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Open AccessJournal ArticleDOI

Organization and Ca2+ Regulation of Adenylyl Cyclases in cAMP Microdomains

Debbie Willoughby, +1 more
- 01 Jul 2007 - 
- Vol. 87, Iss: 3, pp 965-1010
TLDR
The regulation of many of the ACs by the ubiquitous second messenger Ca(2+) provides an overarching mechanism for integrating the activities of these two major signaling systems, and cAMP will exhibit distinct kinetics in discrete cellular domains.
Abstract
The adenylyl cyclases are variously regulated by G protein subunits, a number of serine/threonine and tyrosine protein kinases, and Ca2+. In some physiological situations, this regulation can be re...

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Citations
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Principles of c-di-GMP signalling in bacteria.

TL;DR: This Review focuses on emerging principles of c-di-GMP signalling using selected systems in different bacteria as examples.
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A Coupled SYSTEM of Intracellular Ca2+ Clocks and Surface Membrane Voltage Clocks Controls the Timekeeping Mechanism of the Heart’s Pacemaker

TL;DR: Evidence is examined that forms the basis of this coupled-clock system concept in cardiac SANCs, where G protein-coupled receptors signaling creates pacemaker flexibility, ie, effects changes in the rhythmic action potential firing rate, by impacting on these very same factors that regulate robust basal coupled- clock system function.
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Caveolae as Organizers of Pharmacologically Relevant Signal Transduction Molecules

TL;DR: The role of Caveolae/caveolin in cardiac and pulmonary pathophysiology, pharmacologic implications of caveolar localization of signaling molecules, and the possibility that caveolae might serve as a therapeutic target are reviewed.
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Underpinning compartmentalised cAMP signalling through targeted cAMP breakdown

TL;DR: Genes for these important regulatory enzymes are linked to schizophrenia, stroke and asthma, thus indicating the therapeutic potential that selective inhibitors could have as anti-inflammatory, anti-depressant and cognitive enhancer agents.
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Physiological roles for G protein-regulated adenylyl cyclase isoforms: insights from knockout and overexpression studies.

TL;DR: The latest on AC knockout and overexpression studies are explored to better understand the roles of G protein regulation of ACs in the brain, olfactory bulb, and heart.
References
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Journal ArticleDOI

Altered Stress-Induced Anxiety in Adenylyl Cyclase Type VIII-Deficient Mice

TL;DR: A novel role for AC8 in the modulation of anxiety is demonstrated as a compromise in calcium-stimulated AC activity in the hippocampus, hypothalamus, thalamus, and brainstem and the behavioral consequences of AC8 deficiency are evaluated.
Journal ArticleDOI

Biochemical studies of stimulus convergence during classical conditioning in Aplysia: dual regulation of adenylate cyclase by Ca2+/calmodulin and transmitter

TL;DR: The dependence of cyclase activation on the temporal pattern of Ca2+ and transmitter addition is explored and it is suggested that the dually regulated adenylate cyclase might underlie the temporal requirements for effective classical conditioning in this system.
Journal ArticleDOI

Regulation of adenylyl cyclase from Paramecium by an intrinsic potassium conductance

TL;DR: A hyperpolarization-activated K+ efflux appears to directly regulate adenylyl cyclase activity in vivo, and is associated with secondary function as carrier of the K+ resting conductance.
Journal ArticleDOI

Capacitative Ca2+ entry exclusively inhibits cAMP synthesis in C6-2B glioma cells. Evidence that physiologically evoked Ca2+ entry regulates Ca(2+)-inhibitable adenylyl cyclase in non-excitable cells.

TL;DR: It is demonstrated not only that Ca2+ entry mediates the inhibitory effects of Ca2+, but also that diffuse elevations in [Ca2+]i are ineffective in modulating cAMP synthesis, which suggests that, as with certain Ca(2+)-sensitive ion channels, Ca(1-)-sensitive adenylyl cyclases may be functionally colocalized with Ca2- entry channels.
Journal ArticleDOI

Molecular cloning and characterization of the type VII isoform of mammalian adenylyl cyclase expressed widely in mouse tissues and in S49 mouse lymphoma cells.

TL;DR: The ability of phorbol ester to increase basal and isoproterenol-stimulated type VII activity appears to be a direct effect on this adenylyl cyclase isoform and not the result of modification of the inhibitory G protein, Gi.
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