ライフサイエンスコーパス: Y-27632

1 s in the presence of a Rho kinase inhibitor (Y-27632).

2 nstrate direct relaxation of the IAS SMCs by Y-27632.

3 1, or totally abolished by pretreatment with Y-27632.

4 1(G93A) mice with and without treatment with Y-27632.

5 were inhibited by the Rho-kinase inhibitor, Y-27632.

6 of dominant-negative RhoA and treatment with Y-27632.

7 (C3) or the blocking of ROCK activation with Y-27632.

8 le actin in myofibroblasts was attenuated by Y-27632.

9 OCK was inhibited with a specific inhibitor, Y-27632.

10 bited by the Rho-associated kinase inhibitor Y-27632.

11 hibitor C3 exoenzyme or Rho-kinase inhibitor Y-27632.

12 etely inhibited by the p160(ROCK) inhibitor, Y-27632.

13 nocodazole, and/or the Rho kinase inhibitor, Y-27632.

14 mpletely relaxed by the Rho kinase inhibitor Y-27632.

15 o, and this was inhibited in the presence of Y-27632.

16 the Rho-associated protein kinase inhibitor Y-27632.

17 o-associated protein kinase (ROCK) inhibitor Y-27632.

18 and (3) exposed to S aureus exoproducts and Y-27632.

19 conjunctival vasculature in the presence of Y-27632.

20 that was abolished with the ROCK inhibitor, Y-27632.

21 icantly reduced by calphostin-C but not with Y-27632.

22 icantly reduced by calphostin-C but not with Y-27632.

23 Rho-associated coiled-coil kinase inhibitor Y-27632.

24 r blocker BQ123 and completely by fasudil or Y-27632.

25 tion in response to the Rho-kinase inhibitor Y-27632.

26 TR90 was blunted by the Rho kinase inhibitor Y-27632.

27 irtually abolished by the rho kinase blocker Y-27632 (1 mum) and attenuated by the protein kinase C i

28 Treatment of HTM and SC cells with Y-27632 (10 microM) led to significant but reversible ch

29 iber formation with the Rho kinase inhibitor Y-27632 (10 microm) or actin polymerization with latrunc

30 rmeability increased (by 80%) in response to Y-27632 (10 microM) treatment, whereas myosin light-chai

31 n (0.1 micromol/L), the Rho kinase inhibitor Y-27632 (10 micromol/L), or L-citrulline (1 mmol/L).

32 -associated protein kinase (ROCK) inhibitors Y-27632 (10 muM) and GSK-269962 (50 nM) both abrogated t

33 0%) in enucleated porcine eyes perfused with Y-27632 (10-100 microM), and this effect was associated

34 Inhibition of Rho kinase with Y-27632 (30 microM) for 90-120 min induced F-actin reduc

35 Perfusion of microvessels with Y-27632 (30 microM) for up to 100 min reduced basal L(p)

36 iated protein kinase (ROCK) inhibition using Y-27632 (3T3+Y).

37 tment with the Rho kinase-specific inhibitor Y-27632 (5 microM).

38 The effects of Y-27632 (a Rho-kinase inhibitor) were assessed in first-

39 Experiments were repeated in the presence of Y 27632, a ROCK inhibitor.

40 esults that led to this model, we found that Y-27632, a Rho kinase inhibitor used to implicate myosin

41 ting from 3 different anatomical sites) with Y-27632, a Rho kinase inhibitor, greatly increased their

42 On the other hand, Y-27632, a Rho kinase-specific inhibitor, diminished myo

43 Y-27632, a Rho-dependent serine/threonine protein kinase

44 Administration of Y-27632, a selective Rock inhibitor, also preferentially

45 e report that a cocktail of small molecules, Y-27632, A-83-01, and CHIR99021, can convert rat and mou

46 The Rho kinase inhibitor Y-27632 abolished the antagonistic effect of mevalonate.

47 Chronic treatment with Rho-kinase inhibitor Y-27632 after chronic social defeat stress reverses depr

48 es and the small molecule inhibitor of ROCK, Y-27632, against the reciprocals of the peptide concentr

49 xin B or the Rho-associated kinase inhibitor Y-27632 also blocked TGF-beta1-stimulated alpha1(I) mRNA

50 Inhibition of p160ROCK with Y-27632 also promotes neurite outgrowth on myelin-associ

51 Y-27632 also significantly inhibited focus formation by

52 In addition, Y-27632, an inhibitor of the Rho effector p160ROCK/Rho k

53 Y-27632, an inhibitor of the Rho-associated kinase p160R

54 Y-27632, an inhibitor of the Rho-associated kinase ROCK,

55 rammed cells is mediated by a combination of Y-27632 and a diffusible factor (or factors) released by

56 Pretreatment with Y-27632 and blebbistatin (as inhibitors of actomyosin co

57 bited PdBU-induced force generation, whereas Y-27632 and c3 exoenzyme did not.

58 sts of the Rho-Rho kinase pathway, including Y-27632 and dominant-negative RhoA (RhoA-N19).

59 perty of stem cells, we investigated whether Y-27632 and feeder cells induced a stem-like phenotype.

60 n of CRCs is also reversible, and removal of Y-27632 and feeders allows the cells to differentiate no

61 In 5,5'-dimethyl-BAPTA-treated platelets, Y-27632 and HA 1077 completely abolished both ADP-induce

62 Both Y-27632 and HA 1077 reduced peak levels of ADP-induced p

63 The Rho kinase inhibitors Y-27632 and HA-1077 and expression of a dominant negativ

64 ent of HUVEC with the RhoA kinase inhibitors Y-27632 and HA-1077 caused dose-dependent cell death.

65 o) and Galpha(12/13) because pertussis toxin Y-27632 and had no effect, whereas U-73122 inhibition of

66 changing the substratum to type I collagen, Y-27632 and RhoA-N19 failed to inhibit the response.

67 Paradoxically, Y-27632 and RhoA-N19 increased ERK phosphorylation in MC

68 The Rho-kinase inhibitor Y-27632 and the protein kinase C (PKC) inhibitor GF10920

69 gh administration of the selective inhibitor Y-27632 and Western blot analysis.

70 hacrynic acid (ECA), a Rho kinase inhibitor (Y-27632), and H-7 (serine/threonine kinase inhibitor), w

71 ity and measured mechano-IC(50) for aspirin, Y-27632, and eptifibatide.

72 lls were treated with toxin B, exoenzyme C3, Y-27632, and HA1077.

73 recently developed specific ROCK inhibitor, Y-27632, and ROCK truncation mutants to investigate the

74 ration is dependent on both feeder cells and Y-27632, and the conditionally reprogrammed cells (CRCs)

75 Y-27632 blocked focus formation by RhoA and its guanine-

76 nhibitor, ML-7, or the rho kinase inhibitor, Y-27632, blocked lamella formation, myosin phosphorylati

77 nt of the cells with a RhoA kinase inhibitor Y-27632 blocks TGF-beta-induced stress fiber formation.

78 Y-27632 blocks the phosphorylation of profilin in HEK293

79 This effect was not attenuated by Y-27632 but could be inhibited by the MEK inhibitor, UO1

80 f Rho-effector kinase inhibitors Fasudil and Y-27632, but ATP-induced IL-1 beta release was unaffecte

81 , apart from neuroprotection, ROCK inhibitor Y-27632 can also accelerate regeneration of motor axons,

82 Although acute oral Y-27632 caused a marked and sustained decrease in mean p

83 In in vivo studies, the lower doses of Y-27632 caused a potent and selective decrease in the IA

84 In these phenotypes, Y-27632 caused marked (twofold or more) increases or dec

85 cantly higher and resistant to relaxation by Y 27632, compared with the H-ras(+/+) IAS.

86 kinase p160ROCK with the pyridine derivative Y-27632 completely abolished activation of NHE1 by integ

87 blast feeder cells and Rho kinase inhibitor, Y-27632, conditionally induces an indefinite proliferati

88 The IAS relaxation by Y-27632 correlated specifically with the decrease in ROK

89 Whereas Y-27632 decreased basal and depolarization-induced SRF e

90 these observations, the Rho kinase inhibitor Y-27632 decreased cell impedance (stiffness) of TM and S

91 In contrast, 5 minutes of inhaled Y-27632 decreased MPAP without reducing MSAP.

92 Inhibition of rho-kinase (Y-27632) decreased tonic force more than phasic, but had

93 Nocodazole alone or in combination with Y-27632 did not change the discoid shape of epitheliocyt

94 Y-27632 did not inhibit other well known survival pathwa

95 ent with the Rho-associated kinase inhibitor Y-27632 did not prevent FAK translocation and tyrosine p

96 In NIH3T3 cells, Y-27632 did not prevent the activation of serum response

97 inant negative Rho kinase, or treatment with Y-27632 disassembled microfilaments in normal NIH3T3 and

98 lockade of Rho-associated kinase (ROCK) with Y-27632 down-regulates adhesion strength in stationary,

99 s were treated with the Rho-kinase inhibitor Y-27632 either 30 minutes before, or 1 hour after they w

100 Y 27632 eliminated this difference.

101 ion of RhoA kinase by the specific inhibitor Y-27632 enhanced phorbol ester-stimulated alpha(4)beta(1

102 Furthermore, Y-27632 enhances sprouting of CST fibers in vivo and acc

103 Embryos treated with ROCK inhibitor Y-27632 exhibited elevated expression of ICM marker NANO

104 t ATP-competitive small molecule inhibitors (Y-27632, fasudil, hydroxyfasudil, and H-1152P).

105 + medium containing the Rho-kinase inhibitor Y-27632 for 1 to 2 hours.

106 combination with Rho-kinase inhibitor (ROCK) Y-27632 for the cultivation of HCEnCs from older donor c

107 partial reduction in the enhanced potency of Y-27632 found 24 hours after LPS.

108 nea-pig ureter, three Rho-kinase inhibitors, Y-27632, HA-1077 and H-1152, significantly decreased pha

109 However, Y-27632 had no effect on PIP(2) synthesis in lysates, al

110 1-aminoethyl)-cyclohexanecarboxamide, 2 HCl (Y-27632) had no effect on agonist-induced inhibition of

111 Repeated treatment of NIH3T3 cells with Y-27632, however, substantially disrupted their actin fi

112 RhoA/ROCK inhibitors (C3-exoenzmye, fasudil, Y-27632, ibuprofen, siRhoA, and p21) in experimental spi

113 Treatment with Y-27632 improved functional and morphological measures o

114 ation of RhoA signaling in the dKO mice with Y-27632 improved muscle regeneration and reduced the exp

115 Y-27632 improved RBC deformability (RCTT: 8.228 +/- 0.08

116 terial toxin, or inhibition of Rho kinase by Y-27632 in HTM cells led to significant but contrasting

117 vestigated the effects of the ROCK inhibitor Y-27632 in immunocompromised (CD-1 Nu) mice with orthoto

118 tudies examined the effects of ROK inhibitor Y-27632 in the tonic smooth muscle of the rat internal a

119 We demonstrate that a Rho kinase inhibitor (Y-27632), in combination with fibroblast feeder cells, i

120 Fibroblasts incubated with Y-27632 increased their degree of polarization by develo

121 The Rho kinase-specific inhibitor (Y-27632)-induced changes in actin stress fibers, focal a

122 crease in p53 protein level concomitant with Y-27632-induced cell death.

123 Y-27632-induced changes in SC cell monolayer permeabilit

124 Treatment with Y-27632 influenced neither integrin activation epitope n

125 a from all groups identified ROCK-supported (Y-27632 inhibitable) expression of 10 transcripts, inclu

126 e Rho adenovirus and inhibition of ROCK with Y-27632 inhibited Cch-stimulated PLD1 activity, increase

127 In addition, the p160ROCK-specific inhibitor Y-27632 inhibited increases in NHE1 activity in response

128 ition of the ROCK activity by treatment with Y-27632 inhibited the assembly of E-cadherin-based cell-

129 rix metalloproteinase had no effect, whereas Y-27632 inhibition of the Galpha(12/13)-mediated Rho kin

130 mutant or treatment with the ROCK inhibitor Y-27632 inhibits the apoptotic effect of PMA in LNCaP ce

131 f RhoA in the cells with RhoA/ROCK inhibitor Y-27632 led to reduced osteogenic potential and improved

132 on studies with pharmacological inhibitors (Y-27632, LY294002, PF271 and PP2) and inhibitory protein

133 s administration of the Rho kinase inhibitor Y-27632 nearly normalizes the pulmonary hypertension (PH

134 leuprolide, interferon alpha-2b, letrozole, Y-27632, octreotide, and human growth hormone, all deliv

135 hat of protein kinase A, H89, of Rho kinase, Y-27632, of mTOR, rapamycin, or of JNK, SP600125, preven

136 of profilin blocks the inhibitory effect of Y-27632 on both AR and Htt aggregation.

137 ine, resulted in a reversal of the effect of Y-27632 on diminished timolol maleate intraocular penetr

138 The hypotensive effect of inhaled Y-27632 on hypoxic PH was greater than that of inhaled n

139 could also reverse the inhibitory effect of Y-27632 on the action potential and Ca(2+) transient.

140 rum-coated plastic or endothelial cells with Y-27632 or C3 exoenzyme markedly reduced the rate of de-

141 Preincubation with Y-27632 or cytochalasin D blocked both the initial contr

142 h the Rho-associated kinase (ROCK) inhibitor Y-27632 or introduction of dominant negative ROCK or Rho

143 Treatment with Y-27632 or ML-7 that inhibits myosin phosphorylation and

144 as preincubation with the specific inhibitor Y-27632 or transfection with dominant negative ROCK, pre

145 Cells were exposed to the ROCK inhibitor Y-27632 or vehicle for 12 hours, and transcript levels a

146 led-coil-containing protein kinase inhibitor Y-27632, or by HA 1077.

147 ruses overnight or the inhibitors 1-butanol, Y-27632, or C3 exotoxin before stimulation with the chol

148 In contrast, treatment with ECA, Y-27632, or H-7 triggered changes in cell shape and redu

149 Treatment with Y-27632 partially inhibited the effects of vasopressin o

150 C inhibitor calphostin-C, Rho/ROCK inhibitor Y-27632, permeable Rho/ROCK inhibitor c3-exoenzyme, and

151 The Rho-associated kinase (ROCK) inhibitor Y-27632 permits hPSC survival upon dissociation; however

152 r, lens, and iris) versus eyes not receiving Y-27632 pretreatment.

153 Rho kinase inhibition by Y-27632 prevented CTGF and hydroxyproline, whereas the R

154 Finally, Y-27632 prevented the deleterious effects of S aureus ex

155 Both nifedipine and Y-27632 prevented the depolarization-induced increase in

156 The ROK inhibitor, Y-27632, prevented depolarization-induced increase in SM

157 pe of epitheliocytes, however treatment with Y-27632 produced thinning of the lamellar cytoplasm.

158 pletely blocked S1P-mediated contraction and Y-27632 reduced it.

159 ive, treatment with the Rho-kinase inhibitor Y-27632 reduced vessel constriction and PH in Pbx-mutant

160 The ROCK inhibitor Y-27632 reduces Htt toxicity in fly and mouse models.

161 Using pharmacologic antagonism (Y-27632, ref.

162 nd treatment with a ROCK specific inhibitor (Y-27632), respectively.

163 associated protein kinase (ROCK) with C3 and Y-27632, respectively.

164 alpha]quinoxalin-1-one was able to bring the Y-27632 response back to normal both 6 and 24 hours afte

165 Importantly, Y-27632 restored epithelial repair and lamellipodial dyn

166 o-associated protein kinase (ROCK) inhibitor Y-27632 restored migration suggesting that ROCK-dependen

167 Further, the ROCK inhibitor Y-27632 restored terminal differentiation in rapamycin-t

168 Blocking Rho kinase by means of Y-27632 resulted in a 50% and greater reduction in power

169 Pretreatment of the eyes of NZW rabbits with Y-27632 resulted in aggregate fold reductions (1 hour, 0

170 sociated coiled-coil kinase (ROCK) inhibitor Y-27632 reversed this effect by MK2-K339R, which strongl

171 bitor of RhoA signalling (the ROCK inhibitor Y-27632) reversed the increased cell migration phenotype

172 lipopolysaccharide groups, administration of Y-27632 reverted the hyperreactivity to vasopressin.

173 ess fibers was comparable to that induced by Y-27632 (Rho kinase inhibitor).

174 rase technique following RBC incubation with Y-27632 (Rho-kinase inhibitor to increase deformability)

175 r, respectively) normalized the responses to Y-27632 seen 6 hours after LPS.

176 rase or ROK-alpha by the specific inhibitor, Y-27632, showed a decrease in the phosphorylation mediat

177 e demonstrated that the Rho kinase inhibitor Y-27632, significantly suppresses keratinocyte different

178 activated receptor-gamma agonist, along with Y-27632 synergistically diminished dissociation-induced

179 ogical inhibition of ROCK1/2 using 10 microM Y-27632 (the IC(50) for this compound in ECs) strongly d

180 When treated with Y-27632, the cells acquired a polarized, elongate shape

181 203580, simvastatin, or Rho-kinase inhibitor Y-27632, the detrimental effect of CRP on bradykinin-ind

182 of RhoA or treated with Rho-kinase inhibitor Y-27632 transformed most edge cells into leader-like cel

183 Y-27632-treated embryos failed to accumulate YAP in the

184 Y-27632 treatment did not increase the lifespan of sympt

185 her hand, CC-RCCVHL cells were sensitized to Y-27632 treatment in hypoxia (2% O2).

186 Similarly, Y-27632 treatment increased stimulated beta(2) integrin-

187 Finally, Y-27632 treatment inhibited growth of subcutaneous 786-O

188 cient CC-RCC had a protective effect against Y-27632 treatment, mimicking VHL reintroduction.

189 ficient CC-RCC, thus mimicking the effect of Y-27632 treatment, whereas downregulation of ROCK2 had n

190 6B, PRKCZ, SCRIB, and LLGL1, was dampened by Y-27632 treatment, whereas some of the polarization even

191 In both fibroblast groups Y-27632-treatment increased expression of endothelin rec

192 e, or brinzolamide incubated with or without Y-27632 was determined in vertical Franz diffusion cells

193 These results suggested that inhaled Y-27632 was more effective than inhaled nitric oxide as

194 The increased potency of Y-27632 was partially reversed by endothelium removal at

195 The ROCK inhibitor, Y-27632, was identified and validated for selective targ

196 A specific inhibitor of ROCK, Y-27632, was used to examine the role of ROCK in the reg

197 The ATP-competitive inhibitors AMP-PCP and Y-27632 were noncompetitive inhibitors versus S6 peptide

198 Proregenerative effects of Y-27632 were studied during the disease course in the SO

199 gative rhoA and by the rho-kinase inhibitor, Y-27632, which also inhibited myosin light-chain phospho

200 thelial cells with either the ROCK inhibitor Y-27632, which destabilizes stress fibers, or the actin

201 pretreatment of cells with either HA1077 or Y-27632, which inhibit the kinases downstream of RhoA.

202 ncreased cloning efficiency (2-3-fold versus Y-27632) without affecting pluripotency of hPSCs.

203 In this study, we tested if oral or inhaled Y-27632 would be an effective and selective pulmonary va

204 of RhoA signaling, the Rho kinase inhibitor Y-27632, yielded similar results.