TRPC3, an underestimated, universal pacemaker channel?

Cell Calcium ◽  
2021 ◽  
pp. 102484
Author(s):  
Oleksandra Tiapko ◽  
Klaus Groschner
Keyword(s):  
Pacemaker Channel

Familial Sinus Bradycardia Associated with a Mutation in the Cardiac Pacemaker Channel

2006 ◽  
Vol 354 (2) ◽  
pp. 151-157 ◽  
Author(s):  
Raffaella Milanesi ◽  
Mirko Baruscotti ◽  
Tomaso Gnecchi-Ruscone ◽  
Dario DiFrancesco
Keyword(s):  
Sinus Bradycardia ◽  
Cardiac Pacemaker ◽  
Pacemaker Channel

scholarly journals Functional stabilization of weakened thalamic pacemaker channel regulation in rat absence epilepsy

2006 ◽  
Vol 575 (1) ◽  
pp. 83-100 ◽  
Author(s):  
Mira Kuisle ◽  
Nicolas Wanaverbecq ◽  
Amy L. Brewster ◽  
Samuel G. A. Frère ◽  
Didier Pinault ◽  
...  
Keyword(s):  
Absence Epilepsy ◽  
Channel Regulation ◽  
Pacemaker Channel

Selective Pharmacological Inhibition of the Pacemaker Channel Isoforms (HCN1-4) as New Possible Therapeutical Targets

2011 ◽  
Vol 18 (24) ◽  
pp. 3662-3674 ◽  
Author(s):  
I. Koncz ◽  
T. Szel ◽  
K. Jaeger ◽  
I. Baczko ◽  
E. Cerbai ◽  
...  
Keyword(s):  
Pharmacological Inhibition ◽  
Pacemaker Channel

scholarly journals Reversal of HCN Channel Voltage Dependence via Bridging of the S4–S5 Linker and Post-S6

2006 ◽  
Vol 128 (3) ◽  
pp. 273-282 ◽  
Author(s):  
David L. Prole ◽  
Gary Yellen
Keyword(s):  
Voltage Dependence ◽  
Disulfide Bridges ◽  
Hcn Channel ◽  
Channel Activation ◽  
Transmembrane Voltage ◽  
Pacemaker Channel ◽  
Positive Voltage ◽  
Close Proximity ◽  
Inactivation Process ◽  
Voltage Gated Ion Channels

Voltage-gated ion channels possess charged domains that move in response to changes in transmembrane voltage. How this movement is transduced into gating of the channel pore is largely unknown. Here we show directly that two functionally important regions of the spHCN1 pacemaker channel, the S4–S5 linker and the C-linker, come into close proximity during gating. Cross-linking these regions with high-affinity metal bridges or disulfide bridges dramatically alters channel gating in the absence of cAMP; after modification the polarity of voltage dependence is reversed. Instead of being closed at positive voltage and activating with hyperpolarization, modified channels are closed at negative voltage and activate with depolarization. Mechanistically, this reversal of voltage dependence occurs as a result of selectively eliminating channel deactivation, while retaining an existing inactivation process. Bridging also alters channel activation by cAMP, showing that interaction of these two regions can also affect the efficacy of physiological ligands.

Role of caveolar lipid rafts in pacemaker channel kinetics

Heart Rhythm ◽  
2005 ◽  
Vol 2 (5) ◽  
pp. S34-S35
Author(s):  
Bin Ye ◽  
Nianqing Shi ◽  
Jason Foell ◽  
Ravi C. Balijepalli ◽  
Timothy J. Kamp ◽  
...  
Keyword(s):  
Lipid Rafts ◽  
Channel Kinetics ◽  
Pacemaker Channel

scholarly journals Down-regulation ofmiR-1/miR-133contributes to re-expression of pacemaker channel genesHCN2andHCN4in hypertrophic heart.

2011 ◽  
Vol 286 (32) ◽  
pp. 28656.2-28656 ◽  
Author(s):  
Xiaobin Luo ◽  
Huixian Lin ◽  
Zhengwei Pan ◽  
Jiening Xiao ◽  
Yong Zhang ◽  
...  
Keyword(s):  
Down Regulation ◽  
Pacemaker Channel
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