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

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

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

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

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

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

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

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

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

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

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

13 conjunctival vasculature in the presence of Y-27632.

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

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

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

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

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

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

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

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

22 1, or totally abolished by pretreatment with Y-27632.

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

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

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

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

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

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

29 0%) in enucleated porcine eyes perfused with Y-27632 (10-100 microM), and this effect was associated

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

46 Y-27632 also significantly inhibited focus formation by

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

72 Y-27632 blocks the phosphorylation of profilin in HEK293

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

93 Y 27632 eliminated this difference.

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

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

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

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

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

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

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

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

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

103 1-aminoethyl)-cyclohexanecarboxamide, 2 HCl (Y-27632) had no effect on agonist-induced inhibition of

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

151 Using pharmacologic antagonism (Y-27632, ref.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

169 203580, simvastatin, or Rho-kinase inhibitor Y-27632, the detrimental effect of CRP on bradykinin-ind

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

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

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

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

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

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

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

177 6B, PRKCZ, SCRIB, and LLGL1, was dampened by Y-27632 treatment, whereas some of the polarization even

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

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

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

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

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

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

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

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

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

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

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

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

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