ライフサイエンスコーパス: MLCK

1 MLCK activation alters size selectivity to enhance parac

2 MLCK activation at 10 Hz also resulted in more vesicles

3 MLCK activation partially declined at 3 s of stimulation

4 MLCK activity influences cell polarity by increasing myo

5 MLCK inhibition also delayed barrier function recovery.

6 MLCK inhibition increased barrier function and stabilize

7 MLCK inhibition slowed and then stopped contraction but

8 MLCK is known to regulate vesicle trafficking and synapt

9 MLCK-mediated MLC phosphorylation is required for microv

10 ion with intraluminally administered ML-7 (a MLCK inhibitor) or Y27632 (a Rho-associated kinase inhib

11 y PKC (protein kinase C) activation, or by a MLCK agonist peptide, reduces the amount of dye lost eve

12 as a key regulator of cardiac contraction, a MLCK that is preferentially expressed in cardiac muscle

13 Expression of Rho(v14) and activated MLCK (ctMLCK) synergistically increase ectopic crossover

14 ne induces MLC phosphorylation by activating MLCK and partly inhibiting MLC phosphatase.

15 (Tg) mice that express constitutively active MLCK (CA-MLCK) specifically within intestinal epithelia.

16 sgenic mice expressing constitutively active MLCK.

17 eby IKK2 regulates MLC phosphorylation as an MLCK and, thus, vascular function and blood pressure.

18 g the physiological importance of IKK2 as an MLCK.

19 g the physiological importance of IKK2 as an MLCK.

20 Therefore, we tested whether IKK2 is an MLCK in living cells and the role of IKK2 in mediating v

21 phosphorylation, suggesting that IKK2 is an MLCK in living cells.

22 pre-exposure to either ML-7 (50 microM), an MLCK (MLC kinase) inhibitor, or chelerythrine (10 microM

23 force and phosphorylation of RLC, CPI-17 and MLCK.

24 hasic, but had little effect on [Ca(2+)] and MLCK activation.

25 Nuclear factor-B and MLCK signalling appear to be important downstream mediat

26 PAH, HIF-1alpha expression is decreased, and MLCK activity, MLC phosphorylation, and cell contraction

27 [Ca2+]i transient is rapidly dissipated and MLCK inactivated, whereas MLC20 and muscle contraction a

28 )] (fura-2 ratio or fluo-4 fluorescence) and MLCK activity both increased rapidly to an initial peak

29 cells mediated by lamellipodia formation and MLCK activity may be important for T cells to access inf

30 The dependence of force on [Ca2+]i and MLCK activation decreased with time suggesting increased

31 Src kinase and MLCK inhibitors blocked this synergistic effect of ethan

32 ng calcium, oxidative stress, Src kinase and MLCK.

33 revented the activation of MLCK promoter and MLCK mRNA transcription.

34 blebs with actin just before retraction, and MLCK inhibition led to persistent blebbing and attenuate

35 es, consistent with the concept that Src and MLCK form a swelling-induced protein complex that regula

36 nd rapid CPI-17 dephosphorylation as well as MLCK inactivation, resulting in rapid MLC dephosphorylat

37 A genetically-encoded biosensor MLCK for measuring Ca(2+)-dependent CaM binding and acti

38 nd is maintained through cytokinesis by both MLCK- and Rho-dependent signaling.

39 a-primed monolayers caused increases in both MLCK expression and MLC phosphorylation, suggesting that

40 out mice was the same site phosphorylated by MLCK, indicating a potential alternative signaling pathw

41 R-anchored exchangeable pool is regulated by MLCK.

42 e selectivity and can be rapidly reversed by MLCK inhibition.

43 n binding region (ABR) was not stabilized by MLCK inhibition, either in the presence or absence of en

44 nction size selectivity but is unaffected by MLCK inhibition in vitro.

45 CA-MLCK Tg mice demonstrated significant barrier loss but g

46 CA-MLCK Tg mice did, however, develop mucosal immune activa

47 that express constitutively active MLCK (CA-MLCK) specifically within intestinal epithelia.

48 Cardiac MLCK is phosphorylated and the level of phosphorylation

49 nown that a more recently discovered cardiac MLCK (cMLCK) is necessary for normal RLC phosphorylation

50 ne homologous to mylk1 and -2, named cardiac MLCK, which is specifically expressed in the heart in bo

51 Both overexpression and knockdown of cardiac MLCK in cultured cardiomyocytes revealed that cardiac ML

52 In fact, expression of cardiac MLCK is highly regulated by the cardiac homeobox protein

53 The overall structure of cardiac MLCK protein is conserved with skeletal and smooth muscl

54 ultured cardiomyocytes revealed that cardiac MLCK is likely a new regulator of MLC2 phosphorylation,

55 human Caco-2BBe cells with IFN-gamma caused MLCK-dependent TW arc formation and brush border fanning

56 Both TNF and LIGHT caused MLCK-dependent barrier dysfunction.

57 At the base of the cell, MLCK also localized to dynamic actin-coated rings and pa

58 At the sides of the cell, MLCK and myosin II localized to swelling-induced membran

59 rs were comparable with those of the classic MLCK.

60 In conclusion, MLCK activity of arterial smooth muscle during KCl-induc

61 skeletal muscle Ca(2+)/calmodulin-dependent MLCK as a primary biochemical mechanism for tension pote

62 is required for the development of diarrhea, MLCK inhibition does not completely restore water absorp

63 d myocardium following treatment with either MLCK or PKA.

64 ch signaling in VSM cells induced endogenous MLCK transcript levels.

65 In conclusion, epithelial MLCK-activated brush border fanning by IFN-gamma promote

66 also indicate that inhibition of epithelial MLCK may be an effective non-immunosuppressive therapy f

67 These data show that epithelial MLCK is essential for intestinal barrier dysfunction and

68 nted increases in barrier function following MLCK inhibition in a manner that required endogenous ZO-

69 nhibitor of CaMK II, markedly reduced force, MLCK FRET and [Ca(2+)].

70 At the same tonic force, MLCK FRET ratio activated by alpha(1)-adrenoceptors was

71 luorescence resonance energy transfer (FRET) MLCK activity biosensor.

72 Further, MLCK treatment increases Ca(2+)-independent force and ma

73 1 gene) and skeletal (encoded by mylk2 gene) MLCK, have been shown to be expressed in mammals.

74 We show that graded MLCK overexpression increases RLC monophosphorylation (p

75 Hence, MLCK activation in IAS-SMCs caused by a global rise in [

76 ations of the relationships among [Ca2+](i), MLCK activation, and contraction in urinary bladder smoo

77 ation leads to rapid increases in [Ca2+](i), MLCK activation, and RLC phosphorylation in phasic smoot

78 c field stimulation (EFS) increased [Ca2+]i, MLCK activation and concomitant force in a frequency-dep

79 on neurally stimulated elevation of [Ca2+]i, MLCK activation, force and phosphorylation of RLC, myosi

80 We identified MLCK as a direct target of activated Notch receptor as d

81 force, forskolin caused a rapid decrease in MLCK FRET ratio and force, but no change in Ca(2+), sugg

82 In contrast, a 50% decrease in MLCK in aortic smooth muscle resulted in 40% inhibition

83 A 50% decrease in MLCK in urinary bladder smooth muscle had no effect on R

84 osphorylation but sensitivity differences in MLCK, MYPT1 T853, MYPT1 T696, myosin binding subunit 85

85 hibition of the IL-1beta-induced increase in MLCK activity also prevented the increase in Caco-2 TJ p

86 lmodulin (Ca(2+)/CaM) induces an increase in MLCK activity and a change in FRET.

87 permeability was mediated by an increase in MLCK expression and activity.

88 aused a dose- and time-dependent increase in MLCK expression and kinase activity in Caco-2 monolayers

89 al permeability also required an increase in MLCK expression.

90 diated by an NF-kappaB-dependent increase in MLCK gene transcription.

91 time course of IL-1beta-induced increase in MLCK level correlated linearly with increase in Caco-2 T

92 in expression was preceded by an increase in MLCK mRNA expression.

93 The IL-1beta-induced increase in MLCK mRNA transcription and subsequent increase in MLCK

94 A frequency- and time-dependent increase in MLCK phosphorylation explained the desensitization of ML

95 RNA transcription and subsequent increase in MLCK protein expression and Caco-2 TJ permeability was m

96 dicate that the IL-1beta-induced increase in MLCK protein expression and Caco-2 TJ permeability was m

97 hibition of the IL-1beta-induced increase in MLCK protein expression prevented the increase in Caco-2

98 The IL-1beta-induced increase in MLCK protein expression was preceded by an increase in M

99 IL-1beta caused a progressive increase in MLCK protein expression.

100 An initial Notch1-induced increase in MLCK transcription was followed by loss in promoter sens

101 in intestinal permeability was inhibited in MLCK(-/-) and TLR-4(-/-) mice.

102 of MLC phosphatase but also by inactivating MLCK.

103 ma(i), PI 3-kinase, and the Ca2+-independent MLCK, integrin-linked kinase.

104 is probably induced by the Ca2+-independent MLCK, ZIP kinase.

105 implying participation of a Ca2+-independent MLCK.

106 MLC20 phosphorylation via a Ca2+-independent MLCK.

107 p50/p65 axis mediated the TNF-alpha-induced MLCK gene activation and the subsequent MLCK increase in

108 ession of both myocardin- and Notch1-induced MLCK promoter activity.

109 In vivo experiments showed that inhibiting MLCK increased the number of apoptotic cells and retarde

110 ciated kinase (PAK), which directly inhibits MLCK.

111 nstrate that it acts via a pathway involving MLCK and probably myosin light chain (MLC) and myosin II

112 without affecting expression of the 220-kDa MLCK or telokin.

113 fic smooth muscle myosin light chain kinase (MLCK) (smMLCK) and skeletal muscle MLCK (skMLCK) are ded

114 e associated with myosin light chain kinase (MLCK) activation and increased claudin-2 expression, res

115 ng and epithelial myosin light chain kinase (MLCK) activation.

116 by Ca2+-dependent myosin light chain kinase (MLCK) activity and is maintained through cytokinesis by

117 both cell types, myosin light chain kinase (MLCK) also appeared to control myosin II activity in CM

118 ht chain (RLC) by myosin light chain kinase (MLCK) and myosin binding protein-C (cMyBP-C) by protein

119 ases MEK and ERK, myosin light chain kinase (MLCK) and Myosin IIB.

120 modulin-dependent myosin light chain kinase (MLCK) and myosin light chain phosphatase (MLCP).

121 modulin-dependent myosin light chain kinase (MLCK) and myosin light chain phosphatase (MLCP).

122 Activation of myosin light chain kinase (MLCK) and other kinases was studied in the arteries of t

123 hich is driven by myosin light chain kinase (MLCK) and Rho-associated kinase (ROCK).

124 e have identified myosin light chain kinase (MLCK) as a regulator of membrane internalization in resp

125 ress a FRET-based myosin light chain kinase (MLCK) biosensor molecule, we report a technique for dyna

126 Inhibition of myosin light chain kinase (MLCK) blocked the effects of both morphine and TLR ligan

127 due to increased myosin light chain kinase (MLCK) expression.

128 calmodulin sensor myosin light chain kinase (MLCK) in smooth muscles, the effects of suramin/alpha,be

129 and 5, as well as myosin light chain kinase (MLCK) in these cells.

130 of IFN-gamma and myosin light chain kinase (MLCK) in TW myosin phosphorylation and brush border fann

131 e of the specific myosin light chain kinase (MLCK) inhibitor ML-7 under both isobaric and isometric c

132 lin activation of myosin light chain kinase (MLCK) initiates myosin regulatory light chain (RLC) phos

133 Myosin light-chain kinase (MLCK) is a downstream target of TNF-alpha and was phosph

134 modulin-dependent myosin light-chain kinase (MLCK) is essential for initiation of smooth muscle contr

135 Myosin light chain kinase (MLCK) is expressed as long and short isoforms from uniqu

136 tic agent or when myosin light chain kinase (MLCK) is inhibited pharmacologically or by microinjectin

137 nction induced by myosin light chain kinase (MLCK) is required for the development of diarrhea, MLCK

138 knockout of long myosin light chain kinase (MLCK) or treatment of wild-type mice with a highly speci

139 modulin-dependent myosin light chain kinase (MLCK) phosphorylates smooth muscle myosin regulatory lig

140 ein, we show that myosin light chain kinase (MLCK) plays a central role in the LPS-induced increase i

141 ding motif on the myosin light chain kinase (MLCK) promoter region, leading to the activation of MLCK

142 binding motif on the myosin L chain kinase (MLCK) promoter region, leading to the activation of MLCK

143 e myosin (SMM) by myosin light-chain kinase (MLCK) proposes that MLCK is bound tightly to actin but w

144 lear factor-B and myosin light-chain kinase (MLCK) signalling, and these changes were almost complete

145 se II (CaMKII) to myosin light chain kinase (MLCK) to myosin light chain, the last of which controls

146 ifically, the role of myosin L chain kinase (MLCK) was investigated.

147 inase (ROCK), and myosin light chain kinase (MLCK) were also recruited to lateral membranes.

148 ht chain (RLC) by myosin light chain kinase (MLCK) were determined.

149 lity regulated by myosin light chain kinase (MLCK) were responsible for the intriguing turning behavi

150 220-kDa nonmuscle myosin light chain kinase (MLCK), a 130-kDa smooth muscle MLCK (smMLCK), as well as

151 o upregulation of myosin light chain kinase (MLCK), a hallmark of the pathogenesis of inflammatory bo

152 n and activity of myosin light chain kinase (MLCK), a primary regulator of VSM force production.

153 kinase (ROCK) and myosin light chain kinase (MLCK), culminating in the activation of non-muscle myosi

154 Last, myosin light chain kinase (MLCK), which can be directly phosphorylated and activate

155 stinal epithelial myosin light chain kinase (MLCK), which is the primary mechanism of tumor necrosis

156 Myosin light chain kinase (MLCK)-dependent phosphorylation of the regulatory light

157 ng contributes to myosin light chain kinase (MLCK)-dependent tight junction regulation.

158 previously that a myosin light chain kinase (MLCK)-myosin II pathway was required for effective trans

159 tes and activates myosin light-chain kinase (MLCK).

160 se (ROCK) but not myosin light chain kinase (MLCK).

161 argets, including myosin light chain kinase (MLCK).

162 ity by activating myosin light chain kinase (MLCK; official name MYLK3) gene.

163 chain (MLC) phosphorylation and MLC kinase (MLCK) activity-major determinants of vascular tone-were

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

165 phosphorylation were reversed by MLC kinase (MLCK) inhibition.

166 that these are both reversed by MLC kinase (MLCK) inhibition.

167 of Syk, Ca(2+) mobilization, and MLC kinase (MLCK) only partially inhibited MLC phosphorylation, sugg

168 regulatory light chain (MLC) by MLC kinase (MLCK) regulates tight junction function.

169 n of myosin light chain (MLC) by MLC kinase (MLCK) through integrin beta1 is required for actin stres

170 Positive expression of MLC kinase (MLCK) was found at the mRNA and protein levels by RT-PCR

171 o the classic Ca(2)(+)-dependent MLC kinase (MLCK), another unidentified kinase(s) also contributes t

172 egulated by myosin light chain (MLC) kinase (MLCK) and rho kinase (ROCK).

173 Two myosin light chain (MLC) kinase (MLCK) proteins, smooth muscle (encoded by mylk1 gene) an

174 that deletion of myosin light-chain kinases (MLCK) in the smooth muscle cells from internal anal sphi

175 Limiting MLCK activity combined with modest Ca(2+) sensitization

176 ntial Sp1 sites upstream of the exon 1A long MLCK transcriptional start site.

177 ns, 1A and 1B, which encode alternative long MLCK transcriptional start sites.

178 or (TNF) augments intestinal epithelial long MLCK expression, which is critical to cytoskeletal regul

179 TNF up-regulates intestinal epithelial long MLCK transcription from exon 1A are differentiation-depe

180 seen in mice genetically deficient for long MLCK-210 or IFN-gamma.

181 We found that TNF increases long MLCK mRNA transcription, both in human enterocytes in vi

182 entiated enterocytes activated the 4-kb long MLCK promoter in response to TNF, and consensus promoter

183 ivo ZO-1 exchange in wild-type, but not long MLCK(-/-), mice.

184 either AP-1 or NFkappaB can up-regulate long MLCK transcription, but the mechanisms by which TNF up-r

185 are protein kinases (CaMKII, PKC, MPF, MAPK, MLCK) whose activity is directly or indirectly regulated

186 m of purinergic receptors suppressed maximal MLCK activation to a greater extent in the early contrac

187 n kinase (MLCK) (smMLCK) and skeletal muscle MLCK (skMLCK) are dedicated protein kinases regulated by

188 issue-specific expression of skeletal muscle MLCK and in contrast to the ubiquitous expression of smo

189 Loss of skeletal muscle MLCK expression had no effect on cardiac RLC phosphoryla

190 in mice resulted in loss of skeletal muscle MLCK expression, with no change in smooth muscle MLCK ex

191 chain kinase (MLCK), a 130-kDa smooth muscle MLCK (smMLCK), as well as the non-catalytic product telo

192 expression, with no change in smooth muscle MLCK expression.

193 In contrast, smooth muscle MLCK had a more ubiquitous tissue distribution, with the

194 o the ubiquitous expression of smooth muscle MLCK.

195 is conserved with skeletal and smooth muscle MLCK; however, the amino terminus is quite unique, witho

196 1 is mediated through Rok-dependent, but not MLCK-dependent, stimulation of myosin II activity yet in

197 In support of this notion, MLCK-induced phosphorylation of D166V-mutated hearts was

198 These results suggest a novel MLCK-specific mechanism for controlling cell polarity vi

199 Fifteen to 30% of MLCK was associated with CaM at approximately 1 nM free

200 ry and ROS production, whereas abrogation of MLCK using specific siRNA significantly inhibited the ab

201 ther, our results suggest that activation of MLCK accelerates both slow and rapid forms of vesicle en

202 osphorylation through the dual activation of MLCK and inhibition of MLCP.

203 role in the TNF-alpha-induced activation of MLCK gene and increase in intestinal TJ permeability.

204 mediate the TNF-alpha-induced activation of MLCK gene and increase in TJ permeability remain unclear

205 Recruitment and activation of MLCK occurred after ring assembly was complete and coinc

206 romoter region, leading to the activation of MLCK promoter activity and gene transcription.

207 romoter region, leading to the activation of MLCK promoter activity and gene transcription.

208 -2 binding motif prevented the activation of MLCK promoter and MLCK mRNA transcription.

209 2+ signals provide the initial activation of MLCK with muscarinic receptors supporting sustained resp

210 Here, we confirm the activation of MLCK, based on increased nerve terminal phospho-MLC immu

211 We further demonstrate that activation of MLCK, by increased extracellular Ca(2+), by PKC (protein

212 r actin ring assembly, while the activity of MLCK drives contraction.

213 MP cause a rapid decrease in the affinity of MLCK for Ca(2+)/CaM.

214 ting a cAMP mediated decrease in affinity of MLCK for Ca(2+)/CaM.

215 urther demonstrate a partial contribution of MLCK to intestinal barrier dysfunction and liver disease

216 sults indicate differential contributions of MLCK to signaling.

217 The apparent desensitization of MLCK to Ca2+ activation appears to be due to phosphoryla

218 phorylation explained the desensitization of MLCK to Ca2+, since MLCK activation declined more rapidl

219 phosphorylation-dependent desensitization of MLCK.

220 K inhibition and siRNA-induced knock-down of MLCK inhibited the LPS-induced increase in Caco-2 TJ per

221 Additionally, knock-down of MLCK protein expression by small interference RNA preven

222 The effects of MLCK and ROCK on single-SF mechanics may be correspondin

223 dings that activation of a small fraction of MLCK by limiting amounts of free Ca(2+)/calmodulin combi

224 vide insights into how haploinsufficiency of MLCK may result in contractile dysfunction in vivo, lead

225 ated, smooth muscle-specific inactivation of MLCK expression in adult mice to determine whether MLCK

226 Combined inhibition of MLCK and calmodulin did not induce synergistic inhibitio

227 was significantly decreased by inhibition of MLCK or Rho kinase or by loss of UreB.

228 Inhibition of MLCK significantly reduces metastatic outgrowth in vivo.

229 Acute inhibition of MLCK with pharmacological agents was found to slow down

230 ism of action involves a tonic inhibition of MLCK, presumably through PAK phosphorylation.

231 pathogenesis and suggest that inhibition of MLCK-dependent caveolar endocytosis may represent an app

232 h muscle cells revealed a bimodal pattern of MLCK promoter activity and gene expression upon stimulat

233 signal-transduction pathway up-regulation of MLCK expression.

234 tivation of ATF-2 and by ATF-2 regulation of MLCK gene activity.

235 gnaling in the transcriptional regulation of MLCK gene expression.

236 cally observing activation and regulation of MLCK within the smooth muscle cells of intact, functioni

237 signal-transduction pathway up-regulation of MLCK.

238 hine and TLR ligands, suggesting the role of MLCK in tight junction modulation by TLR.

239 leal smooth muscle appear to be dependent on MLCK and MLCP activities without changes in constitutive

240 The effects of KENESKA and other peptides on MLCK and MLC activation and on failures in both wild-typ

241 causing relaxation, changes in [Ca(2+)], or MLCK FRET.

242 Arp2/3 or MLCK inhibition substantially reduced probability of T c

243 Inhibition of integrin beta1 or MLCK prevents transition from a quiescent to proliferati

244 s since unilateral microinjection of ROCK or MLCK inhibitors into the hypoglossal nucleus reduced or

245 Inhibition of either Src or MLCK led to altered patch and ring lifetimes, consistent

246 ith either a RhoA/Rock inhibitor (Y27632) or MLCK inhibitor (ML7) abrogated ATP release in response t

247 alytic domain sequence similarity with other MLCKs but lacking an autoinhibitory segment.

248 ild-type mice with a highly specific peptide MLCK inhibitor prevented epithelial MLC phosphorylation,

249 Pharmacologic MLCK inhibition also blocked in vivo ZO-1 exchange in wi

250 The pharmacologic MLCK inhibition and siRNA-induced knock-down of MLCK inh

251 n redistribution, and reduced phosphorylated MLCK than sham monolayers.

252 light-chain kinase (nmMLCK), the predominant MLCK isoform in endothelial cells, has been shown to con

253 velocities, we showed that the co-purifying MLCK-CaM was activated by Ca(2+) and phosphorylation of

254 properties were observed from reconstituted MLCK-CaM-SMM.

255 This requires MLCK activation and caveolar endocytosis.

256 uncations and siHRT2 treatments that rescued MLCK promoter activity and gene expression.

257 We conclude that reversible, MLCK-dependent permeability increases cause mucosal immu

258 required microfilament remodeling and ROCK, MLCK, and dynamin II activities.

259 ered signalling pathways PI(3)K-Akt and ROCK-MLCK.

260 d the desensitization of MLCK to Ca2+, since MLCK activation declined more rapidly than [Ca2+]i.

261 Smooth muscle myosin light chain kinase (SM-MLCK) is the key enzyme responsible for phosphorylation

262 oordinating transcriptional regulation of SM-MLCK.

263 Taken together, SM-MLCK promoter activity appears highly sensitive to the r

264 uced MLCK gene activation and the subsequent MLCK increase in intestinal TJ permeability.

265 These data demonstrate that MLCK activation triggers caveolin-1-dependent endocytosi

266 We found that MLCK and calmodulin (CaM) co-purify with unphosphorylate

267 osin light-chain kinase (MLCK) proposes that MLCK is bound tightly to actin but weakly to SMM.

268 with subcellular laser ablation reveals that MLCK and ROCK quantitatively regulate the viscoelastic p

269 estern blot and quantitative-PCR showed that MLCK is expressed predominantly in fast-twitch skeletal

270 O-1 ABR in barrier function and suggest that MLCK-dependent ZO-1 exchange is essential to this mechan

271 ion and MLC phosphorylation, suggesting that MLCK is a TNF-alpha-inducible protein.

272 Although previous work suggests that MLCK and ROCK control distinct pools of cellular SFs, it

273 Although the MLCK:SMM molar ratio in SMM preparations was well below

274 n of the canonical NF-kappaB pathway and the MLCK gene.

275 in TM and CM cells by the Rho kinase and the MLCK pathways despite their compositional similarity in

276 vated by MAPK, appears involved, because the MLCK inhibitors ML-7 and Peptide 18 prevent sperm chroma

277 we provide strong evidence that most of the MLCK is bound directly to SMM through the telokin domain

278 re was time-dependent phosphorylation of the MLCK substrate myosin II regulatory light chain.

279 onserved Notch-responsive element within the MLCK promoter that binds the Notch receptor complex and

280 These results suggest that this MLCK may play a role in the initiation of contraction.

281 agnitude lower than those of the other three MLCK family members, whereas its Km (RLC and ATP) and KC

282 Thus, MLCK activation by 100 Hz stimulation switches the mecha

283 Thus, MLCK content is limiting for contraction in aortic smoot

284 by microinjecting an inhibitory antibody to MLCK.

285 thoracic duct has an enhanced sensitivity to MLCK inhibition when compared to cervical lymphatics and

286 There were two MLCK pools that bound unphosphorylated SMM with K(d) app

287 Overexpression of FLAG-tagged wild type MLCK in human pulmonary artery endothelial cells enhance

288 We find that a fourth uncharacterized MLCK, MLCK4, is also expressed in cardiac muscle with hi

289 otor protein that can be phosphorylated upon MLCK activation.

290 Using MLCK-deficient mice, we further demonstrate a partial co

291 junction morphology and barrier function via MLCK up-regulation and MLC phosphorylation.

292 In vivo, MLCK activation increases paracellular flux of uncharged

293 pase activation increased cell survival when MLCK is inhibited or when cells are treated with tumor n

294 xpression in adult mice to determine whether MLCK was differentially limiting in distinct smooth musc

295 We determined whether MLCK was activated by H pylori and defined the mechanism

296 Our results point to a model in which MLCK and ROCK regulate peripheral and central SF viscoel

297 However, while MLCK treatment has been shown to increase the Ca(2+) sen

298 ment spacing was reduced by 2 nm (3.5%) with MLCK treatment, but did not change with PKA treatment.

299 iation of the cell volume regulator Src with MLCK and with the endocytosis regulators cortactin and d

300 /I(1,0) and, as hypothesized, treatment with MLCK also increased I(1,1)/I(1,0), which can explain the