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1 ling pathways, myosin light chain kinase and Rho-associated kinase.
3 ets pretreated with a P2Y(1) antagonist or a Rho-associated kinase 1 inhibitor, confirming the crucia
7 but also on well-known players such as PAR1, Rho-associated kinase 2, phospholipase C, and proteins r
9 Inhibition of either beta(2) integrins or Rho-associated kinase, a kinase downstream from RhoA, gr
12 treated with FGF-2 and Y27632 (inhibitor of Rho-associated kinase) achieved an 84% recovery of the w
16 FLCN positively regulates RhoA activity and Rho-associated kinase activity, consistent with the only
19 ncreased actin polymerization in response to Rho-associated kinase and PKC signaling contributes sign
20 evering is partially slowed by inhibition of Rho-associated kinase and virtually abolished by direct
21 ted protein kinase, Src tyrosine kinase, and rho-associated kinase are required for initiation in bot
22 ivity was dependent on actin, Cav1, Src, and Rho-associated kinase as well as downstream protein kina
23 tide-based proteomic screen identified ROCK (Rho-associated kinase) as a putative substrate for SNRK,
25 actin remodeling, myosin light chain kinase, Rho-associated kinase, calcium, and VEGF and its recepto
27 and higher plateau retraction distances than Rho-associated kinase-dependent SFs located in the cell
28 neuropeptides and bioactive lipids (Rho- and Rho-associated kinase-dependent), tyrosine kinase recept
30 r beta (TGF-beta) and the migratory proteins rho-associated kinase, focal adhesion kinase, and matrix
34 bed regulation of the RhoA downstream target Rho-associated kinase I/II (ROCK), the patients' lymphoc
35 phosphorylation at Thr(697) and Thr(855) by Rho-associated kinase inhibited phosphatase activity and
36 is localized at the mitotic cell cortex, and Rho-associated kinase inhibition increases the degree of
40 GTPase inhibitor C. difficile toxin B or the Rho-associated kinase inhibitor Y-27632 also blocked TGF
41 FAK to focal contacts and treatment with the Rho-associated kinase inhibitor Y-27632 did not prevent
44 n, and pretreatment of HUVECs with Y27632, a Rho-associated kinase inhibitor, rescued TP-impaired ins
47 o-effector protein kinase that is related to Rho-associated kinases of ROCK/ROK/Rho-kinase family.
48 sphorylation of MLC phosphatase (SMPP-1M) by Rho-associated kinase or endogenous SMPP-1M-associated k
50 n of cell contractility through RhoA GTPase, Rho-associated kinase, or myosin light chain kinase rest
51 ere, we describe the purification of a novel Rho-associated kinase, p140, which appears to be the maj
54 ltered the Ras homolog gene family, member A/Rho-associated kinase pathway with increased stress acti
55 arget the transforming growth factor-beta or Rho-associated kinase pathways converts embryonic fibrob
60 cyclin E acquires a high binding affinity to Rho-associated kinase (ROCK II), and physically associat
61 Ras-MAPK leads to loss of apically localized Rho-associated kinase (Rock) 2a, which results in failed
64 Fasudil is a small molecule inhibitor of Rho-associated kinase (ROCK) and is approved for the tre
68 ation with inhibition of EMT by inclusion of Rho-associated kinase (ROCK) and transforming growth fac
69 n was only partially dependent on Rho kinase/Rho-associated kinase (ROCK) and was independent of RhoA
70 I3-kinase or phospholipase-C, but inhibiting Rho-associated kinase (ROCK) blocked only E13K-induced i
71 d endocytosis of TJ proteins was mediated by Rho-associated kinase (ROCK) but not myosin light chain
74 ibition analysis revealed a critical role of Rho-associated kinase (ROCK) in AJC disassembly in calci
77 h WT and KO vessels were equally affected by Rho-associated kinase (ROCK) inhibition; however, augmen
78 cells could be rescued by treatment with the Rho-associated kinase (ROCK) inhibitor Y-27632 or introd
80 ays, impedance-based assays with a selective Rho-associated kinase (ROCK) inhibitor, Galpha12/13 knoc
83 We investigated the involvement of the RhoA/Rho-associated kinase (ROCK) pathway in regulating ICAM-
87 ive phenotype was due, in part, to increased Rho-associated kinase (ROCK) signaling concomitant with
88 4c channel through its downstream Rap1A-RhoA-Rho-associated kinase (ROCK) signaling pathway for susta
89 eviously demonstrated that activation of the Rho-associated kinase (ROCK) signaling pathway promotes
92 ally exposed to high stress display elevated Rho-associated kinase (ROCK) signalling and an increased
93 he nocodazole-induced activation of RhoA and Rho-associated kinase (ROCK) that mediates phosphorylati
95 MLC phosphorylation in MKs is regulated by Rho-associated kinase (ROCK), and consistent with our mo
96 Claudins, E-cadherin, F-actin, myosin II, Rho-associated kinase (ROCK), and myosin light chain kin
97 Na,K-ATPase exocytosis was regulated by the Rho-associated kinase (ROCK), as preincubation with the
99 inhibition of RhoA, its downstream effector, Rho-associated kinase (ROCK), or a microtubule-associate
100 ments show that Vangl2, as well as Daam1 and Rho-associated kinase (Rock), regulate apical constricti
101 in to direct the subcellular localization of Rho-associated kinase (Rock), which in turn drives chang
108 lastoma patients, and elevated expression of Rho-associated kinase (ROCK)2 is associated with poor pa
109 cognized that an increased expression of the Rho-associated kinase (ROCK-I), a downstream target of R
114 appears necessary for downregulation of the Rho-associated kinase (ROCK1) that occurs during myogeni
119 -induced STAT3 activation partly depended on Rho-associated kinase (ROK) and involved multiple effect
121 muscle myosin II (Myo-II) by kinases such as Rho-associated kinase (Rok) is important to generate con
122 e myosin targeting subunit (MYPT1) by either Rho-associated kinase (ROK) or an unknown SMPP-1M-associ
124 eously decreases RhoA affinity to its target Rho-associated kinase (ROK), a key mediator of neurite o
125 the activities of protein kinases, including Rho-associated kinase, that phosphorylate the myosin pho
126 the WERDS complex, which in turn, activates Rho-associated kinase to induce apical constriction.
127 ation and extracellular signal-regulated and Rho-associated kinases to regulate gene expression.
128 he fenestration structure, such as targeting Rho-associated kinase, VEGF-A, NF[Formula: see text]B, a
130 over, dominant-negative RhoA or inhibitor of Rho-associated kinase (Y27632) substantially negated the