Go but not Gi2 or Gi3 is required for muscarinic regulation of heart rate and heart rate variability in mice
- 30 March 2007
- journal article
- Published by Elsevier in Biochemical and Biophysical Research Communications
- Vol. 357 (1) , 139-143
- https://doi.org/10.1016/j.bbrc.2007.03.130
Abstract
No abstract availableKeywords
This publication has 14 references indexed in Scilit:
- G Protein-Activated Inwardly Rectifying Potassium Channels as Potential Therapeutic TargetsCurrent Pharmaceutical Design, 2006
- Endogenous RGS Proteins and Gα Subtypes Differentially Control Muscarinic and Adenosine-Mediated Chronotropic EffectsCirculation Research, 2006
- Mammalian G Proteins and Their Cell Type Specific FunctionsPhysiological Reviews, 2005
- Multiple neurological abnormalities in mice deficient in the G protein G oProceedings of the National Academy of Sciences, 1998
- Targeted inactivation of αi2or αi3disrupts activation of the cardiac muscarinic K+channel, IK+Ach, in intact cellsProceedings of the National Academy of Sciences, 1997
- Gα o is necessary for muscarinic regulation of Ca 2+ channels in mouse heartProceedings of the National Academy of Sciences, 1997
- Production of homozygous mutant ES cells with a single targeting construct.Molecular and Cellular Biology, 1992
- Heart Rate Regulation by G Proteins Acting on the Cardiac Pacemaker ChannelScience, 1990
- Decreased heart rate variability and its association with increased mortality after acute myocardial infarctionThe American Journal of Cardiology, 1987
- Power Spectrum Analysis of Heart Rate Fluctuation: A Quantitative Probe of Beat-to-Beat Cardiovascular ControlScience, 1981