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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
8 Inhibition of either beta(2) integrins or Rho-associated kinase, a kinase downstream from RhoA, gr
11 treated with FGF-2 and Y27632 (inhibitor of Rho-associated kinase) achieved an 84% recovery of the w
15 FLCN positively regulates RhoA activity and Rho-associated kinase activity, consistent with the only
18 ncreased actin polymerization in response to Rho-associated kinase and PKC signaling contributes sign
19 evering is partially slowed by inhibition of Rho-associated kinase and virtually abolished by direct
20 ivity was dependent on actin, Cav1, Src, and Rho-associated kinase as well as downstream protein kina
21 tide-based proteomic screen identified ROCK (Rho-associated kinase) as a putative substrate for SNRK,
24 and higher plateau retraction distances than Rho-associated kinase-dependent SFs located in the cell
25 neuropeptides and bioactive lipids (Rho- and Rho-associated kinase-dependent), tyrosine kinase recept
27 r beta (TGF-beta) and the migratory proteins rho-associated kinase, focal adhesion kinase, and matrix
31 phosphorylation at Thr(697) and Thr(855) by Rho-associated kinase inhibited phosphatase activity and
32 is localized at the mitotic cell cortex, and Rho-associated kinase inhibition increases the degree of
36 GTPase inhibitor C. difficile toxin B or the Rho-associated kinase inhibitor Y-27632 also blocked TGF
37 FAK to focal contacts and treatment with the Rho-associated kinase inhibitor Y-27632 did not prevent
40 n, and pretreatment of HUVECs with Y27632, a Rho-associated kinase inhibitor, rescued TP-impaired ins
43 o-effector protein kinase that is related to Rho-associated kinases of ROCK/ROK/Rho-kinase family.
44 sphorylation of MLC phosphatase (SMPP-1M) by Rho-associated kinase or endogenous SMPP-1M-associated k
45 n of cell contractility through RhoA GTPase, Rho-associated kinase, or myosin light chain kinase rest
46 ere, we describe the purification of a novel Rho-associated kinase, p140, which appears to be the maj
49 ltered the Ras homolog gene family, member A/Rho-associated kinase pathway with increased stress acti
50 arget the transforming growth factor-beta or Rho-associated kinase pathways converts embryonic fibrob
55 cyclin E acquires a high binding affinity to Rho-associated kinase (ROCK II), and physically associat
56 Ras-MAPK leads to loss of apically localized Rho-associated kinase (Rock) 2a, which results in failed
62 ation with inhibition of EMT by inclusion of Rho-associated kinase (ROCK) and transforming growth fac
63 n was only partially dependent on Rho kinase/Rho-associated kinase (ROCK) and was independent of RhoA
64 I3-kinase or phospholipase-C, but inhibiting Rho-associated kinase (ROCK) blocked only E13K-induced i
65 d endocytosis of TJ proteins was mediated by Rho-associated kinase (ROCK) but not myosin light chain
68 ibition analysis revealed a critical role of Rho-associated kinase (ROCK) in AJC disassembly in calci
70 cells could be rescued by treatment with the Rho-associated kinase (ROCK) inhibitor Y-27632 or introd
72 ays, impedance-based assays with a selective Rho-associated kinase (ROCK) inhibitor, Galpha12/13 knoc
75 We investigated the involvement of the RhoA/Rho-associated kinase (ROCK) pathway in regulating ICAM-
79 ive phenotype was due, in part, to increased Rho-associated kinase (ROCK) signaling concomitant with
80 4c channel through its downstream Rap1A-RhoA-Rho-associated kinase (ROCK) signaling pathway for susta
81 eviously demonstrated that activation of the Rho-associated kinase (ROCK) signaling pathway promotes
83 he nocodazole-induced activation of RhoA and Rho-associated kinase (ROCK) that mediates phosphorylati
85 MLC phosphorylation in MKs is regulated by Rho-associated kinase (ROCK), and consistent with our mo
86 Claudins, E-cadherin, F-actin, myosin II, Rho-associated kinase (ROCK), and myosin light chain kin
87 Na,K-ATPase exocytosis was regulated by the Rho-associated kinase (ROCK), as preincubation with the
89 inhibition of RhoA, its downstream effector, Rho-associated kinase (ROCK), or a microtubule-associate
90 ments show that Vangl2, as well as Daam1 and Rho-associated kinase (Rock), regulate apical constricti
91 in to direct the subcellular localization of Rho-associated kinase (Rock), which in turn drives chang
98 lastoma patients, and elevated expression of Rho-associated kinase (ROCK)2 is associated with poor pa
99 cognized that an increased expression of the Rho-associated kinase (ROCK-I), a downstream target of R
102 appears necessary for downregulation of the Rho-associated kinase (ROCK1) that occurs during myogeni
105 -induced STAT3 activation partly depended on Rho-associated kinase (ROK) and involved multiple effect
107 muscle myosin II (Myo-II) by kinases such as Rho-associated kinase (Rok) is important to generate con
108 e myosin targeting subunit (MYPT1) by either Rho-associated kinase (ROK) or an unknown SMPP-1M-associ
110 eously decreases RhoA affinity to its target Rho-associated kinase (ROK), a key mediator of neurite o
111 the activities of protein kinases, including Rho-associated kinase, that phosphorylate the myosin pho
112 ation and extracellular signal-regulated and Rho-associated kinases to regulate gene expression.
114 over, dominant-negative RhoA or inhibitor of Rho-associated kinase (Y27632) substantially negated the
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