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1 re preceded by long-duration waves of airway smooth muscle contraction.
2 implicated in Rho-mediated cell adhesion and smooth muscle contraction.
3 a crucial and selective role in ETA-mediated smooth muscle contraction.
4 and play an important role in regulating the smooth muscle contraction.
5 tase activity in the absence of Ca2+ induces smooth muscle contraction.
6 kinase (MLCK) is essential for initiation of smooth muscle contraction.
7 of myosin (MLC20) phosphorylation and airway smooth muscle contraction.
8 aggregation, lipolysis, glycogenolysis, and smooth muscle contraction.
9 PT1.PP1C.P-CPI-17, leading to an increase in smooth muscle contraction.
10 take part in the thin filament regulation of smooth muscle contraction.
11 depletion of paxillin by antisense inhibits smooth muscle contraction.
12 in filament dynamics and organization during smooth muscle contraction.
13 thought to be involved in the regulation of smooth muscle contraction.
14 +) sensitivity of myosin phosphorylation and smooth muscle contraction.
15 ing pathways, important regulators of airway smooth muscle contraction.
16 in filament dynamics and organization during smooth muscle contraction.
17 that paxillin may be involved in regulating smooth muscle contraction.
18 oconstriction of human airway by stimulating smooth muscle contraction.
19 heads plays a key role in the regulation of smooth muscle contraction.
20 of CPI-17 to produce Ca(2+) sensitization of smooth muscle contraction.
21 on and subsequent inhibition (relaxation) of smooth muscle contraction.
22 which might play a role in the regulation of smooth muscle contraction.
23 re involved in blood pressure regulation and smooth muscle contraction.
24 hectomy, parasympathetic stimulation elicits smooth muscle contraction.
25 proliferation and airway as well as vascular smooth muscle contraction.
26 oteins known to regulate aortic and tracheal smooth muscle contraction.
27 gests that NO may be closely associated with smooth muscle contraction.
28 ability persisted beyond the duration of the smooth muscle contraction.
29 of myosin light chain, which induces airway smooth muscle contraction.
30 the involvement of ZIPK in the regulation of smooth muscle contraction.
31 enin by lentivirus-mediated shRNA attenuated smooth muscle contraction.
32 oA, inactivating RhoA and suppressing airway smooth muscle contraction.
33 latory protein that has a role in modulating smooth muscle contraction.
34 ructural alterations of epithelial cells and smooth muscle contraction.
35 n plays a critical role in the regulation of smooth muscle contraction.
36 ssed ovalbumin-mediated guinea pig bronchial smooth muscle contraction.
37 regulation of thick filament length, such as smooth muscle contraction.
38 dying mechanical stress-mediated decrease in smooth muscle contraction.
39 ural remodelling of the artery, or increased smooth muscle contraction.
40 substrate (CAS) have been shown to regulate smooth muscle contraction.
41 s interaction inhibited IP3-dependent airway smooth muscle contraction.
42 intracellular Ca(++) (via IP(3) release) and smooth muscle contraction.
43 tion process in response to agonist -induced smooth muscle contraction.
44 ch have been implicated commonly in vascular smooth muscle contraction.
45 ing that RGS5 negatively regulates bronchial smooth muscle contraction.
46 tion, cardiac and neuronal excitability, and smooth muscle contraction.
47 ts in the fetal period, requires coordinated smooth muscle contraction.
48 ine release from nerve terminals, and airway smooth muscle contraction.
49 e for lysophosphatidic acid-induced vascular smooth muscle contraction.
50 n to both motion and force generation during smooth muscle contraction.
51 protein caldesmon (CaD) reversibly inhibits smooth muscle contraction.
52 ajal (ICC), the pacemaker cells that control smooth muscle contraction.
53 secretion, sensory signal transduction, and smooth muscle contraction.
54 sory transduction, epithelial secretion, and smooth muscle contraction.
55 negatively modulate force development during smooth muscle contraction.
56 directly inhibited various tonic and phasic smooth muscle contractions.
57 s system, including cardiac, arteriolar, and smooth muscle contractions.
58 requency of spontaneous colonic longitudinal smooth muscle contractions.
59 oded by TMEM16A control neuronal signalling, smooth muscle contraction, airway and exocrine gland sec
61 elieved to be important in the regulation of smooth muscle contraction, although the precise mechanis
62 inflammatory mechanisms that lead to airway smooth muscle contraction and airway hyperresponsiveness
64 There is emerging evidence indicating that smooth muscle contraction and Ca2+ influx through voltag
65 oth muscle cells (VSMCs) which could enhance smooth muscle contraction and cell growth activated by c
66 kinase that is involved in the regulation of smooth muscle contraction and cytoskeletal reorganizatio
67 al lipopolysaccharide (LPS, 20 mg/kg, IP) on smooth muscle contraction and endothelial relaxation in
68 ing genes with potential regulatory roles in smooth muscle contraction and extracellular matrix-recep
69 ion of Vh peptide also inhibited ACh-induced smooth muscle contraction and inhibited ACh-induced acti
70 , red wine, and green tea inhibited arterial smooth muscle contraction and intestinal Cl(-) secretion
72 ential for many biological processes such as smooth muscle contraction and neurotransmitter release.
73 The major mechanism of Ca2+ sensitization of smooth muscle contraction and non-muscle cell motility i
74 ain kinase is important in the initiation of smooth muscle contraction and other contractile processe
75 ial permeability; it also triggers bronchial smooth muscle contraction and participates in autoregula
77 ys an important role in cardiac development, smooth muscle contraction and psychiatric disorders.
78 y myosin light chain kinase (MLCK) initiates smooth muscle contraction and regulates actomyosin-based
79 noid signaling impedes coordinated oviductal smooth muscle contraction and relaxation crucial to norm
82 lays a significant role in the regulation of smooth muscle contraction and suggest that CaMKII activa
83 ermine how Tyr(1065) phosphorylation affects smooth muscle contraction and the conformation and cellu
84 a vital mechanism for the control of airway smooth muscle contraction and thus are a critical factor
85 a vital mechanism for the control of airway smooth muscle contraction and thus are a critical factor
86 ce receptors and cause leukocyte activation, smooth muscle contraction and vascular permeability.
87 uences endothelin (ET) ETA receptor-mediated smooth muscle contraction and, if so, to define the unde
88 ) participates in the regulation of vascular smooth muscle contraction and, if so, to investigate the
89 vestigation may identify agents that inhibit smooth muscle contraction and/or restrain or reverse obs
90 sure decreases the interval between systemic smooth muscle contractions and increases the rate of mor
91 egulation of breathing, gas exchange, airway smooth-muscle contraction and relaxation, blood flow thr
93 a pivotal role in regulating actin dynamics, smooth muscle contraction, and airway hyperresponsivenes
95 ) participates in the regulation of vascular smooth muscle contraction, and if so, to investigate the
98 e pharmacomechanical coupling that activates smooth muscle contraction, and possibly regulation of di
102 n, transforming growth factor-beta, vascular smooth muscle contraction, and the hedgehog and Wnt sign
103 ching morphogenesis, the frequency of airway smooth muscle contraction, and the rate of developmental
104 le cells may be dynamically regulated during smooth muscle contraction, and this dynamic regulation m
105 ing pathways, induce inhibition of the ileal smooth muscle contractions, and affect distinct physiolo
106 affect Ca2+-sensitive pathways implicated in smooth muscle contraction, as tested with alpha-toxin pe
107 ha1 adrenergic receptors not only stimulates smooth muscle contraction but also modifies gene express
108 ator release, and allergen-induced bronchial smooth muscle contraction by CRACM-channel blockers supp
109 m by which RhoA regulates actin dynamics and smooth muscle contraction by expressing the dominant neg
110 , these findings suggest that Plk1 regulates smooth muscle contraction by modulating vimentin phospho
111 9beta1 appears to serve as a brake on airway smooth muscle contraction by recruiting SSAT, which faci
112 n phosphatase (MLCP) plays a pivotal role in smooth muscle contraction by regulating Ca(2+) sensitivi
115 in network have been implicated in mediating smooth muscle contraction, cell migration, and mitosis.
116 n which the magnitude of an agonist-mediated smooth muscle contraction depends on a rapid but limited
117 ht chain phosphorylation (RLC) necessary for smooth muscle contraction depends on the respective acti
123 d in alpha(1)-adrenoceptor-mediated vascular smooth muscle contraction in distinctive time-dependent
125 le for M3-mAChR phosphorylation in bronchial smooth muscle contraction in health and in a disease sta
127 creased in vitro airway narrowing and airway smooth muscle contraction in murine and human airways.
128 sphatase plays a critical role in modulating smooth muscle contraction in response to a variety of ph
129 y is now well recognized to mediate vascular smooth muscle contraction in response to vasoconstrictor
130 The inhibition of myosin phosphatase evokes smooth muscle contraction in the absence of Ca(2+), yet
131 is a multifunctional hormone that regulates smooth muscle contraction in the airways, acid secretion
132 congenital disorder characterized by loss of smooth muscle contraction in the bladder and intestine.
133 ther homologues in inducing well-coordinated smooth muscle contractions in an in vitro rabbit duodena
134 2+) channel expression may suppress circular smooth muscle contractions in the inflamed colon and con
135 its, inhibited adenylyl cyclase, and induced smooth muscle contraction, in similar fashion to the sel
136 hree well-studied pharmacological functions, smooth muscle contraction, increased vascular permeabili
137 , and identified distinct pathways linked to smooth muscle contraction, inflammatory cytokines, immun
140 itiation of force generation during vascular smooth muscle contraction involves a rise in intracellul
142 ption, protein transport, protein synthesis, smooth muscle contraction, ion transport, chemotaxis, an
150 t are unresponsive to capsaicin, bradykinin, smooth muscle contraction, longitudinal or transverse st
151 II) from mast cell renin elicited bronchial smooth muscle contraction mediated by ANG II type 1 rece
152 , many features of bronchial asthma, such as smooth muscle contraction, mucus secretion and recruitme
153 ion transport, olfaction, phototransduction, smooth muscle contraction, nociception, cell proliferati
156 ding mucus secretion, neuronal excitability, smooth muscle contraction, olfactory signal transduction
157 ry effects on inflammation, anaphylaxis, and smooth muscle contraction, PDE-IV inhibitors also produc
158 or a variety of functions including vascular smooth muscle contraction, platelet aggregation, and the
159 ysiological processes as diverse as vascular smooth muscle contraction, platelet aggregation, percept
162 nderstanding of the regulation of myometrial smooth muscle contraction-relaxation is incomplete.
164 l responsiveness was not associated with the smooth muscle contraction since leukotriene C4, histamin
165 ck of PAR-2-mediated platelet aggregation or smooth muscle contraction suggested it might not share t
166 se (approximately total tissue content), and smooth muscle contraction that was rapid in onset and sh
167 cemakers set the origin and frequency of the smooth muscle contractions that propel wastes from the k
169 e ZIPK is involved in regulation of vascular smooth muscle contraction through direct phosphorylation
170 tial cells of Cajal (ICC) control intestinal smooth muscle contraction to regulate gut motility.
171 Excitatory agonists can induce significant smooth muscle contraction under constant free Ca(2+) thr
173 stimulate secretion, cell proliferation, and smooth muscle contraction via a family of G protein-coup
175 sent study, the role of alpha-actinin during smooth muscle contraction was evaluated in tracheal smoo
177 to myosin by caldesmon in the regulation of smooth muscle contraction, we investigated the effects o
178 functions as a second messenger in tracheal smooth muscle contraction, we used the criteria set out
179 ting Ins(1,4,5)P3-dependent Ca2+ release and smooth muscle contraction, whereas the alpha subunits in
180 tly reduced by functionally antagonizing the smooth muscle contraction with isoproterenol, or by bloc
181 latory light chain (RLC) phosphorylation for smooth muscle contraction with subsequent dephosphorylat
182 peptide) attenuated actin polymerization and smooth muscle contraction without affecting myosin light
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