ライフサイエンスコーパス: ROCK

1 ROCK activity and 8-isoprostane-induced ROCK activation

2 ROCK and myosin II inhibition reduced long-term contract

3 ROCK could increase the transcriptional activity of c-My

4 ROCK inhibition enables maintenance of stem cell phenoty

5 ROCK inhibition reversed established fibrosis in a chron

6 ROCK inhibitor (ROCK-I) prevented upregulation of RhoA/R

7 ROCK inhibitors may be useful for the various pathologie

8 ROCK is expressed in fibroblastic, epithelial, endotheli

9 ROCK-I maintained the intracavernous pressure and non-ad

10 ROCKs also play a role in lymphocyte proliferation and m

11 , the properties and development of over 170 ROCK inhibitors as well as their therapeutic potential,

12 1 acted through Rho-dependent kinase LET-502/ROCK and activated a conserved, retrograde DLK-1 MAPK (D

13 es or the activity of the Rho kinase LET-502/ROCK were partially compromised.

14 Similarly, fasudil, a ROCK inhibitor used clinically to treat cerebral vasospa

15 In particular, the ability for a ROCK-inhibitor to diminish the effect of TGFbeta on TM w

16 ent chemical screen, revealing that H1152, a ROCK inhibitor, promotes the robust generation of insuli

17 In the presence of a ROCK inhibitor, PAIP2 expression is enhanced by the tran

18 of these cells, similar to the effects of a ROCK inhibitor.

19 Depletion or inactivation of a ROCK-dependent regulator of actin remodelling, the formi

20 we evaluated the effects of a locally acting ROCK inhibitor (AMA0825) on intestinal fibrosis.

21 he bone marrow supernatants, which activated ROCK in LSK cells and sensitized them for stromal-derive

22 The fact that the active ROCK inhibitor RKI-18, but not the inactive closely rela

23 (22) To develop more advanced ROCK inhibitors targeting various potential applications

24 pounds display subnanomolar activity against ROCK and strong differences of functional activity betwe

25 IC50 < 25 nM), excellent selectivity against ROCK and JNK kinases (>400-fold), potent inhibition of c

26 ured cells (through a pathway involving AKT, ROCK and CDK2/Cyclin E-nucleophosmin) and in mouse tissu

27 unds also inhibit the Rho-kinases ROCK 1 and ROCK 2 and we show they potently inhibit ROCK activity i

28 triggered signalling pathways PI(3)K-Akt and ROCK-MLCK.

29 d the protective function of antioxidant and ROCK-inhibitor treatments.

30 3T3-J2 feeder cells and ROCK inhibition allowed rapid expansion of airway basal

31 activity, which could be rescued by IKK and ROCK inhibitors.

32 lthough previous work suggests that MLCK and ROCK control distinct pools of cellular SFs, it remains

33 The effects of MLCK and ROCK on single-SF mechanics may be correspondingly pheno

34 ellular laser ablation reveals that MLCK and ROCK quantitatively regulate the viscoelastic properties

35 r results point to a model in which MLCK and ROCK regulate peripheral and central SF viscoelastic pro

36 transport and reveals a new role for PAK and ROCK in the regulation of IF precursor transport.

37 e of their effector proteins such as PAK and ROCK, are likely anti-cancer targets for treating K-Ras-

38 Upregulation of both PKA and ROCK has been reported in Ophn1(-/y) mice, but it remain

39 sequential activation of PI3 kinase, Rho and ROCK, leading to activation of Myc through phosphorylati

40 Inhibition of RhoA and ROCK activity partially restores osteogenic differentiat

41 Interfering with RhoA and ROCK function abolishes endothelial permeability, while

42 nown ROCK target, and inhibitors of RhoA and ROCK reversed the suppressive effect of 5-HT on efferocy

43 rs, activated glioma Rho/ROCK signaling, and ROCK inhibition decreased invasion toward SVZ NPC-secret

44 yc by promoting c-Myc protein stability, and ROCK inhibition reduced c-Myc-mediated expression of mRN

45 d passive cutaneous anaphylaxis in vivo, and ROCK inhibitors protect from lethal systemic anaphylaxis

46 , suggesting that centrally localized apical ROCK/myosin activity promotes contraction.

47 Fasudil, a clinically approved ROCK inhibitor, suppressed rough eye phenotype and mitig

48 ROCK1 knockdown, treatment with the approved ROCK inhibitor fasudil resulted in increased apoptosis a

49 ith SMAD4-independent BMP signaling, such as ROCK inhibitors, might be developed as therapeutics for

50 mics analysis identified differences between ROCK-treated and untreated cells as early as 12 hrs.

51 lts suggest that synthetic lethality between ROCK inhibition and VHL deficiency is dependent on HIF a

52 Here, we report the identification of a BMP7-ROCK signaling axis regulating beige adipocyte formation

53 cell lines and its levels are controlled by ROCK-JAK-STAT3 signalling.

54 The regulation of miRNA function by ROCK inhibitors is mediated, at least in part, by poly(A

55 ic homeostasis, which is mediated in part by ROCK, and alteration of this homeostasis influences card

56 chronic myeloid leukemia (aCML), preceded by ROCK hyperactivation, centrosome amplification, and cyto

57 activity in the MPG, which were prevented by ROCK-I.

58 In these cells, ROCK inhibition potentiated autophagy, which was require

59 Consequently, ROCK inhibitors are of interest for treating multiple in

60 ilized F-actin polymerization by controlling ROCK signaling.

61 1 signaling in adipose tissue by controlling ROCK-dependent phosphorylation of the insulin receptor s

62 Dysregulated ROCK activity has been implicated in several human patho

63 e physiological and biological functions for ROCK, the properties and development of over 170 ROCK in

64 izes to the plasma membrane, is required for ROCK-mediated cell contraction from 2 hr post infection.

65 ar, the molecular mechanisms responsible for ROCK-governed tumor cell growth have not been clearly el

66 Our results reveal an indispensable role for ROCK, yet redundant role for isoforms 1 and 2, in cell c

67 Conversely, graded ROCK overexpression preferentially increases RLC diphosp

68 Four conditions including and excluding HA + ROCK and its effect on early attachment rates and prolif

69 ce within 10-15 days when cultured with HA + ROCK.

70 phopeptide-based proteomic screen identified ROCK (Rho-associated kinase) as a putative substrate for

71 Importantly, ROCK inhibition in the BM of patients underexpressing mo

72 dependent manner, in part via a decrease in ROCK 1 expression through inhibition of the phosphorylat

73 tiation, except for known targets, including ROCK and ezrin, claudin-4 expression, and barrier permea

74 cell morphology and motility, and increased ROCK activity contributes to cancer cell invasion and me

75 RK knockdown cardiomyocytes showed increased ROCK activity.

76 sults in a blockade of 8-isoprostane-induced ROCK activation and restoration of VEGF activity.

77 ROCK activity and 8-isoprostane-induced ROCK activation were significantly higher in SSc ECs, wh

78 and ROCK 2 and we show they potently inhibit ROCK activity in melanoma cells in culture and in vivo.

79 , to translocate to EC junctions, to inhibit ROCK activity, and to maintain EC junctional integrity.

80 ication and genomic stability, by inhibiting ROCK.

81 A) in combination with Rho-kinase inhibitor (ROCK) Y-27632 for the cultivation of HCEnCs from older d

82 No Rho-associated kinase inhibitor (ROCK-i), or centrifugation was needed and the side effec

83 ROCK inhibitor (ROCK-I) prevented upregulation of RhoA/ROCK pathway as w

84 K1/PAK-1, and a RhoA-like pathway, involving ROCK/LET-502, control the remodeling of apical junctions

85 K14.ROCK(er)/HK1.ras(1205) papillomatogenesis also required

86 romotion stimulus, confirmed by breeding K14.ROCK(er) into promotion-insensitive HK1.ras(1276) mice,

87 ilar to HK1.ras(1205) controls; however, K14.ROCK(er)/HK1.ras(1205) histotypes comprised a mixed papi

88 .ras(1276) mice, suggesting a permissive K14.ROCK(er)/HK1.ras(1205) papilloma context (wound-promoted

89 ted/NF-kappaB(+)/p53(-)/p21(+)) preceded K14.ROCK(er)-mediated (p-Mypt1/tenascin C/rigidity) malignan

90 -hydroxytamoxifen (4HT)-activated ROCK2 (K14.ROCK(er)) were crossed with mice expressing epidermal-ac

91 At 8 weeks, 4HT-treated K14.ROCK(er)/HK1.ras(1205) cohorts exhibited papillomas simi

92 By 12 weeks, K14.ROCK(er)/HK1.ras(1205) wdSCCs exhibited increased NF-kap

93 s process requires the RhoA-activated kinase ROCK, suggesting that Cdc42 activation at one side of a

94 ivity against the closely related AGC kinase ROCK.

95 on, via activation of Rho-associated kinase (ROCK) and the stress kinase p38, leads to further p53 el

96 Rho-associated kinase (ROCK) has an essential role in governing cell morphology

97 The Rho-associated kinase (ROCK) inhibitor Y-27632 permits hPSC survival upon disso

98 says with a selective Rho-associated kinase (ROCK) inhibitor, Galpha12/13 knockdown and activated Rho

99 ceptor (TXAR) and the Rho-associated kinase (ROCK) pathway.

100 Inhibition of Rho-associated kinase (ROCK) prevented cytoskeletal defects, while inhibiting m

101 ough a Rho-GTPase and Rho-associated kinase (ROCK).

102 ain kinase (MLCK) and Rho-associated kinase (ROCK).

103 argeted inhibition of Rho-associated kinase (ROCK)2 downregulates the proinflammatory T cell response

104 levated expression of Rho-associated kinase (ROCK)2 is associated with poor patient survival.

105 [Rho-associated coiled-coil-forming kinase (ROCK)]/LIM domain kinase signaling pathway in DCs, which

106 ncreased in a Rho-associated protein kinase (ROCK) activation and cell contraction-dependent manner.

107 y to activate Rho-associated protein kinase (ROCK) in WTs.

108 NI), RhoA and Rho-associated protein kinase (ROCK) increase in penile endothelial and smooth muscle c

109 broblasts and Rho-associated protein kinase (ROCK) inhibition using Y-27632 (3T3+Y).

110 based on the Rho-associated protein kinase (ROCK) inhibitor Y-27632.

111 however, the Rho-associated protein kinase (ROCK) inhibitors Y-27632 (10 muM) and GSK-269962 (50 nM)

112 ated, coiled-coil-containing protein kinase (ROCK) inhibitors.

113 Rho-associated protein kinase (ROCK) is required for both high-speed migration and stra

114 ated, coiled-coil containing protein kinase (ROCK) pathway.

115 n of RhoA and Rho-associated protein kinase (ROCK) with C3 and Y-27632, respectively.

116 ated, coiled-coil-containing protein kinase (ROCK), ERK, or PI3K.

117 tream target, Rho-associated protein kinase (ROCK), restored megakaryocyte proplatelet formation in t

118 nd downstream Rho-associated protein kinase (ROCK).

119 ated, coiled-coil containing protein kinase (ROCK).

120 stiffness sensing by increasing Rho kinase (ROCK) activity, resulting in increased transcription med

121 contractility pathway involving Rho kinase (ROCK) and myosin light chain kinase (MLCK), culminating

122 asts was dependent on intact Rho/Rho kinase (ROCK) and myosin signals inasmuch as treatment with Y276

123 e anomalies are primarily due to Rho kinase (ROCK) controlled excessive contractile myosin-II activit

124 Rho kinase (ROCK) is a serine/threonine protein kinase that regulate

125 n of polo-like kinase 1 and RhoA/Rho kinase (ROCK) leads to the synergistic effects in KRAS-mutant ca

126 -HT signals to activate the RhoA/Rho kinase (ROCK) pathway, a pathway known for its ability to regula

127 In contrast, Rho kinase (ROCK) regulates myosin accumulation at the cell rear and

128 loss of function, we found that Rho kinase (ROCK) signaling was constitutively activated, resulting

129 rho-Kinase (ROCK) activity was increased specifically in bone marrow

130 tin ULFs is further regulated by Rho-kinase (ROCK) and p21-activated kinase (PAK): ROCK inhibits ULF

131 Inhibition of Rho-kinase (ROCK) with fasudil blocked HG-induced podocyte MP format

132 oA through its effector kinase, RhoA kinase (ROCK), activates myosin II to form actomyosin filament b

133 ant version of the myosin-activating kinase, ROCK, that localizes diffusely, rather than centrally, i

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

135 Rho kinases (ROCKs) are involved in regulating a variety of physiolog

136 Rho kinases (ROCKs) belong to the serine-threonine family, the inhibi

137 Rho kinases (ROCKs) contribute to allergic airways disease.

138 Rho kinases (ROCKs) play multiple roles in TGFbeta-induced myofibrobl

139 osin phosphatase subunit 1 (Mypt-1), a known ROCK target, and inhibitors of RhoA and ROCK reversed th

140 Local ROCK inhibition prevents and reverses intestinal fibrosi

141 Overall, our results show that local ROCK inhibition is promising for counteracting fibrosis

142 Molecularly, ROCK inhibition induced glycogen synthase kinase 3beta-d

143 hPSCs were exposed to 10 muM ROCK inhibitor for varying exposure times.

144 EBs from dissociated hESCs in the absence of ROCK-i and centrifugation was achieved within an optimal

145 BB disruption is caused by the activation of ROCK/MLC signalling, persistent actin polymerization and

146 the notion that anti-fibrotic activities of ROCK-inhibitors could counteract the elevation of IOP an

147 In contrast, there was no effect of ROCK insufficiency on allergic airways inflammation, alt

148 ifugation was needed and the side effects of ROCK-i can be avoided.

149 a continuing effort toward identification of ROCK inhibitors, we here report the design, synthesis, a

150 Inhibition of ROCK (Rho-associated protein kinase), downstream of RhoA

151 Accordingly, inhibition of ROCK activity or MLC function promotes enrichment of DOC

152 sin II ATPase activity than to inhibition of ROCK activity, but viscosity is highly sensitive to both

153 destabilization was rescued by inhibition of ROCK and histone deacetylase 6 but not by a GAP-mutant f

154 Therefore, inhibition of ROCK and its stimulated signaling might prove to be a pr

155 anotransducers were rescued by inhibition of ROCK and phenocopied by JAM-A, JACOP, or p114RhoGEF down

156 However, systemic inhibition of ROCK is expected to result in significant side effects.

157 Here we showed that inhibition of ROCK kinase activity, either by a selective ROCK inhibit

158 In addition, in vivo inhibition of ROCK partially rescued the in vivo Snrk cmcKO cardiac fu

159 Pharmacologic inhibition of ROCK reduced metastasis of colorectal xenograft tumors i

160 tically, our data suggest that inhibition of ROCK reduces the ability of melanoma cells to efficientl

161 nts raise the possibility that inhibition of ROCK signaling could be a useful therapeutic approach to

162 Small-molecule inhibition of ROCK suppressed MYCN-driven neuroblastoma growth in TH-M

163 t transformation suggests that inhibition of ROCK with RKI-18 results in preventing migration, invasi

164 Inhibition of ROCK, a key regulator of cell migration, in neuroblastom

165 Inhibition of ROCK, ERK, or PI3K/Akt blocked sHA/TSG-6-mediated AHR.

166 sults suggest that these novel inhibitors of ROCK may be beneficial in the treatment of metastasis.

167 c signaling module for spatial regulation of ROCK activity, actomyosin contractility, and epithelial

168 Importantly, the role of ROCK in hematopoiesis or leukemogenesis in the context o

169 d some light into the physiologic role(s) of ROCK in both normal and abnormal hematopoiesis.

170 1 signaling, coupled with the suppression of ROCK and activation of cofilin-mediated actin reorganiza

171 Suppression of ROCK-c-Myc downstream molecules, such as c-Myc-regulated

172 le cell cultures that are achieved by use of ROCK (Rho kinase) inhibitors.

173 e conclusions with regard to the function of ROCKs have involved the use of cell line models, pharmac

174 models identify pharmacologic inhibition of ROCKs as a mechanism-based approach to reduce tau levels

175 invasive potential of ARMS cells depended on ROCK activity, which is regulated by the GTPase RhoE.

176 Malignancy depended on ROCK(er)/p-Mypt1 expression, as cessation of 4HT treatme

177 n to exert a positive feedback regulation on ROCK by increasing RhoA mRNA expression.

178 nalysis confirmed key amino acid residues on ROCK that are phosphorylated by SNRK.

179 The Rho kinases, or ROCKs, are a family of serine-threonine kinases that ser

180 o-inflammatory cytokine secretion from other ROCK-positive cell types, corroborating the selective in

181 In addition, two other ROCK inhibitors, RKI 1447 and GSK 429286, selectively ta

182 inase (ROCK) and p21-activated kinase (PAK): ROCK inhibits ULF transport, while PAK stimulates it.

183 s use actomyosin contractility driven by Rho-ROCK and JAK-STAT3 to migrate efficiently.

184 rthermore, pharmacological inhibition of Rho-ROCK effectively reduced PTHLH production and breast can

185 Here, we showed that inhibition of RHO-ROCK signaling enhances ICM and suppresses TE characteri

186 Activation of Rho-ROCK signaling in the absence of DLC1 mediated SMAD3 lin

187 tegrity, which is partially dependent on Rho-ROCK signalling, and that disruption of MEKK3:CCM2 inter

188 ic navigation, was modestly dependent on Rho-ROCK-myosin II signaling on a 2D substrate or in a loose

189 These results suggest that RHO-ROCK signaling plays an essential role in regulating Hip

190 ar envelope rupture sites and define the Rho-ROCK pathway as the driver of nuclear damage.

191 t GIT2 is targeted to FAs in response to Rho-ROCK signaling and actomyosin contractility.

192 er, we found that myosin IIA responds to Rho-ROCK signaling to support junctional tension in MCF-7 ce

193 eover, the activation of the Galpha12/13/Rho/ROCK pathway in myofibroblasts by FTY720-P caused potent

194 -P selectively activated the Galpha12/13/Rho/ROCK pathway via the S1P2 receptor.

195 S1P similarly activated Galpha12/13/Rho/ROCK signaling via S1P2 receptors, whereas the two selec

196 FTY720-P potently activated Galpha12/13/Rho/ROCK signaling.

197 additional pathways, such as Galpha12/13/Rho/ROCK signaling.

198 Caspase-3 inhibition and a Rho/ROCK inhibitor prevented rapamycin-induced increases in

199 ay, via the Galphaq-11, PLCbeta/PKC, and Rho/ROCK signaling pathways.

200 by suppression of Rho pathway either by Rho/ROCK inhibitors, or by shRNA repression.

201 of these effects was likely mitigated by Rho/ROCK, Rho/ROCK pathway inhibition via Y27632 disrupted c

202 h the binding partners, activated glioma Rho/ROCK signaling, and ROCK inhibition decreased invasion t

203 Application of Rho/ROCK inhibitors produced the same effect as introduction

204 ens junction formation via activation of Rho/ROCK, CDC42, and caveolin endocytosis-dependent pathways

205 ffects was likely mitigated by Rho/ROCK, Rho/ROCK pathway inhibition via Y27632 disrupted cell-cell j

206 al activity of CAFs, as regulated by the Rho/ROCK pathway, contributes to increased blood vessel grow

207 We also show that platelets, via the Rho/ROCK pathway, synergistically couple mechanical and bioc

208 rix adhesion molecule, vinculin, and the Rho/ROCK pathway, which transduces signals provided by extra

209 tly promote myometrial contractility via Rho/ROCK signaling, thus contributing to preterm labor-media

210 gnalling to inhibit Rac1 and activate a RhoA-ROCK-Formin homology domain-containing 3 (FHOD3) pathway

211 ogue, to modulate cell contraction in a RhoA-ROCK-independent manner.

212 s by altering synaptic connections, and RhoA-ROCK inhibition enhances functional recovery by blocking

213 To test this hypothesis, RhoA-ROCK signaling was blocked by RhoA deletion from postnat

214 nd cognitive performance and inhibiting RhoA-ROCK signaling alleviates these deficits.

215 TAT3 signaling downstream of p120-Kaiso-RhoA-ROCK signaling.

216 st progenitors by activating p120-Kaiso-RhoA-ROCK-canonical BMP signaling.

217 ette formation, whereas G12/13-mediated RhoA-ROCK signaling suppresses the remodeling process.

218 Moreover, RhoA-ROCK inhibition prevents TBI-induced spine remodeling an

219 olecules involved in metastasis, namely RhoA-ROCK and N-WASP.

220 l adhesions, resulting in activation of RhoA-ROCK signalling to myosin II and cell contraction.

221 The RhoA-ROCK signaling pathway is a potential therapeutic target

222 Moreover, we identified a role for the RhoA-ROCK-myosin II signaling axis in this MeV internalizatio

223 dent upon LKB1 farnesylation leading to RhoA-ROCK-mediated stress fiber formation, but membrane dynam

224 RhoA/ROCK inhibition was found to improve locomotor outcome b

225 RhoA/ROCK signalling regulates an activity-dependent Rdx phos

226 AK/p190RhoGAP complex to downregulate a RhoA/ROCK/Ezrin pathway at the ECM interface.

227 Here we show that TGFbeta-activated RhoA/ROCK signalling functions as a molecular switch regardin

228 Taking into account publication bias, RhoA/ROCK inhibition improves functional outcome in experimen

229 distinct signaling pathways mediated by RhoA/ROCK and Src Family Kinases, respectively.

230 aining 3 (FHOD3), which is activated by RhoA/ROCK, establishing a novel mechanism through which the R

231 as a cytoskeletal rheostat controlling RhoA/ROCK protein expression during PDAC cell migration and m

232 on of this network uncovered a critical RhoA/ROCK signaling node that operates downstream of eIF5A in

233 Our findings also implicate the eIF5A/RhoA/ROCK module as a potential new therapeutic target to tre

234 de and cell shortening, and facilitated RhoA/ROCK/LIMK1-mediated cofilin phosphorylation.

235 ll migration and invasion by modulating RhoA/ROCK protein expression levels.

236 egulated gene and protein expression of RhoA/ROCK and caspase-3 mediated apoptosis in the major pelvi

237 Inactivation of RhoA/ROCK in MSCs induces matrix metalloproteinase-3-mediated

238 esults indicate that the combination of RhoA/ROCK inhibition and glucocorticoid treatment in dystroph

239 also revealed the synergistic effect of RhoA/ROCK inhibition and glucocorticoid treatment, which coul

240 selected if they reported the effect of RhoA/ROCK inhibitors (C3-exoenzmye, fasudil, Y-27632, ibuprof

241 itor (ROCK-I) prevented upregulation of RhoA/ROCK pathway as well as activation of caspase-3 in the M

242 We evaluated the role of RhoA/ROCK pathway in CN regulation following CNI using a vali

243 hese results suggest that activation of RhoA/ROCK pathway mediates caspase-3 dependent apoptosis of n

244 capitulate the effects of inhibition of RhoA/ROCK pathway on NMII isoform localization; thus, cytokin

245 generation is hampered by activation of RhoA/ROCK pathway.

246 Inhibition of RhoA/ROCK signaling abolished the localization of NMIIB, wher

247 by co-administration of an inhibitor of RhoA/ROCK signaling, which can be activated by glucocorticoid

248 uppress efferocytosis via activation of RhoA/ROCK.

249 calize at the furrow by focusing on the RhoA/ROCK pathway that has a low activity in polyploid megaka

250 teins including proteins activating the RhoA/ROCK pathway, known to induce amoeboid properties and de

251 mmune response that is inhibited by the RhoA/ROCK pathway.

252 tribute the resultant repolarization to RhoA/ROCK-mediated redistribution of beta-Pix, which activate

253 erferes with the metastatic process via RhoA/ROCK signaling in neuroblastoma cells.

254 differentiate into myofibroblasts when RhoA/ROCK is turned on, endothelial cells when turned off.

255 Our results indicate that the RhoE/ROCK/ARHGAP25 signaling pathway promotes ARMS invasive p

256 ROCK kinase activity, either by a selective ROCK inhibitor Y27632 or by specific ROCK small interfer

257 re-based design, led to potent and selective ROCK inhibitors.

258 ign, synthesis, and evaluation of novel soft ROCK inhibitors displaying an ester function allowing th

259 lective ROCK inhibitor Y27632 or by specific ROCK small interfering RNA (siRNA) molecules, attenuated

260 As such, ROCK inhibitors have potential therapeutic applicability

261 RKI-18 suppresses ROCK-mediated actin fiber formation, following stimulati

262 Because systemic ROCK inhibition causes cardiovascular side effects, we e

263 of molecular targeting (fibronectin, talin, ROCK), including 'adaptive switching' between Continuous

264 ic neurons in the MPG following CNI and that ROCK-I can prevent post-prostatectomy ED.

265 These data identify that ROCK-dependent intermittent T cell migration regulates t

266 Our observations indicate that ROCK activation is a tumor promoter in human cutaneous S

267 tly, mechanistic investigation revealed that ROCK endowed cancer cells with tumorigenic capability, m

268 Burgeoning data suggest that ROCK is also involved in the growth regulation of tumor

269 In blood cells, emerging data suggest that ROCK plays an essential role in negatively regulating in

270 Findings, thus far, suggest that ROCK plays an essential role in regulating growth and su

271 matinib to induce apoptosis, suggesting that ROCK inhibitors, combined with imatinib treatment, can o

272 The ROCK inhibitor, fasudil, also reduced airway responsiven

273 The ROCK inhibitor, Y-27632, was identified and validated fo

274 and cardiac looping defects observed in the ROCK inhibitor treated zebrafish.

275 We investigated the effects of the ROCK inhibitor Y-27632 in immunocompromised (CD-1 Nu) mi

276 ppresses potently the phosphorylation of the ROCK substrate myosin light chain 2 (MLC2) in intact hum

277 dopodia maturation by acting upstream of the ROCK-LIMK-Cofilin pathway through the control of RhoC GT

278 n, chemotaxis and adhesion downstream of the ROCK-LIMK-cofilin signalling axis.

279 A new study reveals that the ROCK proteins play key roles in the formation of tumours

280 from postnatal neurons or treatment with the ROCK inhibitor fasudil.

281 The ROCKs are increasingly recognized as critical coordinato

282 In recent years, an important role for the ROCKs in the regulation of immune responses is also bein

283 oaches that could be employed to inhibit the ROCKs in autoimmune disorders.

284 Given the potential promise of the ROCKs as therapeutic targets, we also outline the approa

285 We provide an overview of the role of the ROCKs in immune cells and discuss studies that highlight

286 rt differential functional effects for these ROCKs at the epithelial zonula adherens (ZA).

287 complex, which attracts glioma cells through ROCK/Rho activation.

288 regulates transendothelial migration through ROCK signaling.

289 Thus, ROCK inhibitors represent potential therapeutics for VHL

290 dependent on RhoC and not RhoA signaling to ROCK.

291 VHL cells is sufficient to sensitize them to ROCK inhibition.

292 n of upstream TGF-beta signaling, triggering ROCK activity and its downstream effects on desmosomal g

293 To date, two ROCK inhibitors have been approved for clinical use in J

294 We have found that the two ROCK isoforms, ROCK1 and ROCK2, differentially regulate

295 ed to determine the contributions of the two ROCK isoforms, ROCK1 and ROCK2, to AHR, inflammation and

296 ucleation) and Rho-mediated contraction (via ROCK phosphorylation of myosin light chain), which are c

297 nt BMP signaling activated Rho signaling via ROCK and LIM domain kinase (LIMK).

298 Embryos treated with ROCK inhibitor Y-27632 exhibited elevated expression of

299 CC-RCC treatment with ROCK inhibitors is cytotoxic and cytostatic based on bro

300 lly defined and xeno-free conditions without ROCK inhibitors.