ライフサイエンスコーパス: Rho-kinase

1 kinases and is upstream of the activation by Rho kinase.

2 lphaq-coupled downstream pathways, including Rho kinase.

3 raising intracellular calcium and activating rho kinase.

4 osphatase) at Thr-696/Thr-853 or activity of Rho kinase.

5 the apical and basolateral membranes through Rho kinase.

6 of Spry1 protein and promoted activation of Rho kinase.

7 inhibition or short hairpin RNA knockdown of Rho kinase.

8 fect correlated with increased activation of Rho kinase.

9 inhibited the cytoskeletal regulatory factor Rho kinase.

10 chanisms involving redox-sensitive PKG-1 and Rho kinase.

11 on that involved TRPC6, phospholipase C, and rho kinase.

12 normalized by pharmacological inhibition of Rho kinase.

13 scle possibly due to increased activation of Rho-kinase.

14 Overexpression of Rho kinase 1 (ROCK1) and the G protein RhoA is implicate

15 The Ser/Thr Rho kinase 1 (ROCK1) is known to have major roles in a w

16 cruitment of 1-phosphomyosin light chain and Rho kinase 1, contraction of the actomyosin ring, and ex

17 We found that Rho-kinase 1 (ROCK1) regulates leptin action on body wei

18 omoter of and activated the transcription of Rho-kinase 2 (Rock2), and Bmal1 deletion abolished the t

19 We previously demonstrated that Rho kinase 2b (Rock2b) is required for anteroposterior a

20 , L-type calcium channels, protein kinase C, Rho-kinase, actin polymerization, and myocardin-related

21 enotype, and the molecular signaling between Rho kinase activation in cardiomyocytes and extracellula

22 n on zebrafish cardiovascular development or Rho kinase activation in EC.

23 Recent studies have found aberrant Rho kinase activation in inherited CCM pathogenesis, and

24 -kappaB pathway had no impact on LPA-induced Rho kinase activation, but inhibited adhesion molecule e

25 result in phospholipase C-mediated TRPC6 and rho kinase activation, which conjointly trigger vasocons

26 induces pulmonary hypertension through Rho A/Rho kinase activation-mediated vasoconstriction and pulm

27 n Prkg1(-/-) lung tissues, which resulted in Rho kinase activation.

28 gnized signaling cascade involving Spry1 and Rho kinase activation.

29 nanofibers associated with an attenuation of Rho kinase activation.

30 phosphorylation of JAK2 and subsequent RhoA/Rho-kinase activation.

31 der smooth muscle cells through upregulating Rho kinase activity and phosphorylating myosin light cha

32 at NPY promotes AHR through the induction of Rho kinase activity and phosphorylation of myosin light

33 hieve spatiotemporally limited inhibition of Rho kinase activity in vivo.

34 RhoA/Rho kinase activity is required for EMT and for differen

35 tes and focused on redox-sensitive pathways, Rho kinase activity, and protein kinase G type-1 (PKG-1)

36 e that TTC7A deficiency results in increased Rho kinase activity, which disrupts polarity, growth, an

37 rp2/3 complex inhibition were independent of Rho kinase activity.

38 redox-sensitive PKG-1, and downregulation of Rho kinase activity.

39 thelial dysfunction, liver fibrosis, hepatic Rho-kinase activity (a marker of hepatic stellate cell c

40 revented the effects of TGF-beta on RhoA and Rho-kinase activity and contraction, respectively.

41 -beta target gene, an important regulator of Rho-kinase activity and therefore a potential therapeuti

42 ase in miR-21-null mice, RhoB expression and Rho-kinase activity are increased, accompanied by exagge

43 The mechanisms that direct localized Rho-kinase activity are not well understood.

44 ix (ECM) in polarizing cells determined RhoA/Rho-kinase activity at cell-cell contact sites.

45 -induced contraction, RhoA translocation and Rho-kinase activity in airway smooth muscle largely via

46 ts, endothelial dysfunction was improved and Rho-kinase activity was significantly reduced.

47 iR-21 directly represses RhoB expression and Rho-kinase activity, inducing molecular changes consiste

48 polymerization, and ROCKOUT, an inhibitor of Rho-kinase activity, prevent gastrulation.

49 endothelial cell proliferation and increased Rho-kinase activity.

50 se branching defects following inhibition of Rho kinase, an important downstream effector of the PCP

51 Using H1152 (IC50 6.1 mum) to inhibit Rho kinase and 6.3G9 to inhibit alphavbeta6 integrins, w

52 AR-13324 is a small-molecule inhibitor of Rho kinase and a norepinephrine transporter.

53 se GM-CSF via S1P receptor 3 (S1pr3) through Rho kinase and extracellular signal-regulated kinase-dep

54 ated KATP channels trigger signaling through Rho kinase and Janus kinase-3, and cause actin remodelin

55 Rac, and their downstream effectors such as Rho kinase and nicotinamide adenine dinucleotide phospha

56 is required for apicomedial accumulation of Rho kinase and non-muscle myosin II, which coordinate ap

57 n in a NO-independent manner, presumably via rho kinase and p38 MAPK, and Syk inhibition might presen

58 NF-kappaB further induces activation of Rho kinase and shedding of endothelial microparticles ca

59 Thus, a Rho kinase and the MAPK modules ERK1/2 and JNK act upstr

60 ted differentially in TM and CM cells by the Rho kinase and the MLCK pathways despite their compositi

61 se was associated with increased endothelial Rho kinases and ERK1/2 activities and cytoskeletal reorg

62 L-NAME and SNAP did not affect Rho kinases and ERK1/2 activities.

63 stimulates EMP release through activation of Rho kinases and ERK1/2 pathways, whereas atheroprotectiv

64 ls to transactivate latent TGF-beta in a Rho/Rho-kinase and alphavbeta6 integrin-dependent manner.

65 TGF-beta on expression and activity of RhoA, Rho-kinase and ARHGEF1, an activator of RhoA, as well as

66 which, in TAA, related to down-regulation of Rho-kinase and in BDL to up-regulation of DDAH-2.

67 In Shroom mutants, Rho-kinase and myosin II achieve reduced levels of plana

68 ecruitment at force-bearing sites depends on Rho-kinase and myosin II activation, suggesting that zyx

69 n- and Rho-kinase-binding protein, amplifies Rho-kinase and myosin II planar polarity and junctional

70 sforming growth factor-beta (TGF-beta), RhoA/Rho-kinase and Src-family kinases (SrcFK) have independe

71 ., endothelial nitric oxide synthase [eNOS], Rho-kinase, and dimethylarginine dimethylaminohydrolase

72 ts RhoGEF2, reducing membrane recruitment of Rho-kinase, and increasing a specific E-cadherin pool th

73 rming growth-factor-beta (TGF-beta) and RhoA/Rho-kinase are independently implicated in the airway hy

74 The results define Rho kinase as a therapeutic target to rescue endothelial

75 duced HUVEC barrier dysfunction through RhoA/Rho kinase as downstream intermediates.

76 Inhibitors of Rho kinase as well as TGFbetaR1 and NF-kappaB decreased

77 Collectively, these findings highlight the Rho kinases as rational therapeutic targets to combat ta

78 hen inhibited the activity of Abl family and Rho kinases as well as NR2B-containing N-methyl-D-aspart

79 n collectively, our data are consistent with Rho kinase being upstream of NF-kappaB in driving LPA-me

80 room, an asymmetrically localized actin- and Rho-kinase-binding protein, amplifies Rho-kinase and myo

81 hibitors of the downstream effector of RhoA, Rho kinase, block oscillatory behavior.

82 Inhibiting Rho kinase blocked both TGFbeta- and FGF2-induced stress

83 Inhibition of Rho kinase blocked these changes and reduced t-PA/plasmi

84 HPV was virtually abolished by the rho kinase blocker Y-27632 (1 mum) and attenuated by the

85 Blocking Rho kinase by means of Y-27632 resulted in a 50% and gre

86 Rac1, RhoA, and their effectors cofilin and Rho kinase by perturbing the plasma membrane lipids.

87 GTPase by bacterial toxin, or inhibition of Rho kinase by Y-27632 in HTM cells led to significant bu

88 Rho-kinase can phosphorylate this domain and inhibit its

89 Inhibition of myosin-II (MII) or Rho-kinase collapsed bridges, whereas extension continue

90 Optogenetic control of Rho-kinase combined with computational modeling reveals

91 tral to cGMP-mediated inhibition of the VSMC Rho kinase contractile pathway.

92 rane lipids, suggesting a mechanism by which Rho-kinase could regulate Baz association with the cell

93 a) is required for high glucose-induced RhoA/Rho kinase/CPI-17 activation and thereby contributes to

94 udies suggest that high glucose-induced RhoA/Rho kinase/CPI-17 activation is involved in diabetes-ass

95 m signaling that links high glucose and RhoA/Rho kinase/CPI-17 activation is unknown.

96 deletion abolishes high glucose-induced RhoA/Rho kinase/CPI-17 activation, and restoring expression o

97 iPLA(2)beta up-regulation activates the RhoA/Rho kinase/CPI-17 via 12/15-lipoxygenases and thereby co

98 inase signaling leads to cell sorting by the Rho kinase-dependent generation of a cortical actin diff

99 of the actomyosin contractile machinery in a Rho kinase-dependent manner then lead to rapid and prono

100 express its ligand, semaphorin 4D, in a Rho/Rho kinase-dependent manner.

101 pathway increases intraocular pressure in a Rho kinase-dependent manner.

102 ncreased RhoA activation was associated with Rho kinase-dependent phosphorylation of myosin light cha

103 nd apoptosis in renal cells by controlling a Rho kinase-dependent signaling network.

104 ell migration, and proliferation through the Rho kinase-dependent signaling pathway.

105 cells constrict their apices because of Rho/Rho-kinase-dependent apical enrichment of 1P-myosin.

106 n drives apico-basal shortening, whereas Rho/Rho-kinase-dependent enrichment of 1P and 2P myosin in c

107 uires sphingosine 1-phosphate signalling and Rho-kinase-dependent myosin contraction, but is distingu

108 anced bradykinin-induced RhoA translocation, Rho-kinase-dependent phosphorylation and contraction, bu

109 Rho-kinase-dependent vasoconstriction accounted for appr

110 h computational modeling reveals that active Rho-kinase diffuses to growing other immature neurites a

111 Significantly, Drk signals engage the Rho kinase Drok, implicating dynamic cytoskeletal change

112 ites within myosin regulatory light chain by Rho kinase drove NMII clustering in areas behind the cen

113 cells and inhibiting the activity of Rac or Rho kinase effectively reduces the migration of venous,

114 , randomized noninferiority clinical trials: Rho Kinase Elevated IOP Treatment Trial 1 and 2 (ROCKET-

115 y to facilitate lamellipodia formation while Rho kinase exhibited a significantly lower activity lead

116 Other epithelia need Rho-kinase for planar cell polarity but it is not known

117 for fibronectin-stimulated Rho-GTP loading, Rho-kinase function, and the maturation of focal adhesio

118 So far, activation of RhoA/Rho kinase has not been associated with RGS molecules.

119 Although the protein levels of Rho-A and Rho-kinase I and II had not been impaired, the levels of

120 and CM cells, was regulated predominantly by Rho kinase in both cell types, myosin light chain kinase

121 g pathways indicated involvement of RhoA and Rho kinase in JAM-A relocalization.

122 Pharmacologic inhibition of Rho kinases in neurons diminished detergent-soluble and

123 Our data demonstrate the importance of Rho-kinase in normal nephron tubulogenesis and patternin

124 asured mucus secretion and the expression of Rho-kinase in the airway tissue of patients with asthma.

125 The role of Rho-kinase in the renal and systemic effects of vasopres

126 vel mechanism we call collared rounding: Rho/Rho-kinase-independent basolateral enrichment of 1P-myos

127 ted in elevated RhoA activity and associated Rho kinase-induced nonmuscle myosin II activity.

128 hanous-induced actin polymerization and RhoA/Rho kinase-induced phosphorylation of myosin light chain

129 The possibility that Rho kinase inhibition and statins sustain K(Ca)2.3 hyper

130 Rho kinase inhibition and the absence of the lectin-like

131 Both feeder cells and Rho kinase inhibition are required for the conditional r

132 MP reversed phagocytic impairment induced by Rho kinase inhibition but was ineffective in the presenc

133 Rho kinase inhibition by Y-27632 prevented CTGF and hydr

134 these neurobehavioral deficiencies, whereas Rho kinase inhibition corrected response strategies.

135 Morphological rescue is possible following Rho kinase inhibition in an oligodendrocyte subset.

136 L-NAME-treated arteries, but was restored by Rho kinase inhibition or statin treatment.

137 We suggest that Rho kinase inhibition promotes goal-oriented action sele

138 ion to the TP agonist, U46619 was reduced by Rho kinase inhibition.

139 lated kinase, B-cell lymphoma protein-2, and Rho kinase inhibition.

140 d specific FLNA repeats and was sensitive to Rho kinase inhibition.

141 Rho-kinase inhibition also rescues goal-directed respons

142 Rho-kinase inhibition reduced PAR4-AP-mediated peak thro

143 We demonstrate that a Rho kinase inhibitor (Y-27632), in combination with fibr

144 human epithelial cells in the presence of a Rho kinase inhibitor (Y-27632).

145 rectly or through photo-release of the caged Rho kinase inhibitor also reduced the rate of VE-cadheri

146 or was less appreciable in the presence of a rho kinase inhibitor and in 2D monolayer cocultures.

147 Treatment with a Rho kinase inhibitor attenuated the fibrotic phenotype.

148 tion were abrogated by pretreatment with the rho kinase inhibitor fasudil.

149 Moreover, Rho kinase inhibitor or JNK inhibitor treatment suppress

150 sely, in cells in which LRP1 was silenced, a Rho kinase inhibitor promoted migration and inhibited ad

151 Consistent with these observations, the Rho kinase inhibitor Y-27632 decreased cell impedance (s

152 the present study, we demonstrated that the Rho kinase inhibitor Y-27632, significantly suppresses k

153 s was comparable to that induced by Y-27632 (Rho kinase inhibitor).

154 examined whether fasudil, a selective Rho-A/Rho kinase inhibitor, affects the mucus hypersecretion b

155 The Rho kinase inhibitor, but not nicardipine, significantly

156 These findings indicate that the Rho-A/Rho kinase inhibitor, fasudil, plays a negative regulato

157 different anatomical sites) with Y-27632, a Rho kinase inhibitor, greatly increased their proliferat

158 Fasudil, a selective Rho-A/Rho kinase inhibitor, has been used in clinical trials t

159 Furthermore, Y27632, a Rho kinase inhibitor, reduced the antiapoptotic effect o

160 The i.t. administration of fasudil, a Rho kinase inhibitor, reversed the hypertensive pulmonar

161 on of irradiated fibroblast feeder cells and Rho kinase inhibitor, Y-27632, conditionally induces an

162 e retina with a RhoA antagonist, CT-04, or a Rho kinase inhibitor, Y27632, at multiple concentrations

163 ling and SRF, as they were attenuated by the Rho kinase inhibitor, Y27632, or by the SRF inhibitor, C

164 s were ameliorated by topical application of Rho kinase inhibitor.

165 of hyaluronic acid (HA) in combination with Rho-kinase inhibitor (ROCK) Y-27632 for the cultivation

166 y of netarsudil 0.02% ophthalmic solution, a rho-kinase inhibitor and norepinephrine transporter inhi

167 Further studies revealed that the Rho-kinase inhibitor fasudil (1 micromol/L) significantl

168 ction, was not effective, treatment with the Rho-kinase inhibitor Y-27632 reduced vessel constriction

169 ional anti-PAH molecule fasudil (HA-1077), a Rho-kinase inhibitor, into liposomal vesicles results in

170 effects are prevented by treatment with the Rho-kinase inhibitor, Y27632.

171 cytosis induced by Stx2B were reduced by Rho/Rho kinase inhibitors and dominant-negative RhoA, wherea

172 Rho kinase inhibitors cause a reversible decline in the

173 polarization, an effect that was reversed by Rho kinase inhibitors or simvastatin.

174 These actions, similar to those of the Rho kinase inhibitors, possibly underlie the reported in

175 g but were only moderately reduced by Rho or Rho kinase inhibitors.

176 d is the target of a new class of drugs, the Rho kinase inhibitors.

177 gulated protein kinases 1 and 2 (ERK1/2) and Rho kinases inhibitors but unaffected by caspase inhibit

178 eported on the design and synthesis of novel Rho-kinase inhibitors (RKIs).

179 e the development and evaluation of emerging Rho-kinase inhibitors and adenosine receptor ligands tha

180 uided design, we discovered a novel class of Rho-kinase inhibitors.

181 l cultures that are achieved by use of ROCK (Rho kinase) inhibitors.

182 is mediated by a cytoskeletal rearrangement-Rho kinase-integrin system, and both protein-tyrosine ki

183 zyxin promotes actin reinforcement even when Rho kinase is inhibited.

184 Whereas Rho kinase is necessary to induce cell intercalation and

185 role of some RhoA effectors like formins and Rho kinase is reasonably understood, the functions of an

186 The myosin II activator Rho-kinase is asymmetrically enriched at the anterior an

187 We show that Rho-kinase is essential for the morphogenesis of nephron

188 ar cell polarity but it is not known whether Rho-kinase is involved in this way in the nephron.

189 Moreover, the localized myosin activator Rho-kinase is required for spatially regulated myosin ac

190 n expansion of the Baz domain, and activated Rho-kinase is sufficient to exclude Baz from the cortex.

191 and to investigate the contributions of the Rho kinase isoforms ROCK1 and ROCK2 to adhesion molecule

192 n of cells - processes that are dependent on Rho kinase, JNK and, to some extent, planar cell polarit

193 mediated via downstream PCP targets such as Rho kinase, Jun kinase (JNK), and both actin and microtu

194 of the small GTPase, RhoA, and its effector Rho kinase leads to down-regulation of smooth muscle (SM

195 n when hemidesmosomes or the activity of the Rho kinase LET-502/ROCK were partially compromised.

196 gulation was shown to be responsible for the Rho kinase-mediated activation of TGFbeta1 signaling.

197 1 and NF-kappaB signaling contributes to the Rho kinase-mediated pathological fibrosis.

198 on that stimulates alpha2C-adrenoceptors and Rho-kinase-mediated MLC phosphorylation, downstream of T

199 ted by master kinase Par-4/LKB1 via the RhoA-Rho kinase-myosin II pathway, and inhibition of this pat

200 ic abnormalities are associated with altered Rho-kinase/myosin II signaling and loss of apically dist

201 otein kinase pathway that, together with the Rho-kinase nuclear factor kappa B pathway (NF-kB), are r

202 ace by shadow mask-plating, or inhibition of Rho kinase or nonmuscle myosin attenuated stress fiber a

203 ects, whereas combined inhibition of Syk and rho kinase or Syk and p38 MAPK did not cause additive br

204 ed with pharmacological inhibitors of either Rho-kinase or Myosin II ATPase.

205 The Rho kinases, or ROCKs, are a family of serine-threonine

206 affected by inhibition of protein kinase C, Rho-kinase, or extracellular signal-regulated protein ki

207 The Rho/Rho kinase pathway is central for TP signalling and stat

208 Blockade of the Rho/Rho kinase pathway may have beneficial consequences duri

209 Furthermore, the Rho/Rho kinase pathway regulates filamin accumulation and fi

210 n also be elicited by inhibitors of the RhoA/Rho kinase pathway via inhibition of myosin light chain

211 isms by which elevated cAMP opposes the RhoA-Rho kinase pathway, leading to the relaxation of the act

212 e of the renal vascular system and the Rho-A/Rho-kinase pathway in the maintenance of the pressor eff

213 se to adherens junctions and is required for Rho-kinase planar polarity.

214 These results demonstrate that Rho-kinase plays an instructive role in planar polarity

215 Our data suggest that activation of Rho-kinase potentiates the vascular effects of vasopress

216 PKGI is known to phosphorylate Rho kinase, preventing Rho-mediated inhibition of MLC ph

217 ic markers to demonstrate that inhibition of Rho-kinase prevents proper proximal-distal axis formatio

218 y regulated activity of the myosin activator Rho-kinase promotes actomyosin contraction at specific p

219 fectors, such as RhoGTPases (RhoA and Rac1), Rho-kinase, protein kinase-Ngamma, and phosphoinositide-

220 In contrast, inhibition of Rho kinase reduced phosphorylation of JNK but not p38, d

221 Inhibition of Rho-kinase reduced PAR4-AP-mediated FV secretion and mic

222 reased RhoA activity, with the activation of Rho kinase responsible for endothelial cell dysregulatio

223 Loss of Rho-kinase results in expansion of the Baz domain, and a

224 a mechanotransduction pathway involving Rho/Rho kinase (Rho/ROCK), actin cytoskeletal remodeling, an

225 ative key regulator of the Rho/RhoA effector Rho-kinase [Rho-associated coiled-coil-forming kinase (R

226 In the current study, we have found that the Rho kinases, Rho-associated, coiled-coil containing prot

227 The droxidopa effect on the Rho kinase (RhoK) / protein kinase B (AKT) / endothelial

228 These compounds also inhibit the Rho-kinases ROCK 1 and ROCK 2 and we show they potently

229 ediated this stiffness sensing by increasing Rho kinase (ROCK) activity, resulting in increased trans

230 n actomyosin contractility pathway involving Rho kinase (ROCK) and myosin light chain kinase (MLCK),

231 y myofibroblasts was dependent on intact Rho/Rho kinase (ROCK) and myosin signals inasmuch as treatme

232 GTPase RhoA and its key downstream effector Rho kinase (ROCK) are critical mediators of growth cone

233 ell-cell adhesions, and contains a conserved Rho kinase (Rock) binding domain, we hypothesized that S

234 ce that these anomalies are primarily due to Rho kinase (ROCK) controlled excessive contractile myosi

235 Here, we report that Rho kinase (ROCK) controls coordinated tissue organizati

236 RhoA/Rho kinase (ROCK) function is required for 5-HT-induced

237 strongly activates RhoA and the Rho effector Rho kinase (ROCK) in breast cancer cells and induces the

238 The Rho kinase (ROCK) inhibitor SAR1x blocked increases in p

239 Rho kinase (ROCK) is a promising drug target for the tre

240 Rho kinase (ROCK) is a serine/threonine protein kinase t

241 al inhibition of polo-like kinase 1 and RhoA/Rho kinase (ROCK) leads to the synergistic effects in KR

242 5-HT signals to activate the RhoA/Rho kinase (ROCK) pathway, a pathway known for its abili

243 In contrast, Rho kinase (ROCK) regulates myosin accumulation at the c

244 ting cellular morphogenesis through the RhoA/Rho kinase (ROCK) signaling cascade.

245 calization of CD44 polypeptides via the S1P3/Rho kinase (ROCK) signaling pathway.

246 with mTORC1 loss of function, we found that Rho kinase (ROCK) signaling was constitutively activated

247 voltage-operated calcium channels (L-VOCCs), Rho kinase (ROCK), and protein kinase C (PKC) to ET-1-in

248 ting directly with the coiled-coil region of Rho kinase (Rock).

249 sustaining activity of RhoA and its effector Rho kinase (ROCK).

250 rho-Kinase (ROCK) activity was increased specifically in

251 ort of vimentin ULFs is further regulated by Rho-kinase (ROCK) and p21-activated kinase (PAK): ROCK i

252 EMT in vivo, and analyze effects of Rho and Rho-kinase (ROCK) manipulation on cell motility in vivo.

253 being associated with activation of the Rho/Rho-kinase (ROCK) pathway.

254 Inhibition of Rho-kinase (ROCK) with fasudil blocked HG-induced podocy

255 to a variety of signaling pathways including Rho-kinase (ROCK).

256 The Rho kinases (ROCK1 and ROCK2) are highly homologous seri

257 Rho kinases (ROCK1 and ROCK2) function downstream of the

258 s installed on a small-molecule inhibitor of Rho kinase, Rockout, to generate a 'caged Rockout' deriv

259 Rho kinases (ROCKs) are involved in regulating a variety

260 Rho kinases (ROCKs) belong to a family of serine/threoni

261 Rho kinases (ROCKs) belong to the serine-threonine famil

262 Rho kinases (ROCKs) contribute to allergic airways disea

263 Rho kinases (ROCKs) play multiple roles in TGFbeta-induc

264 in activity sensor, we found that Drosophila Rho kinase (Rok) enriches for activated Myosin on the ne

265 r protein (HOXD10), RhoA/RhoC up-regulation, Rho-kinase (ROK) activation, and breast tumor cell invas

266 s tension in the epithelial layer increases, Rho kinase signaling activates myosin assembly and contr

267 to cell--cell junctions, where it suppressed Rho kinase signaling and stabilized the junctions.

268 Pharmacologic inhibition of Rho kinase signaling blocked LPA-induced p65 phosphoryla

269 EGF activates ERK/p90RSK and Rho/Rho kinase signaling in A431 and DiFi colon cancer cells

270 ed sphingosine kinase-1 (SK1) expression via Rho kinase signaling in renal proximal tubules; the S1P(

271 nal effect involving local regulation of the Rho kinase signaling pathway that controls these dynamic

272 o and in vitro, caused downregulation of the Rho kinase signaling pathway, a key mediator of cell sur

273 e/extracellular signal-regulated kinase, and Rho kinase signaling pathways are major effectors of RGS

274 ctivated the EGF receptor/ERK/p90RSK and Rho/Rho kinase signaling pathways.

275 Pharmacological inhibition of Rho kinase signaling re-established the synergistic apop

276 R and by cytoskeletal modulation via ERM and Rho kinase signaling.

277 o serum or LPA, nor any detectable change in Rho-kinase signaling activity.

278 to bone morphogenetic protein (BMP) and Rho/Rho-kinase signaling as well as functional pathways asso

279 ucose activated the protein kinase C and Rho/Rho-kinase signaling pathways and stimulated actin polym

280 Rho/Rho kinase signalling following TP stimulation and L-NAM

281 in and F-actin levels, and aberrantly mobile Rho-kinase structures.

282 ently of Rac, myosin light chain kinase, and Rho kinase, suggesting a passive physical mechanism.

283 and partially attenuated by an inhibitor of Rho kinase, suggesting that both pathways converge on FL

284 itors for Ser/Thr kinases, including PKC and Rho kinase that are known to activate Ezrin.

285 A, Rho1, promotes apoptosis independently of Rho kinase through its effects on c-Jun NH(2)-terminal k

286 pidermal microtubules function together with Rho kinase to promote the transport of E-cadherin to adh

287 We show that Rho GTPase recruits Rho-kinase to adherens junctions and is required for Rho

288 el molecular pathways/targets including RhoA/Rho kinase, tyrosine kinase, endothelial progenitor cell

289 nase IIIbeta, diacylglycerol kinase, Rho, or Rho-kinase was blocked, agonists of all three receptors

290 f the Wnt5a signaling intermediates Rac1 and Rho kinase, we demonstrated that Wnt5a-mediated inhibiti

291 t of myosin phosphatase that is inhibited by Rho-kinase, were increased in both the renal cortex and

292 GABA-mediated depolarization activates ROCK (Rho kinase), which in turn leads to the upregulation of

293 Thus, in contrast to Rho kinase, which generates actomyosin-based tension and

294 RhoA activates Rho kinase, which phosphorylates the regulatory subunit

295 was up-regulated and the activity of Rac and Rho kinases, which regulate the cytoskeleton and migrati

296 Inhibiting the RhoA pathway upstream of Rho kinase with a safe gene drug could provide a new enh

297 Inhibition of Rho kinase with Y27632 had no effects on ENaC response t

298 n with cytochalasin-D, but not inhibition of Rho kinase with Y27632, blocked TNF-alpha-induced retrac

299 LPA activated Rho kinase within minutes and subsequently the NF-kappaB

300 chioles, and inhibitors of RhoGEFs (Y16) and Rho-kinase (Y27632), but not the SrcFK inhibitor PP2, pr