Epac as a novel effector of airway smooth muscle relaxation.
about
The pharmacological rationale for combining muscarinic receptor antagonists and β-adrenoceptor agonists in the treatment of airway and bladder diseaseSignaling pathways that control rho kinase activity maintain the embryonic epicardial progenitor state.Investigational beta-2 adrenergic agonists for the treatment of chronic obstructive pulmonary disease.Crosstalk between beta-2-adrenoceptor and muscarinic acetylcholine receptors in the airwayβ-Agonist-mediated relaxation of airway smooth muscle is protein kinase A-dependent.Anti-inflammatory role of the cAMP effectors Epac and PKA: implications in chronic obstructive pulmonary diseaseThe expression and relaxant effect of bitter taste receptors in human bronchi.Actions of cAMP on calcium sensitization in human detrusor smooth muscle contraction.cAMP-mediated secretion of brain-derived neurotrophic factor in developing airway smooth muscle.Activation of G protein-coupled bile acid receptor, TGR5, induces smooth muscle relaxation via both Epac- and PKA-mediated inhibition of RhoA/Rho kinase pathwayThe dopamine D1 receptor is expressed and facilitates relaxation in airway smooth muscle.Novel cAMP signalling paradigms: therapeutic implications for airway diseasecAMP regulation of airway smooth muscle function.Multiple facets of cAMP signalling and physiological impact: cAMP compartmentalization in the lung.cAMP signalling in the vasculature: the role of Epac (exchange protein directly activated by cAMP).A-kinase anchoring proteins: cAMP compartmentalization in neurodegenerative and obstructive pulmonary diseases.Update on ultra-long-acting β agonists in chronic obstructive pulmonary disease.Protein kinase A and the exchange protein directly activated by cAMP (Epac) modulate phenotype plasticity in human airway smooth muscle.cAMP inhibits modulation of airway smooth muscle phenotype via the exchange protein activated by cAMP (Epac) and protein kinase AProstaglandin E2 Inhibits Histamine-Evoked Ca2+ Release in Human Aortic Smooth Muscle Cells through Hyperactive cAMP Signalling Junctions and Protein Kinase A.Inhibition of prostate smooth muscle contraction and prostate stromal cell growth by the inhibitors of Rac, NSC23766 and EHT1864.Calcium/calmodulin-dependent kinase 2 mediates Epac-induced spontaneous transient outward currents in rat vascular smooth muscle.Olfactory Receptors Modulate Physiological Processes in Human Airway Smooth Muscle Cells.Real time analysis of β(2)-adrenoceptor-mediated signaling kinetics in human primary airway smooth muscle cells reveals both ligand and dose dependent differences.Ca(2+) signals evoked by histamine H1 receptors are attenuated by activation of prostaglandin EP2 and EP4 receptors in human aortic smooth muscle cells.The cAMP effector EPAC activates Elk1 transcription factor in prostate smooth muscle, and is a minor regulator of α1-adrenergic contraction.Exchange protein activated by cAMP (Epac) induces vascular relaxation by activating Ca2+-sensitive K+ channels in rat mesenteric artery.Epac Function and cAMP Scaffolds in the Heart and Lung.Intracellular cAMP Sensor EPAC: Physiology, Pathophysiology, and Therapeutics Development.Selective inhibition of histamine-evoked Ca2+ signals by compartmentalized cAMP in human bronchial airway smooth muscle cells.
P2860
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P2860
Epac as a novel effector of airway smooth muscle relaxation.
description
2011 nî lūn-bûn
@nan
2011年の論文
@ja
2011年論文
@yue
2011年論文
@zh-hant
2011年論文
@zh-hk
2011年論文
@zh-mo
2011年論文
@zh-tw
2011年论文
@wuu
2011年论文
@zh
2011年论文
@zh-cn
name
Epac as a novel effector of airway smooth muscle relaxation.
@en
type
label
Epac as a novel effector of airway smooth muscle relaxation.
@en
prefLabel
Epac as a novel effector of airway smooth muscle relaxation.
@en
P2093
P2860
P1476
Epac as a novel effector of airway smooth muscle relaxation.
@en
P2093
Carolina R S Elzinga
Harm Maarsingh
Herman Meurs
Janke Schuur
Mark Menzen
Martina Schmidt
Sara S Roscioni
P2860
P304
P356
10.1111/J.1582-4934.2010.01150.X
P577
2011-07-01T00:00:00Z