ライフサイエンスコーパス: MLC

1 MLC phosphatase (MLCP) activity, once decreased by agoni

2 MLC phosphatase is a trimeric complex of a 20-kDa subuni

3 MLC phosphorylation and barrier integrity were determine

4 MLC phosphorylation in MKs is regulated by Rho-associate

5 MLC phosphorylation was assessed by urea-glycerol gel el

6 MLC-4, a nonmuscle myosin regulatory light chain, locali

7 MLC-B localizes to the same extreme apical pole in the c

8 Three hundred thirty patients (SILC = 165, MLC = 165) were evaluated.

9 Since myosin light chain 20 (MLC(20)) phosphorylation appears to underlie the tonic c

10 yn lymphatic vessels, myosin light chain 20, MLC(20) phosphorylation was increased in these vessels.

11 expression is decreased, and MLCK activity, MLC phosphorylation, and cell contraction are increased.

12 eta)-dependent downregulation of actomyosin (MLC-2) contractility.

13 C than after HALC (2.7 vs 3.3 days) or after MLC/HALC (3.4 vs 4.6/4.9 days).

14 arison of the rate of H(2) activation via an MLC pathway between 1 and two widely used ruthenium cata

15 tic study of the 1,2-addition of H(2) via an MLC pathway to the widely used iron catalyst [((iPr)PNP)

16 additives to promote H(2) activation via an MLC pathway.

17 s, in parallel with decreases in Ca(2+) and MLC phosphorylation, followed by a reduction of contract

18 r hypothesis, the contractile activities and MLC(20) phosphorylation of thoracic duct and cervical ly

19 ressions did not alter BSM contractility and MLC(20) phosphorylation in strips isolated from JNK2 kno

20 wound closure by a pathway requiring ERK and MLC kinase.

21 ndependently induced actin stress fibers and MLC phosphorylation in TM cells, and decreased AH outflo

22 ges and decreases in actin stress fibers and MLC phosphorylation.

23 , Rho guanosine triphosphatase (GTPase), and MLC phosphatase was monitored in HTM cells using ELISA,

24 Myosin IIA and MLC phosphorylation are important in platelet responses

25 ulated by the balance between MLC kinase and MLC phosphatase (MLCP) activities.

26 the androgen-dependent cell lines (LNCaP and MLC-SV40) and tumors.

27 (MLC) phosphorylation; both barrier loss and MLC phosphorylation were reversed by MLC kinase (MLCK) i

28 that integrin-induced activation of MAPK and MLC and subsequent clot retraction is Rac1-dependent.

29 7(-/-) ESCs had higher expression of MHC and MLC and enhanced formation of contractile cardiomyocytes

30 cant decreases in phosphorylation of MLC and MLC phosphatase targeting subunit (MYPT1) and a signific

31 Inhibition of Syk, Ca(2+) mobilization, and MLC kinase (MLCK) only partially inhibited MLC phosphory

32 ted from each layer for analyses of MyHC and MLC isoforms.

33 activity toward in vivo substrates, p21 and MLC.

34 Myosin light chain (MLC) phosphorylation and MLC kinase (MLCK) activity-major determinants of vascula

35 to the rapid time course of Ca(2+) rise and MLC phosphorylation.

36 in CD200(tg), with corresponding attenuated MLC responses.

37 Our findings implicate a RAR-beta/MLC-2 pathway in peritumoural stromal remodelling and me

38 is in turn regulated by the balance between MLC kinase and MLC phosphatase (MLCP) activities.

39 ice has the following characteristics: 3 bit MLC, electroforming-free, self-rectifying, much higher c

40 Blocking MLC or ERK phosphorylation inhibited the motogenic effec

41 ; 30 minutes) caused phosphorylation of both MLC and CPI-17.

42 e heterolytic N-H and H-H bond activation by MLC is shown, in which hemilability of the phosphorus li

43 of 5azaD/TSA-expanded cells as determined by MLC were both significantly lower than control.

44 on of myosin regulatory light chain (MLC) by MLC kinase (MLCK) regulates tight junction function.

45 osphorylation of myosin light chain (MLC) by MLC kinase (MLCK) through integrin beta1 is required for

46 oss and MLC phosphorylation were reversed by MLC kinase (MLCK) inhibition.

47 inhibition were fully prevented/reverted by MLC kinase (MLCK) inhibition.

48 Loss of MLC1 function causes MLC.

49 rkedly decreased vascular smooth muscle cell MLC phosphorylation, suggesting that IKK2 is an MLCK in

50 asible candidate to succeed multilevel-cell (MLC) NAND flash memory.

51 In metastatic cells, MLC is organized perpendicularly to the direction of mov

52 Overexpression of IKK2 increased cellular MLC phosphorylation level, and pharmacological inhibitio

53 activation of ROCK regulates myosin L chain (MLC) phosphorylation, stress fiber formation and permeab

54 sphorylation and reduced myosin light chain (MLC(20) ) phosphorylation.

55 lation of the regulatory myosin light chain (MLC(20)) as a biomarker of in vivo cellular contractilit

56 20-kilodalton regulatory myosin light chain (MLC(20)) is critical to the cytoplasmic functions of the

57 quirement for regulatory myosin light chain (MLC(20)) phosphorylation for maximum actin-activated MgA

58 ted Ca(2+) mobilization, myosin light chain (MLC) 2 phosphorylation, and contraction of VSMC upon alp

59 e activity of regulatory myosin light chain (MLC) and cofilin by altering their phosphorylation.

60 essed phosphorylation of myosin light chain (MLC) and CPI-17, but not myosin targeting subunit of myo

61 Myosin light chain (MLC) and extracellular signal-regulated kinase (ERK) wer

62 duced phosphorylation of myosin light chain (MLC) and focal adhesion kinase (FAK), supporting a role

63 intracellular epithelial myosin light chain (MLC) and screened using Caco-2 monolayers in vitro.

64 horylation of myosin regulatory light chain (MLC) by MLC kinase (MLCK) regulates tight junction funct

65 that phosphorylation of myosin light chain (MLC) by MLC kinase (MLCK) through integrin beta1 is requ

66 Phosphorylation of myosin light chain (MLC) is essential for the contractility of the actin cyt

67 horylation of myosin regulatory light chain (MLC) is impaired in GEF-H1-depleted cells.

68 Two myosin light chain (MLC) kinase (MLCK) proteins, smooth muscle (encoded by m

69 the non-muscle ~214-kDa myosin light chain (MLC) kinase (nmMLCK) modulates the interaction between c

70 sed invasion and altered myosin light chain (MLC) organization.

71 ndependent activation of myosin light chain (MLC) phosphatase by protein kinase G Ialpha (PKGIalpha).

72 ndent changes in Ca(2+), myosin light chain (MLC) phosphorylation and contraction to changes in phosp

73 Myosin light chain (MLC) phosphorylation and MLC kinase (MLCK) activity-majo

74 Platelet myosin light chain (MLC) phosphorylation and transcript levels of its gene M

75 Time- and dose-dependent myosin light chain (MLC) phosphorylation in response to S1P and total expres

76 cle stress and decreased myosin light chain (MLC) phosphorylation in vivo, providing an ideal model f

77 on cAMP and cGMP levels, myosin light chain (MLC) phosphorylation, actin filament organization and ac

78 ion, actin cytoskeleton, myosin light chain (MLC) phosphorylation, and extracellular matrix (ECM) pro

79 nt as well as downstream myosin light chain (MLC) phosphorylation, barrier loss, and diarrhea in vitr

80 rrier function, MAPk and myosin light chain (MLC) phosphorylation, tight junction (TJ) protein expres

81 ellular calcium flux and myosin light chain (MLC) phosphorylation, which are prerequisites for contra

82 egulated by the state of myosin light chain (MLC) phosphorylation, which is in turn regulated by the

83 OCK inhibition increased myosin light chain (MLC) phosphorylation, which is known to trigger actomyos

84 mediated by stimulating myosin light chain (MLC) phosphorylation.

85 anied with a decrease in myosin light chain (MLC) phosphorylation.

86 thelia via myosin II regulatory light chain (MLC) phosphorylation; both barrier loss and MLC phosphor

87 A myosin light chain (MLC) tagged with photoactivatable green fluorescent prot

88 lation of the myosin regulatory light chain (MLC), a key regulatory component of cortical contraction

89 lation of its regulatory myosin light chain (MLC), significantly attenuates PPF.

90 horylation of the 20 kDa myosin light chain (MLC), which activates crossbridge cycling and the polyme

91 und ROCK1 phosphorylates myosin light chain (MLC), which is required for actin-myosin contractility.

92 d for phosphorylation of myosin light chain (MLC), which regulates myosin II-mediated cell contractil

93 orylation of endothelial myosin light chain (MLC).

94 e phosphorylation of the myosin light chain (MLC).

95 n the phosphorylation of myosin light chain (MLC).

96 ished phosphorylation of myosin light chain (MLC).

97 A unique MyoB light chain (MLC-B) was identified that contains a calmodulin-like do

98 , and phosphorylation of myosin light chain (MLC-p), a downstream target of RhoA, was assessed by Wes

99 ility by phosphorylating myosin light chain (MLC-P).

100 y, which in turn affects myosin light-chain (MLC) phosphorylation.

101 and phosphorylation of myosin light chains (MLC).

102 M-LC) and by micellar liquid chromatography (MLC) employing sodium dodecyl sulfate (SDS) as surfactan

103 model (VIM), a machine learning classifier (MLC) developed previously.

104 ams are members of the Mobile Lab Coalition (MLC), a nonprofit organization of mobile and other labor

105 entional (multiport) laparoscopic colectomy (MLC) (overall conversion rate, 6.9%).

106 (SILC) to multiport laparoscopic colectomy (MLC) when performed by experienced laparoscopic surgeons

107 ively, and the minimum lethal concentration (MLC) was 1.6 muM and 20 muM, respectively.

108 AK induces acute ATP release and concomitant MLC dephosphorylation in bovine corneal epithelial cells

109 Metal-ligand cooperation (MLC) by dearomatization/aromatization provides a unique

110 The use of metal-ligand cooperation (MLC) by transition metal bifunctional catalysts has emer

111 pathway involving metal-ligand cooperation (MLC) is proposed to be important in many transition meta

112 on/dearomatization metal-ligand cooperation (MLC) were prepared and characterized.

113 that can undergo metal-ligand cooperativity (MLC) at the catalyst.

114 phorylated and non-phosphorylated cortactin, MLC, Src, and p47(phox) to caveolin-enriched microdomain

115 alencephalic leukoencephalopathy with cysts (MLC) is a genetic disease characterized by infantile ons

116 ion of CD8+ FOXP3+ Ts cells in primary 7-day MLC.

117 of DPP1(-/-) CTL generated in early (5-day) MLC in vitro and in peritoneal exudate cells 5 days afte

118 with decreased RhoA activation and decreased MLC-p.

119 d MYPT1 phosphorylation in CCS but decreased MLC and MYPT1 phosphorylation in hISMCs subjected to ECS

120 at 60 days, with antigen-specific decreased MLC responses to BALB/c.

121 A signaling in Pak2-depleted cells decreases MLC phosphorylation and restores cell invasion.

122 n addition to the classic Ca(2)(+)-dependent MLC kinase (MLCK), another unidentified kinase(s) also c

123 in-dependent MAPK activation, MAPK-dependent MLC phosphorylation, and clot retraction are inhibited b

124 sels only at the higher pressures tested did MLC(20) di-phosphorylation decrease.

125 In thoracic duct MLC(20) di-phosphorylation, but not mono-phosphorylation

126 PAK1 enhanced MLC phosphorylation via phosphorylating MYPT1 on Thr-696

127 ulated cells, the depletion of Pak2 enhances MLC phosphorylation.

128 arrier dysfunction nor intestinal epithelial MLC phosphorylation occurred in LT beta R knockout mice.

129 ountering the ramp-like structures exhibited MLC accumulation near head-tail junctions contacting the

130 nism for decreased platelet MYL9 expression, MLC phosphorylation, thrombocytopenia, and platelet dysf

131 ost fibers express conventional slow or fast MLC isoforms, in accordance with the type (slow or fast)

132 Few comparative studies for MLC and SILC have been reported.

133 oxia-inducible factor --> RhoA --> ROCK1 --> MLC --> FAK signaling in breast cancer cells.

134 ular functional defects, described for human MLC, were confirmed.

135 of the regulatory light chain of myosin II (MLC(20)) at the activation sites promotes both the motor

136 hains of the contractile protein myosin IIa (MLC).

137 muscle, exercise capacity was not altered in MLC-Cre:GRK2(fl/fl) mice compared with wild-type control

138 atory cytokines IFN-gamma and IL-17A both in MLC and in culture with autologous DC pulsed with CMV pr

139 uo and Cdc42 expression result in changes in MLC and/or cofilin phosphorylation, which might alter ac

140 ined phase of contraction with a decrease in MLC and MYPT1 phosphorylation in the aorta.

141 f contraction with a significant decrease in MLC but not CPI-17 or MYPT1 phosphorylation.

142 This results in the decrease in MLC phosphorylation and smooth muscle relaxation.

143 lung myofibroblasts demonstrate decreases in MLC(20) phosphorylation and reduced contractility in res

144 a2AR) agonist, was significantly enhanced in MLC-Cre:GRK2(fl/fl) mice; mechanistically, this seems to

145 ion, suggesting that IKK2 may be involved in MLC phosphorylation.

146 f MYPT1 at Thr853, leading to a reduction in MLC phosphorylation and actomyosin contraction.

147 ressor cells and impairs T cell responses in MLC.

148 nd 2 was significantly lower in SILS than in MLC and HALC.

149 astrocytic swelling, substantiating that in MLC the primary defect is in volume regulation by astroc

150 Adoptive transfer of tolerance in MLC to BL/6 grafts was most evident when both skin and s

151 proteins that changed after CP/CPB included: MLC-2a, ATP-synthase delta chain and Enoyl-CoenzymeA hyd

152 PAK activation increased MLC and MYPT1 phosphorylation in CCS but decreased MLC a

153 decreased PAK1 phosphorylation and increased MLC phosphorylation (pMLC), whereas in DLPFC pMLC remain

154 actin stress fiber formation, and increased MLC phosphorylation, fibronectin, and laminin levels, an

155 H pylori increased MLC phosphorylation in epithelial monolayers; this was s

156 S1P increased MLC phosphorylation with a similar time- and dose-depend

157 H pylori increases MLC phosphorylation, occludin internalization and barrie

158 This increases MLC phosphatase activity and induces MLC20 dephosphoryla

159 osphatase coincident with the Ca(2+)-induced MLC kinase activation to synergistically initiate a rapi

160 naling pathways leading to TNF-alpha-induced MLC phosphorylation and permeability increases.

161 TNF-alpha-induced MLC phosphorylation required ROCK activation.

162 ROCK1 was dispensable for TNF-alpha-induced MLC phosphorylation, ROCK1 was required for TNF-alpha-in

163 not sufficient to prevent TNF-alpha-induced MLC phosphorylation, whereas inhibition of ROCK2 prevent

164 AMP in BCECs prevented the histamine-induced MLC phosphorylation and the disruption of the actin cyto

165 The histamine-induced MLC phosphorylation was reduced by pre-exposure to eithe

166 Histamine induces MLC phosphorylation by activating MLCK and partly inhibi

167 rosine kinase-dependent pathway that induces MLC phosphorylation through the dual activation of MLCK

168 ing MYPT1 on Thr-696, whereas PAK1 inhibited MLC phosphorylation via decreasing MYPT1 on both Thr-696

169 d MLC kinase (MLCK) only partially inhibited MLC phosphorylation, suggesting the presence of a second

170 ion by activating MLCK and partly inhibiting MLC phosphatase.

171 bunit of MLC phosphatase, thereby inhibiting MLC phosphatase activity and increasing contraction and

172 ltaneous expression of a dominant inhibitory MLC form.

173 t phosphorylates MLC20 directly and inhibits MLC phosphatase by phosphorylating CPI-17.

174 Exogenous relaxin inhibits MLC(20) phosphorylation and bleomycin-induced lung fibro

175 Activation of RhoA, which inhibits MLC phosphatase through Rho kinase, was examined by immu

176 protein phosphatase (CPI-17), which inhibits MLC phosphatase, was studied using Western blot analysis

177 on of ROCK2 prevented TNF-alpha-induced late MLC phosphorylation at 24 h.

178 echanisms involving not only kinase-mediated MLC phosphorylation but also Src activation.

179 lpha2C-adrenoceptors and Rho-kinase-mediated MLC phosphorylation, downstream of TRPA1 activation.

180 MLCK-mediated MLC phosphorylation is required for microvesicle release

181 xposure to either ML-7 (50 microM), an MLCK (MLC kinase) inhibitor, or chelerythrine (10 microM), an

182 l muscle-specific GRK2 knock-out (KO) mouse (MLC-Cre:GRK2(fl/fl)) to gain a better understanding of t

183 physically and functionally replaced native MLC on the myosin lever arm in a permeabilized skeletal

184 phosphorylation/dephosphorylation of nuclear MLC(20) results in the sliding of myosin and actin molec

185 creases the unphosphorylated form of nuclear MLC(20), resulting in enhanced transcription of ICAM-1.

186 portant for PKGIalpha-mediated activation of MLC phosphatase activity, and changes in LZ+ MYPT1 isofo

187 play an important role in the activation of MLC phosphatase.

188 pients, although there was an attenuation of MLC responses after graft transfer alone.

189 The dephosphorylation of MLC(20) increases the transcription of ICAM-1, whereas i

190 tase is involved in the rapid development of MLC phosphorylation and contraction during Ca(2+) transi

191 Positive expression of MLC kinase (MLCK) was found at the mRNA and protein leve

192 n in response to S1P and total expression of MLC were determined.

193 of the mono- and di-phosphorylation forms of MLC(20) affects both tonic and phasic components of lymp

194 oth the mono- and di-phosphorylated forms of MLC(20).

195 egrity, not only by blocking inactivation of MLC phosphatase but also by inactivating MLCK.

196 rotein kinase (ROCK)-dependent inhibition of MLC phosphatase (MLCP), we examined the effects of cAMP

197 sensitization because complete inhibition of MLC phosphatase activity in the absence of Ca2+ induces

198 The pathways that lead to inhibition of MLC phosphatase by G(q/13)-coupled receptors are initiat

199 id Ca(2+) rise induces a rapid inhibition of MLC phosphatase coincident with the Ca(2+)-induced MLC k

200 tein activation, (b) regulated inhibition of MLC phosphatase, and (c) MLC20 phosphorylation via a Ca2

201 hosphorylation, and 2 modes of inhibition of MLC phosphatase, phosphorylation of CPI-17 Thr38 and MYP

202 inase, preventing Rho-mediated inhibition of MLC phosphatase, promoting vasorelaxation, although the

203 e Ca(2+) sensitization through inhibition of MLC phosphatase.

204 lation of CPI-17, an endogenous inhibitor of MLC phosphatase.

205 RNA interference of MLC-4, as well as of its upstream regulators, LET-502 (R

206 ed levels of active RhoA and lower levels of MLC-p than did NTM-5 cells.

207 would be more sensitive to the modulation of MLC(20) phosphorylation when compared to cervical lympha

208 Both the organization of MLC and force generation are dependent upon ROCK functio

209 e proteins is part of the pathomechanisms of MLC.

210 icroM; 10 minutes) led to phosphorylation of MLC (134% relative to untreated cells) and of CPI-17.

211 pe change, spreading, and phosphorylation of MLC (serine 19) through a pathway that was ablated under

212 ion, and motility through phosphorylation of MLC and FAK.

213 significant decreases in phosphorylation of MLC and MLC phosphatase targeting subunit (MYPT1) and a

214 urthermore, HO stimulated phosphorylation of MLC and recruitment of phosphorylated and non-phosphoryl

215 e that ROCK regulates the phosphorylation of MLC just behind the invading margin of the cell.

216 OCK) to induce inhibitory phosphorylation of MLC phosphatase (MLCP).

217 physiological function of phosphorylation of MLC(20) at the inhibitory sites is unknown.

218 The phosphorylation of MLC(20) at the Ser1 significantly increased during the P

219 d by the status of the di-phosphorylation of MLC(20) in the lymphatics.

220 +), contractile force and phosphorylation of MLC, CPI-17, MYPT1 Thr696 and Thr853 at 10 s after PE st

221 companied by PKC-mediated phosphorylation of MLC, which blocks microvesicle shedding.

222 Phosphorylation of MLC, which increases contractility of the actin cytoskel

223 Aiming at exploration of the possibility of MLC by PCP-type pincer complexes, we report herein the s

224 To test the hypothesis that regulation of MLC phosphatase is involved in the rapid development of

225 e that this occurs through the regulation of MLC phosphorylation.

226 These studies demonstrate the role of MLC activation and myosin isoforms in creating a cell re

227 ed by computation implicates the key role of MLC in facilitating effective catalysis.

228 lly recognizing the phosphorylation sites of MLC(20) at Ser1, and the platelet-derived growth factor

229 phosphorylation of the regulatory subunit of MLC phosphatase (MYPT1) and/or PKC-mediated phosphorylat

230 ich phosphorylates the regulatory subunit of MLC phosphatase, thereby inhibiting MLC phosphatase acti

231 acids inserted into loop 1, are dependent on MLC(20) phosphorylation for both actin-activated MgATPas

232 We show that Pak has no effect on MLC phosphorylation during the contraction of airway smo

233 Consistent with their opposite effects on MLC phosphorylation, Pak1 and Pak2 differentially modula

234 ative in topical ophthalmic formulations, on MLC phosphorylation in primary cultures of bovine cornea

235 both RVM and SSMoG significantly improved on MLC analysis of OCT, but not SAP, measurements alone.

236 ed either using IAM (r(2) (n - 1) = 0.78) or MLC (r(2) (n - 1) = 0.83) derived indexes along with in

237 Accordingly, inhibition of ROCK activity or MLC function promotes enrichment of DOCK5 in membrane pr

238 The inhibition of H-Ras or MLC in endothelial cells inhibited TEM of MDA-MB-231 cel

239 ration but did not abolish [Ca(2+)]i rise or MLC phosphorylation.

240 potential benefits associated with SILC over MLC/HALC but it is yet to be proven objectively.

241 t hearts showed increased phosphorylated (p)-MLC and p-FAK levels, which were mostly attributable to

242 measure the extent of myosin light chain (p-MLC) phosphorylation and ratio of filamentous to globula

243 loss of ROCK1 had no significant effect on p-MLC and p-FAK levels, mTOR signaling, or autophagy at ba

244 itor filamentous actin (F-actin) and phospho-MLC organization and the localization of beta-catenin, a

245 reas the depletion of Pak1 decreases phospho-MLC levels in heregulin-stimulated cells, the depletion

246 CP activity leading to a decrease in phospho-MLC.

247 t mice express higher lung levels of phospho-MLC(20) and develop more severe bleomycin-induced lung f

248 Since thrombin stimulates phospho-MLC through RhoA/Rho-associated, coiled-coil containing

249 K, based on increased nerve terminal phospho-MLC immunostaining, with 100 Hz but not with 10 Hz stimu

250 In response to 1 muM S1P treatment, phospho-MLC concentrated in the SC cell periphery, coincident wi

251 Expression of a phosphomimetic MLC-4 mutant mimicking a constitutively active state als

252 Furthermore, expression of phosphomimetic MLC largely prevented cytokinesis failure in the tested

253 Phosphorylated MLC in response to histamine or PMA was found in a punct

254 Although phosphorylated MLC was redistributed to the leading edge of migrating c

255 rylated MLC(20) form while di-phosphorylated MLC(20) was significantly decreased.

256 showed that recombinant IKK2-phosphorylated MLC and intact myosin in vitro, and the kinetic paramete

257 ochemistry was used to locate phosphorylated MLC in relation to tight junctions.

258 duced an increase in the mono-phosphorylated MLC(20) form while di-phosphorylated MLC(20) was signifi

259 Localization of phosphorylated MLC in proximity to ZO-1 suggests increased contractilit

260 I, phosphorylated-MYPT(1) and phosphorylated-MLC(20).

261 tivation to synergistically initiate a rapid MLC phosphorylation and contraction in arteries with abu

262 ell as MLCK inactivation, resulting in rapid MLC dephosphorylation and relaxation.

263 (2)beta(1) integrin and is mediated by H-Ras/MLC-induced tyrosine phosphorylation of VE-cad.

264 The recombinant MLC physically and functionally replaced native MLC on t

265 Reduced MLC phosphorylation was associated with high expression

266 tions of 0.0005%, 0.001%, and 0.003% reduced MLC phosphorylation by more than 30%.

267 PAK regulated MLC phosphorylation in an activity-dependent biphasic ma

268 ide a novel mechanism whereby IKK2 regulates MLC phosphorylation as an MLCK and, thus, vascular funct

269 onditions, whereas PAK1 negatively regulates MLC phosphorylation via inhibiting MYPT1 phosphorylation

270 We conclude that PAK1 positively regulates MLC phosphorylation in intestinal smooth muscle through

271 aling pathway reveals that relaxin regulates MLC(20) dephosphorylation and lung myofibroblast contrac

272 sed to examine their functions in regulating MLC phosphorylation and permeability increases induced b

273 hat PAK1 plays a critical role in regulating MLC phosphorylation in hISMCs.

274 both the C1 and C2 inserts, does not require MLC(20) phosphorylation for full activity similar to HMM

275 cells and suggest that targeting the ARF/Rho/MLC signaling axis might be a promising strategy to inhi

276 regulator YAP through inhibition of Rho-ROCK-MLC- and FAK-PI3K-dependent signaling pathways.

277 sruption is caused by the activation of ROCK/MLC signalling, persistent actin polymerization and the

278 SpA stimulated a RhoA/ROCK/MLC cascade, resulting in the contraction of the cytoske

279 eveal a critical role for a GEF-H1/RhoA/ROCK/MLC signaling pathway in mediating nocodazole-induced ce

280 cell proliferation in primary and secondary MLC inducing anergy in CD4+ Th cells and suppressing the

281 Ca(2+) transient, we compared Ca(2+) signal, MLC phosphorylation, and 2 modes of inhibition of MLC ph

282 sin light chain 2 (MLC2) by cardiac-specific MLC kinase (cMLCK), located at the neck region of myosin

283 ignificantly attenuates histamine-stimulated MLC-20 phosphorylation.

284 essed phosphorylation of the ROCK substrates MLC-2 and MYPT-1 in human cancer cells, but had no effec

285 We have found that MLC-dependent activation of myosin IIB in migrating cell

286 We propose that MLC-B is a MyoB-specific light chain, and for the short

287 Imaging of live tumors shows that MLC is organized in a similar ROCK-dependent fashion in

288 w alpha-myosin heavy chain MerCreMer and the MLC-2v promoters are active in cardiac progenitor cells.

289 effects on endogenous ROCK activity and the MLC/FAK/AKT/mTOR signaling pathway, which is involved in

290 the actin regulatory proteins and not on the MLC dephosphorylation.

291 compared with TM (EC(50) = 1.33 muM), though MLC expression was significantly greater in TM.

292 r unidentified kinase(s) also contributes to MLC phosphorylation in living cells.

293 uced by both antimycin-A and hypoxia) led to MLC dephosphorylation.

294 Outcomes were similar to MLC, except for a reduction in peak pain score on the fi

295 patients were matched with those undergoing MLC for gender, age, disease, surgery, BMI, and surgeon.

296 ed with the expression of unphosphorylatable MLC(20) at the Ser1/Ser2 phosphorylation sites.

297 ols, or nitriles to regain aromatization via MLC.

298 When MLC effector cells derived from a G14D-CCV-immunized fis

299 gnostic performance marginally compared with MLC analysis of data obtained using each technology alon

300 E augmented endothelial permeability without MLC-P via an actin-binding motif, DVRGLL.