scholarly journals Protein kinase A modulation of CaV1.4 calcium channels

2016 ◽  
Vol 7 (1) ◽  
Author(s):  
Lingjie Sang ◽  
Ivy E. Dick ◽  
David T. Yue
Keyword(s):  
Protein Kinase ◽  
Calcium Channels ◽  
Protein Kinase A ◽  
Kinase A

scholarly journals Functional Regulation of L-type Calcium Channels via Protein Kinase A-mediated Phosphorylation of the β2Subunit

1999 ◽  
Vol 274 (48) ◽  
pp. 33851-33854 ◽  
Author(s):  
Moritz Bünemann ◽  
Brian L. Gerhardstein ◽  
Tianyan Gao ◽  
M. Marlene Hosey
Keyword(s):  
Protein Kinase ◽  
Calcium Channels ◽  
Protein Kinase A ◽  
Functional Regulation ◽  
Kinase A

scholarly journals Antiapolipoprotein A-1 IgG Chronotropic Effects Require Nongenomic Action of Aldosterone on L-Type Calcium Channels

Endocrinology ◽  
2012 ◽  
Vol 153 (3) ◽  
pp. 1269-1278 ◽  
Author(s):  
Michel F. Rossier ◽  
Sabrina Pagano ◽  
Magaly Python ◽  
Andres D. Maturana ◽  
Richard W. James ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Calcium Channels ◽  
Protein Kinase A ◽  
Neonatal Rat ◽  
Chronotropic Effect ◽  
Chronotropic Response ◽  
Nongenomic Action ◽  
Chronotropic Effects ◽  
Spontaneous Contractions ◽  
Kinase A

Autoantibodies to apolipoprotein A-1 (antiapoA-1 IgG) have been shown to be associated with higher resting heart rate and morbidity in myocardial infarction patients and to behave as a chronotropic agent in the presence of aldosterone on isolated neonatal rat ventricular cardiomyocytes (NRVC). We aimed at identifying the pathways accounting for this aldosterone-dependent antiapoA-1 IgG-positive chronotropic effect on NRVC. The rate of regular spontaneous contractions was determined on NRVC in the presence of different steroid hormones and antagonists. AntiapoA-1 IgG chronotropic response was maximal within 20 min and observed only in aldosterone-pretreated cells but not in those exposed to other steroids. The positive antiapoA-1 IgG chronotropic effect was already significant after 5 min aldosterone preincubation, was dependent on 3-kinase and protein kinase A activities, was not inhibited by actinomycin D, and was fully abrogated by eplerenone (but not by spironolactone), demonstrating the dependence on a nongenomic action of aldosterone elicited through the mineralocorticoid receptor (MR). Under oxidative conditions (but not under normal redox state), corticosterone mimicked the permissive action of aldosterone on the antiapoA-1 IgG chronotropic response. Pharmacological and patch-clamp studies identified L-type calcium channels as crucial effectors of antiapoA-1 IgG chronotropic action, involving two converging pathways that increase the channel activity. The first one involves the rapid, nongenomic activation of the phosphatidylinositol 3-kinase enzyme by MR, and the second one requires a constitutive basal protein kinase A activity. In conclusion, our results indicate that, on NRVC, the aldosterone-dependent chronotropic effects of antiapoA-1 IgG involve the nongenomic activation of L-type calcium channels.

Guidance of CNS growth cones by substratum grooves and ridges: effects of inhibitors of the cytoskeleton, calcium channels and signal transduction pathways

1997 ◽  
Vol 110 (23) ◽  
pp. 2915-2924 ◽  
Author(s):  
A. Rajnicek ◽  
C. McCaig
Keyword(s):  
Signal Transduction ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Calcium Channels ◽  
Protein Kinase A ◽  
Growth Cone ◽  
Contact Guidance ◽  
Perpendicular Orientation ◽  
Kinase C ◽  
Kinase A

We exploited our observation that embryonic Xenopus spinal neurites align parallel to grooves in a quartz surface and that embryonic rat hippocampal neurites align perpendicular to shallow, narrow grooves (see companion paper: A. M. Rajnicek, S. Britland and C. D. McCaig, 1997) (J. Cell Sci. 110, 2905–2913) to investigate the mechanism of growth cone contact guidance. Substratum topography affected the pattern of growth cone filopodia and microtubules but parallel orientation of Xenopus neurites and perpendicular orientation of hippocampal neurites were unperturbed by cytochalasin B, which virtually eliminated filopodia. Hippocampal growth cone orientation and turning in response to grooves was unaffected by disruption of microtubules using taxol or nocodazole. Gross cytoskeletal reorganization on grooved substrata was therefore not required for growth cone steering. Inhibitors were used to identify the signal transduction pathway for perpendicular alignment of hippocampal neurites. Alignment persisted in the presence of gadolinium chloride, a blocker of stretch-activated calcium channels, the G protein inhibitor pertussis toxin, the protein tyrosine kinase inhibitor genistein, the protein kinase A and G inhibitor HA1004, the protein kinase A inhibitor KT5720and the protein kinase G inhibitor KT5823. Low concentrations of the protein kinase C inhibitors stauro-sporine, bisindolylmaleimide or H-7 did not affect perpendicular orientation but higher concentrations inhibited it. The calcium channel blockers flunarizine, nifedipine and diltiazem also inhibited perpendicular orientation. Influx of calcium and protein kinase C activity therefore appear to be involved in perpendicular contact guidance.

scholarly journals Integrin Receptor Activation Triggers Converging Regulation of Cav1.2 Calcium Channels by c-Src and Protein Kinase A Pathways

2006 ◽  
Vol 281 (20) ◽  
pp. 14015-14025 ◽  
Author(s):  
Peichun Gui ◽  
Xin Wu ◽  
Shizhang Ling ◽  
Stephanie C. Stotz ◽  
Robert J. Winkfein ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Calcium Channels ◽  
Protein Kinase A ◽  
Receptor Activation ◽  
Integrin Receptor ◽  
Kinase A

scholarly journals Ryanodine receptors, voltage-gated calcium channels and their relationship with protein kinase A in the myocardium

2008 ◽  
pp. 141-149
Author(s):  
MM Petrovic ◽  
K Vales ◽  
B Putnikovic ◽  
V Djulejic ◽  
DM Mitrovic
Keyword(s):  
Protein Kinase ◽  
Calcium Channels ◽  
Cardiac Muscle ◽  
Protein Kinase A ◽  
Ryanodine Receptor ◽  
Ryanodine Receptors ◽  
Physiological Role ◽  
Voltage Gated ◽  
Voltage Gated Calcium Channels ◽  
Kinase A

We present a review about the relationship between ryanodine receptors and voltage-gated calcium channels in myocardium, and also how both of them are related to protein kinase A. Ryanodine receptors, which have three subtypes (RyR1-3), are located on the membrane of sarcoplasmic reticulum. Different subtypes of voltage-gated calcium channels interact with ryanodine receptors in skeletal and cardiac muscle tissue. The mechanism of excitation-contraction coupling is therefore different in the skeletal and cardiac muscle. However, in both tissues ryanodine receptors and voltage-gated calcium channels seem to be physically connected. FK-506 binding proteins (FKBPs) are bound to ryanodine receptors, thus allowing their concerted activity, called coupled gating. The activity of both ryanodine receptors and voltage-gated calcium channels is positively regulated by protein kinase A. These effects are, therefore, components of the mechanism of sympathetic stimulation of myocytes. The specificity of this enzyme’s targeting is achieved by using different A kinase adapting proteins. Different diseases are related to inborn or acquired changes in ryanodine receptor activity in cardiac myocytes. Mutations in the cardiac ryanodine receptor gene can cause catecholamineprovoked ventricular tachycardia. Changes in phosphorylation state of ryanodine receptors can provide a credible explanation for the development of heart failure. The restoration of their normal level of phosphorylation could explain the positive effect of beta-blockers in the treatment of this disease. In conclusion, molecular interactions of ryanodine receptors and voltage-gated calcium channels with PKA have a significant physiological role. However, their defects and alterations can result in serious disturbances.

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