Protein kinase A and the exchange protein directly activated by cAMP (Epac) modulate phenotype plasticity in human airway smooth muscle

Human Bronchial Smooth Muscle Cells Express Adenylyl Cyclase Isoforms 2, 4, and 6 in Distinct Membrane Microdomains

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Epac: Defining a New Mechanism for cAMP Action

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cAMP inhibits modulation of airway smooth muscle phenotype via the exchange protein activated by cAMP (Epac) and protein kinase A

(2010) Sara S Roscioni et al.   BRITISH JOURNAL OF PHARMACOLOGY

A2B receptors mediate the induction of early genes and inhibition of arterial smooth muscle cell proliferation via Epac

(2010) Peter Mayer et al.   CARDIOVASCULAR RESEARCH

Anti-mitogenic effects of β-agonists and PGE2 on airway smooth muscle are PKA dependent

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PKA and Epac synergistically inhibit smooth muscle cell proliferation

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Specificity and spatial dynamics of protein kinase A signaling organized by A-kinase-anchoring proteins

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Insulin-Induced Laminin Expression Promotes a Hypercontractile Airway Smooth Muscle Phenotype

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The role of Epac proteins, novel cAMP mediators, in the regulation of immune, lung and neuronal function

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S-phase kinase-associated protein-2 (Skp2) promotes vascular smooth muscle cell proliferation and neointima formation in vivo

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Underpinning compartmentalised cAMP signalling through targeted cAMP breakdown

(2009) Miles D. Houslay   TRENDS IN BIOCHEMICAL SCIENCES

GSK-3/β-catenin signaling axis in airway smooth muscle: role in mitogenic signaling

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Myosin, Transgelin, and Myosin Light Chain Kinase

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Glucocorticoid- and Protein Kinase A–Dependent Transcriptome Regulation in Airway Smooth Muscle

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Pharmacology of airway smooth muscle proliferation

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The effect of asthma therapeutics on signalling and transcriptional regulation of airway smooth muscle function

(2008) Alaina J. Ammit et al.   PULMONARY PHARMACOLOGY & THERAPEUTICS

Airway smooth muscle in asthma: Phenotype plasticity and function

(2008) Jeremy A. Hirota et al.   PULMONARY PHARMACOLOGY & THERAPEUTICS

Inhibition of human airway smooth muscle cell proliferation by β2-adrenergic receptors and cAMP is PKA independent: evidence for EPAC involvement

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