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 Activated MLC causes an increase in dendritic spine and synapse fo

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

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

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

17 caused increases in both MLCK expression and MLC phosphorylation, suggesting that MLCK is a TNF-alpha

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

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

20 ve Rho activity, stress fiber formation, and MLC phosphorylation.

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

22 Myosin IIA and MLC phosphorylation are important in platelet responses

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

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

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

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

27 7(-/-) ESCs had higher expression of MHC and MLC and enhanced formation of contractile cardiomyocytes

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

29 ts of KENESKA and other peptides on MLCK and MLC activation and on failures in both wild-type and NCA

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

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

32 activity toward in vivo substrates, p21 and MLC.

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

34 barrier function via MLCK up-regulation and MLC phosphorylation.

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

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

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

45 function and that these are both reversed by MLC kinase (MLCK) inhibition.

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

47 Loss of MLC1 function causes MLC.

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

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

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

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

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

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

54 20-kilodalton regulatory myosin light chain (MLC(20)) is critical to the cytoplasmic functions of the

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

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

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

58 rotein-tagged myosin regulatory light chain (MLC) and correlative biochemical analyses, we investigat

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

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

61 olving MLCK and probably myosin light chain (MLC) and myosin II.

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

63 ulated kinase (ERK2) and myosin light chain (MLC) but not cytoplasmic phospholipase A2 upon thrombin-

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 ing that is regulated by myosin light chain (MLC) kinase (MLCK) and rho kinase (ROCK).

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

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

71 ith calmodulin activates myosin light chain (MLC) kinase to initiate a rapid MLC phosphorylation and

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

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

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

75 increases myosin II regulatory light chain (MLC) phosphorylation and decreases barrier function and

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

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

78 ed increases in cortical myosin light chain (MLC) phosphorylation in concert with cortically distribu

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

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

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

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

83 show that ROCK activity, myosin light chain (MLC) phosphorylation, MLC ATPase activity, and an intact

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

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

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

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

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

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

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

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

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

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

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

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

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

97 orylation of endothelial myosin light chain (MLC).

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

99 horylating myosin II regulatory light chain (MLC).

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

101 ished phosphorylation of myosin light chain (MLC).

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

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

104 Changes in myosin light-chain (MLC) phosphorylation were evaluated by Western blot anal

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

106 and phosphorylation of myosin light chains (MLC).

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

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

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

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

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

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

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

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

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

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

117 actin cytoskeletal organization and decrease MLC phosphorylation in PTM and PCB cells, all of which a

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 Both lovastatin and compactin decreased MLC phosphorylation in PTM and PCB cells.

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

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

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

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

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

126 cell alloresponses in MHC class II-disparate MLC and GVHD.

127 leen cells (SpC) in a MHC class II-disparate MLC.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

150 ressor cells and impairs T cell responses in MLC.

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

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

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

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

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

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

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

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

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

160 H pylori increases MLC phosphorylation, occludin internalization and barrie

161 This increases MLC phosphatase activity and induces MLC20 dephosphoryla

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

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

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

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

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

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

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

169 Histamine induces MLC phosphorylation by activating MLCK and partly inhibi

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

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

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

173 ion by activating MLCK and partly inhibiting MLC phosphatase.

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

175 ltaneous expression of a dominant inhibitory MLC form.

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

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

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

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

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

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

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

183 MLCK-mediated MLC phosphorylation is required for microvesicle release

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

212 e proteins is part of the pathomechanisms of MLC.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

260 y, myosin light chain (MLC) phosphorylation, MLC ATPase activity, and an intact actin cytoskeleton, b

261 induced GEnC hyperpermeability by preventing MLC diphosphorylation, and cytoskeletal remodeling.

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

263 light chain (MLC) kinase to initiate a rapid MLC phosphorylation and contraction.

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

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

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

267 Reduced MLC phosphorylation was associated with high expression

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

269 d tumor necrosis factor (TNF)-alpha regulate MLC phosphorylation and disrupt epithelial barrier funct

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

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

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

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

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

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

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

277 on leading to actin cytoskeletal remodeling, MLC diphosphorylation, and enhanced paracellular gap for

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

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

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

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

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

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

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

285 ignificantly attenuates histamine-stimulated MLC-20 phosphorylation.

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

287 st, adhesion to HepII alone does not sustain MLC phosphorylation.

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

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

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

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

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

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

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

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

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

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

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

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

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