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 inhibition enables maintenance of stem cell phenoty

4 ROCK inhibition furthermore selectively decreases the pr

5 ROCK inhibition rescued cytoskeletal or junctional integ

6 ROCK inhibition reversed established fibrosis in a chron

7 ROCK inhibition was associated with normalization of the

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

9 ROCK inhibitors may be useful for the various pathologie

10 ROCK is expressed in fibroblastic, epithelial, endotheli

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

12 ROCK-myosin II ablation specifically kills resistant cel

13 ROCK-Myosin II drives fast rounded-amoeboid migration in

14 ROCKs also play a role in lymphocyte proliferation and m

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

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

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

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

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

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

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

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

23 Abeta(42) oligomers can activate ROCKs.

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

25 Constitutively active ROCK enhanced ARM and impaired PSD-LTM, while decreasing

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

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

28 bortezomib; BTZ) and BMME-disrupting agents (ROCK inhibitor) to overcome BMME-induced drug resistance

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

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

31 by AKT2 and elevated FAK-kinase activity and ROCK-RhoA levels but low levels of paxillin phosphorylat

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

33 c protein kinases such as AKT, RSK, AMPK and ROCK.

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

35 coprotein ligand-1 (PSGL-1)-targeted BTZ and ROCK inhibitor-loaded liposomes is more effective than f

36 3T3-J2 feeder cells and ROCK inhibition allowed rapid expansion of airway basal

37 excellent kinase selectivity for ROCK I and ROCK II against 387 other kinases.

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

39 ng eosinophils exhibit reduced migration and ROCK signalling, as well as both MT dynamic changes and

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

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

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

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

44 reased permeability in experimental NEC, and ROCK inhibitors would be protective against NEC by regul

45 h IRF4- and MYC-controlled gene networks and ROCK inhibition could represent an attractive therapeuti

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

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

48 on proteins through actin polymerization and ROCK-mediated localized contraction of the cell boundary

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

50 Inhibition of RhoA and ROCK activity partially restores osteogenic differentiat

51 Here, we found that active RhoA and ROCK effector phospho-myosin light chain (pMLC) were dow

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

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

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

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

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

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

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

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

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

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

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

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

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

65 nase that can be therapeutically targeted by ROCK inhibitors or statins, is a key downstream effector

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

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

68 ilized F-actin polymerization by controlling ROCK signaling.

69 1 signaling in adipose tissue by controlling ROCK-dependent phosphorylation of the insulin receptor s

70 d ARM and impaired PSD-LTM, while decreasing ROCK activity rescued the enhanced ARM produced by Ras k

71 as 5 d after inducible deletion, the double ROCK knockout hearts exhibited reduced phosphorylation o

72 Mechanistically, the double ROCK knockout promoted age-associated or starvation-indu

73 B light chain 3B was increased in the double ROCK knockout, and these early molecular features persis

74 Dysregulated ROCK activity has been implicated in several human patho

75 ferent, even opposite, effects on endogenous ROCK activity and the MLC/FAK/AKT/mTOR signaling pathway

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

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

78 adhesion kinase (FAK), supporting a role for ROCK activity in regulating the nonsarcomeric cytoskelet

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

80 ound showed excellent kinase selectivity for ROCK I and ROCK II against 387 other kinases.

81 Conversely, graded ROCK overexpression preferentially increases RLC diphosp

82 activates the actin-regulating RhoA-GTPase/ ROCK pathway, which is required for full vascular disrup

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

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

85 High ROCK-myosin II activity correlates with aggressiveness,

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

87 ownstream target Rho-associated kinase I/II (ROCK), the patients' lymphocytes failed to efficiently r

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

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

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

91 rupted cell junctions, mediated by increased ROCK activation.

92 RK knockdown cardiomyocytes showed increased ROCK activity.

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

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

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

96 axonal regeneration, including by inhibiting ROCK, should be further explored.

97 ication and genomic stability, by inhibiting ROCK.

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

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

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

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

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

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

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

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

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

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

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

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

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

111 e equally affected by Rho-associated kinase (ROCK) inhibition; however, augmented protein kinase C (P

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

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

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

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

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

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

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

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

120 d activity of Rho-associated protein kinase (ROCK) and protein kinase A (PKA), we attempted to rescue

121 iated coiled-coil-containing protein kinase (ROCK) are also essential for this process, and active Rh

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

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

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

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

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

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

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

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

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

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

132 re rescued by Rho-associated protein kinase (ROCK)/protein kinase A (PKA) inhibitor fasudil, a drug a

133 iated coiled-coil-containing protein kinase (ROCK)1 and ROCK2 double deletion vs. single deletion on

134 Rho kinase (ROCK) affects cellular permeability and TJ regulation.

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

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

137 ncreased sensitivity to multiple Rho kinase (ROCK) inhibitors.

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

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

140 e demonstrate that the Ras->Raf->rho kinase (ROCK) pathway in MBn suppresses ARM consolidation, allow

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

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

143 which promotes an interaction of Rho kinase (ROCK) with MYPT1 and inhibits myosin targeting.

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

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

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

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

148 containing serine/threonine protein kinases (ROCKs) have recently been suggested as potential targets

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

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

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

152 Local ROCK inhibition prevents and reverses intestinal fibrosi

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

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

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

156 s indicate that, apart from neuroprotection, ROCK inhibitor Y-27632 can also accelerate regeneration

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

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

159 ng and changes in expression and activity of ROCK-myosin II pathway during acquisition of resistance

160 -chromen-4-one derivatives as a new class of ROCK inhibitors.

161 In summary, deletions of ROCK isoforms in cardiomyocytes have different, even opp

162 ation, increased lumenization, disruption of ROCK-mediated myosin II phosphorylation, and SRC signali

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

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

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

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

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

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

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

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

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

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

173 We conclude that MBn Ras/Raf inhibition of ROCK suppresses the consolidation of ARM, which permits

174 Rather, Ras/Raf inhibition of ROCK was found to be responsible for suppressing ARM.

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

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

177 isingly, acute pharmacological inhibition of ROCK-driven actomyosin contractility does not impact the

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

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

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

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

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

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

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

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

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

187 Reduced ROCK signalling preceded cytolysis, which was associated

188 lymerizing drug latrunculin B or by reducing ROCK activity.

189 ation through collagen-rich tissues in a Rho-ROCK-dependent manner consistent with integrin-independe

190 ia, nuclear positioning is controlled by Rho-ROCK-dependent myosin contractility.

191 onal regulator YAP through inhibition of Rho-ROCK-MLC- and FAK-PI3K-dependent signaling pathways.

192 se regulator, NUAK2, or by inhibition of Rho-ROCK-myosin II.

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

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

195 se biological tubing is regulated by the Rho-ROCK (Rho-associated protein kinase) and calcium signali

196 uggest that SPV-1 works through both the Rho-ROCK and calcium signaling pathways to coordinate cellul

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

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

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

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

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

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

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

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

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

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

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

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

209 Altogether, our results suggest that Rho/ROCK and actinomyosin contractility are regulated by AMP

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

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

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

213 , induces metabotropic signaling via the Rho/ROCK pathway.

214 -Fc treatment suppresses autophagy in a RhoA-ROCK dependent manner.

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

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

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

218 uggest that in motile, polarized cells, RhoA-ROCK interactions prevail at the rear, whereas RhoA-DIA

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

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

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

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

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

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

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

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

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

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

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

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

231 CA4P failed to activate RhoA/ROCK/pMLC but its activity was restored upon reoxygenati

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

233 d profound actin filament loss, blocked RhoA/ROCK signalling and rendered microtubules CA4P-resistant

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

252 pendent deacetylation of Miro1 requires RhoA/ROCK activation and downstream intracellular Ca(2+) incr

253 Alteration of the RhoA/ROCK (Rho kinase) pathway has been shown to be neuroprot

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

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

256 Cs), leading to rapid activation of the RhoA/ROCK signaling pathway and breakdown of EC-EC junctions.

257 The RhoA/ROCK-mediated actin cytoskeleton dynamics have been impl

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

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

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

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

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

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

264 As such, ROCK inhibitors have potential therapeutic applicability

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

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

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

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

269 Proteomic analysis shows that ROCK-Myosin II activity in amoeboid cancer cells control

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

271 The ROCK inhibitor, fasudil, also reduced airway responsiven

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

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

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

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

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

277 athological phenotypes by treatment with the ROCK/PKA inhibitor fasudil.

278 The ROCKs are increasingly recognized as critical coordinato

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

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

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

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

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

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

285 regulates transendothelial migration through ROCK signaling.

286 adult stage in Ophn1-dependent XLID through ROCK/PKA inhibition.SIGNIFICANCE STATEMENT In this study

287 Thus, ROCK inhibitors represent potential therapeutics for VHL

288 dependent on RhoC and not RhoA signaling to ROCK.

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

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

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

292 The two ROCK isoforms, ROCK1 and ROCK2, are highly homologous.

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

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

295 d cancer cells perpetuate their behavior via ROCK-Myosin II-driven IL-1alpha secretion and NF-kappaB

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

297 activates Rac1 via DIA and inhibits Rac1 via ROCK, while Rac1 inhibits RhoA through PAK.

298 herapies can be improved by combination with ROCK inhibitors.

299 Our results contrast with ROCK pro-invasive function in other cancers, stressing t

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