modeling shows residue 189 is surface exposed, consistent with the idea that it may form a direct contact with the N-type calcium channel α1 subunit during binding interactions.

Distribution of neurons expressing α1G subunit mRNA of T-type voltage-dependent calcium channel in adult rat central nervous system

1999 ◽  
Vol 268 (2) ◽  
pp. 77-80 ◽  
Author(s):  
Masahiko Kase ◽  
Shingo Kakimoto ◽  
Satoru Sakuma ◽  
Takeshi Houtani ◽  
Hitoshi Ohishi ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Calcium Channel ◽  
Adult Rat ◽  
Subunit Mrna ◽  
Voltage Dependent Calcium Channel ◽  
Voltage Dependent
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