Rho-kinase as a drug target for the treatment of airway hyperrespon-siveness in asthma.
about
Motility, survival, and proliferation.Muscarinic receptor signaling in the pathophysiology of asthma and COPD.Arhgef1 is required by T cells for the development of airway hyperreactivity and inflammation.The whole-genome expression analysis of peripheral blood mononuclear cells from aspirin sensitive asthmatics versus aspirin tolerant patients and healthy donors after in vitro aspirin challenge.The proximal STAT6 and NF-kappaB sites are responsible for IL-13- and TNF-alpha-induced RhoA transcriptions in human bronchial smooth muscle cells.Emerging targets for novel therapy of asthma.alpha-CaMKII controls the growth of human osteosarcoma by regulating cell cycle progression.S100A8/A9: a mediator of severe asthma pathogenesis and morbidity?Inhalation of the Rho-kinase inhibitor Y-27632 reverses allergen-induced airway hyperresponsiveness after the early and late asthmatic reaction.Bronchoprotection and bronchorelaxation in asthma: New targets, and new ways to target the old ones.Interleukin-13 augments bronchial smooth muscle contractility with an up-regulation of RhoA protein.Epac as a novel effector of airway smooth muscle relaxation.Mechanisms underlying the pathogenesis of hyper-contractility of bronchial smooth muscle in allergic asthma.Insulin induces airway smooth muscle contractionBrain-derived neurotrophic factor in TNF-alpha modulation of Ca2+ in human airway smooth muscle.Inhibition of geranylgeranyltransferase inhibits bronchial smooth muscle hyperresponsiveness in mice.Insulin-induced laminin expression promotes a hypercontractile airway smooth muscle phenotype.Short-term roxithromycin treatment attenuates airway inflammation via MAPK/NF-κB activation in a mouse model of allergic asthma.The inhaled Rho kinase inhibitor Y-27632 protects against allergen-induced acute bronchoconstriction, airway hyperresponsiveness, and inflammation.Intranasal administration of recombinant progranulin inhibits bronchial smooth muscle hyperresponsiveness in mouse allergic asthma.Cooperative signaling by TGF-β1 and WNT-11 drives sm-α-actin expression in smooth muscle via Rho kinase-actin-MRTF-A signaling.Rho Kinase (ROCK) collaborates with Pak to Regulate Actin Polymerization and Contraction in Airway Smooth Muscle.
P2860
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P2860
Rho-kinase as a drug target for the treatment of airway hyperrespon-siveness in asthma.
description
2006 nî lūn-bûn
@nan
2006年の論文
@ja
2006年学术文章
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2006年学术文章
@zh-cn
2006年学术文章
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2006年学术文章
@zh-my
2006年学术文章
@zh-sg
2006年學術文章
@yue
2006年學術文章
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2006年學術文章
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name
Rho-kinase as a drug target for the treatment of airway hyperrespon-siveness in asthma.
@ast
Rho-kinase as a drug target for the treatment of airway hyperrespon-siveness in asthma.
@en
type
label
Rho-kinase as a drug target for the treatment of airway hyperrespon-siveness in asthma.
@ast
Rho-kinase as a drug target for the treatment of airway hyperrespon-siveness in asthma.
@en
prefLabel
Rho-kinase as a drug target for the treatment of airway hyperrespon-siveness in asthma.
@ast
Rho-kinase as a drug target for the treatment of airway hyperrespon-siveness in asthma.
@en
P2093
P1476
Rho-kinase as a drug target for the treatment of airway hyperrespon-siveness in asthma.
@en
P2093
Dedmer Schaafsma
Reinoud Gosens
S Adriaan Nelemans
P304
P356
10.2174/138955706776073402
P577
2006-03-01T00:00:00Z