AJP - Heart Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Heart Circ Physiol 280: H2038-H2045, 2001;
0363-6135/01 $5.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (26)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Potet, F.
Right arrow Articles by Baró, I.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Potet, F.
Right arrow Articles by Baró, I.
Vol. 280, Issue 5, H2038-H2045, May 2001

AKAP proteins anchor cAMP-dependent protein kinase to KvLQT1/IsK channel complex

Franck Potet1, John D. Scott2, Raha Mohammad-Panah1, Denis Escande1, and Isabelle Baró1

1 Laboratoire de Physiopathologie et de Pharmacologie Cellulaires et Moléculaires, Hôpital Hôtel-Dieu, Institut National de la Santé et de la Recherche Médicale, 44093 Nantes Cedex, France; and 2 Howard Hughes Medical Institute, Vollum Institute, Portland, Oregon 97201

In cardiac myocytes, the slow component of the delayed rectifier K+ current (IKs) is regulated by cAMP. Elevated cAMP increases IKs amplitude, slows its deactivation kinetics, and shifts its activation curve. At the molecular level, IKs channels are composed of KvLQT1/IsK complexes. In a variety of mammalian heterologous expression systems maintained at physiological temperature, we explored cAMP regulation of recombinant KvLQT1/IsK complexes. In these systems, KvLQT1/IsK complexes were totally insensitive to cAMP regulation. cAMP regulation was not restored by coexpression with the dominant negative isoform of KvLQT1 or with the cystic fibrosis transmembrane regulator. In contrast, coexpression of the neuronal A kinase anchoring protein (AKAP)79, a fragment of a cardiac AKAP (mAKAP), or cardiac AKAP15/18 restored cAMP regulation of KvLQT1/IsK complexes inasmuch as cAMP stimulation increased the IKs amplitude, increased its deactivation time constant, and negatively shifted its activation curve. However, in cells expressing an AKAP, the effects of cAMP stimulation on the IKs amplitude remained modest compared with those previously reported in cardiac myocytes. The effects of cAMP stimulation were fully prevented by including the Ht31 peptide (a global disruptor of protein kinase A anchoring) in the intracellular medium. We concluded that cAMP regulation of IKs requires protein kinase A anchoring by AKAPs, which therefore participate with the channel protein complex underlying IKs.

A kinase anchoring protein; KCNQ1; KCNE1; slow delayed rectifier potassium current


This article has been cited by other articles:


Home page
Biophys. JHome page
H. S. Jensen, M. Grunnet, and S.-P. Olesen
Inactivation as a New Regulatory Mechanism for Neuronal Kv7 Channels
Biophys. J., April 15, 2007; 92(8): 2747 - 2756.
[Abstract] [Full Text] [PDF]


Home page
NeuroscientistHome page
Y. Li, S. Y. Um, and T. V. Mcdonald
Voltage-Gated Potassium Channels: Regulation by Accessory Subunits
Neuroscientist, June 1, 2006; 12(3): 199 - 210.
[Abstract] [PDF]


Home page
Circ. Res.Home page
K. L. Dodge-Kafka, L. Langeberg, and J. D. Scott
Compartmentation of Cyclic Nucleotide Signaling in the Heart: The Role of A-Kinase Anchoring Proteins
Circ. Res., April 28, 2006; 98(8): 993 - 1001.
[Abstract] [Full Text] [PDF]


Home page
PhysiologyHome page
T. Jespersen, M. Grunnet, and S.-P. Olesen
The KCNQ1 Potassium Channel: From Gene to Physiological Function
Physiology, December 1, 2005; 20(6): 408 - 416.
[Abstract] [Full Text] [PDF]


Home page
J. Neurophysiol.Home page
C. Distler, P. K. Rathee, K. S. Lips, O. Obreja, W. Neuhuber, and M. Kress
Fast Ca2+-Induced Potentiation of Heat-Activated Ionic Currents Requires cAMP/PKA Signaling and Functional AKAP Anchoring
J Neurophysiol, May 1, 2003; 89(5): 2499 - 2505.
[Abstract] [Full Text] [PDF]


Home page
DiabetesHome page
P. E. MacDonald, W. El-kholy, M. J. Riedel, A. M. F. Salapatek, P. E. Light, and M. B. Wheeler
The Multiple Actions of GLP-1 on the Process of Glucose-Stimulated Insulin Secretion
Diabetes, December 1, 2002; 51(90003): S434 - 442.
[Abstract] [Full Text] [PDF]


Home page
DiabetesHome page
P. E. MacDonald, A. M. F. Salapatek, and M. B. Wheeler
Glucagon-Like Peptide-1 Receptor Activation Antagonizes Voltage-Dependent Repolarizing K+ Currents in {beta}-Cells: A Possible Glucose-Dependent Insulinotropic Mechanism
Diabetes, December 1, 2002; 51(90003): S443 - 447.
[Abstract] [Full Text] [PDF]


Home page
Cardiovasc ResHome page
S. Kupershmidt, I. C.-H. Yang, M. Sutherland, K.S. Wells, T. Yang, P. Yang, J. R. Balser, and D. M. Roden
Cardiac-enriched LIM domain protein fhl2 is required to generate IKs in a heterologous system
Cardiovasc Res, October 1, 2002; 56(1): 93 - 103.
[Abstract] [Full Text] [PDF]


Home page
Mol. Pharmacol.Home page
M. S. Kapiloff
Contributions of Protein Kinase A Anchoring Proteins to Compartmentation of cAMP Signaling in the Heart
Mol. Pharmacol., August 1, 2002; 62(2): 193 - 199.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online