Channel Activation and Mechanotransduction

2014 ◽  
pp. 433-442
Author(s):  
Henry Donahue ◽  
Randall Duncan ◽  
Damian Genetos
Keyword(s):  
Channel Activation

Inositol lipids and TRPC channel activation

2007 ◽  
Vol 74 ◽  
pp. 37-45 ◽  
Author(s):  
James W. Putney
Keyword(s):  
Plasma Membrane ◽  
Phospholipase C ◽  
Transient Receptor Potential ◽  
Calcium Signalling ◽  
Receptor Potential ◽  
Breakdown Product ◽  
Channel Activation ◽  
Inositol Lipids ◽  
Transient Receptor ◽  
Secondary Mechanism

The original hypothesis put forth by Bob Michell in his seminal 1975 review held that inositol lipid breakdown was involved in the activation of plasma membrane calcium channels or ‘gates’. Subsequently, it was demonstrated that while the interposition of inositol lipid breakdown upstream of calcium signalling was correct, it was predominantly the release of Ca2+ that was activated, through the formation of Ins(1,4,5)P3. Ca2+ entry across the plasma membrane involved a secondary mechanism signalled in an unknown manner by depletion of intracellular Ca2+ stores. In recent years, however, additional non-store-operated mechanisms for Ca2+ entry have emerged. In many instances, these pathways involve homologues of the Drosophila trp (transient receptor potential) gene. In mammalian systems there are seven members of the TRP superfamily, designated TRPC1–TRPC7, which appear to be reasonably close structural and functional homologues of Drosophila TRP. Although these channels can sometimes function as store-operated channels, in the majority of instances they function as channels more directly linked to phospholipase C activity. Three members of this family, TRPC3, 6 and 7, are activated by the phosphoinositide breakdown product, diacylglycerol. Two others, TRPC4 and 5, are also activated as a consequence of phospholipase C activity, although the precise substrate or product molecules involved are still unclear. Thus the TRPCs represent a family of ion channels that are directly activated by inositol lipid breakdown, confirming Bob Michell's original prediction 30 years ago.

Enhanced PIP3 signaling in POMC neurons causes diet-sensitive obesity as the consequence of neuronal silencing via KATP channel activation

2006 ◽  
Vol 1 (S 1) ◽  
Author(s):  
L Plum ◽  
X Ma ◽  
B Hampel ◽  
H Münzberg ◽  
M Shanabrough ◽  
...  
Keyword(s):  
Katp Channel ◽  
Channel Activation

The influence of TRPM8 ion channel activation on immune response at different temperature conditions

2012 ◽  
Vol 37 (8) ◽  
pp. 648-653 ◽  
Author(s):  
Tamara V. Kozyreva ◽  
Galina M. Khramova ◽  
Ludmila S. Eliseeva
Keyword(s):  
Immune Response ◽  
Ion Channel ◽  
Channel Activation ◽  
Temperature Conditions

Opioid receptor activation is involved in neuroprotection induced by TRPV1 channel activation against excitotoxicity in the rat retina

2017 ◽  
Vol 812 ◽  
pp. 57-63 ◽  
Author(s):  
Kenji Sakamoto ◽  
Taiyo Kuroki ◽  
Tomonori Sagawa ◽  
Hiroko Ito ◽  
Asami Mori ◽  
...  
Keyword(s):  
Opioid Receptor ◽  
Receptor Activation ◽  
Trpv1 Channel ◽  
Channel Activation ◽  
Rat Retina
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