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1 ling pathways, myosin light chain kinase and Rho-associated kinase.
2 n of matrix metalloproteinase 15 (MMP15) and Rho-associated kinase 1 (ROCK1).
3 ets pretreated with a P2Y(1) antagonist or a Rho-associated kinase 1 inhibitor, confirming the crucia
4                                              Rho-associated kinases 1 and 2 (ROCK1/2) are Rho-GTPase
5                                              Rho-associated kinase 2 (ROCK2) recently was shown to be
6                                              Rho-associated kinase 2 (ROCK2) regulates the secretion
7 but also on well-known players such as PAR1, Rho-associated kinase 2, phospholipase C, and proteins r
8 ages by suppressing integrin alphaMbeta2 and Rho-associated kinase 2.
9    Inhibition of either beta(2) integrins or Rho-associated kinase, a kinase downstream from RhoA, gr
10               Furthermore, inhibition of the Rho-associated kinase, a regulator of cytokinesis, impro
11                                      ROCK or Rho-associated kinase, a serine/threonine kinase, is an
12  treated with FGF-2 and Y27632 (inhibitor of Rho-associated kinase) achieved an 84% recovery of the w
13           Both myosin light chain kinase and Rho-associated kinase acted as mediators of ERK1/2-depen
14 t extension that could be rescued by RhoA or Rho-associated kinase activation.
15  kinase, p140, which appears to be the major Rho-associated kinase activity in most tissues.
16  FLCN positively regulates RhoA activity and Rho-associated kinase activity, consistent with the only
17  distal cell edge, and the correct levels of Rho-associated kinase activity.
18                                Inhibitors of Rho-associated kinase and PKC prevented the decline in G
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,
24                Inhibition of PI-3K, PKCs, or Rho-associated kinase by pharmacologic inhibitors abroga
25 actin remodeling, myosin light chain kinase, Rho-associated kinase, calcium, and VEGF and its recepto
26                      Selective inhibition of rho-associated kinase decelerated migration in response
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
29                Here, we show that Drosophila Rho-associated kinase (Drok) works downstream of Fz/Dsh
30 r beta (TGF-beta) and the migratory proteins rho-associated kinase, focal adhesion kinase, and matrix
31                                Inhibition of Rho-associated kinase had no effect.
32 dependently of its known associates, p53 and Rho-associated kinase I (ROCK I).
33          We found that RhoE inhibits ROCK I (Rho-associated kinase I) activity during genotoxic stres
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
37                                           No Rho-associated kinase inhibitor (ROCK-i), or centrifugat
38 ll as single-cell survival in the absence of Rho-associated kinase inhibitor (ROCKi).
39                        Administration of the Rho-associated kinase inhibitor fasudil prevented renal
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
42  phosphorylation, which was inhibited by the Rho-associated kinase inhibitor Y-27632.
43 istered ML-7 (a MLCK inhibitor) or Y27632 (a Rho-associated kinase inhibitor).
44 n, and pretreatment of HUVECs with Y27632, a Rho-associated kinase inhibitor, rescued TP-impaired ins
45                   Recent studies using known Rho-associated kinase isoform 1 (ROCK1) inhibitors along
46 lial cells by selectively activating the Rho/Rho-associated kinase/LKB1/PTEN pathway.
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
49                                Inhibition of Rho-associated kinases or Cdc42 caused male neutrophils
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
52                 Y-27632, an inhibitor of the Rho-associated kinase p160ROCK, diminished polyglutamine
53                          The inhibition of a Rho-associated kinase, p160ROCK, decreased the traction
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
56          We found that Rho and its effector, Rho-associated kinase, preferentially regulated the amou
57                                              Rho-associated kinases (Rho kinases), which are downstre
58                 Y-27632, an inhibitor of the Rho-associated kinase ROCK, is a therapeutic lead for Hu
59                      The previously reported Rho-associated kinases ROCK I and II are ubiquitously ex
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
62       These events were dependent on Rho and Rho-Associated Kinase (ROCK) activation.
63                                     Although Rho-associated kinase (ROCK) activity has been implicate
64     Fasudil is a small molecule inhibitor of Rho-associated kinase (ROCK) and is approved for the tre
65 least partially depends on the activation of Rho-associated kinase (ROCK) and LIMK-1.
66 he interaction with its downstream effectors Rho-associated kinase (ROCK) and mDia.
67                Compaction, via activation of Rho-associated kinase (ROCK) and the stress kinase p38,
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
72                                      PKC and Rho-associated kinase (ROCK) Ca(2+)-sensitizing pathways
73                                              Rho-associated kinase (ROCK) has an essential role in go
74 ibition analysis revealed a critical role of Rho-associated kinase (ROCK) in AJC disassembly in calci
75 L-17 production by enhancing the activity of Rho-associated kinase (ROCK) in T cells.
76                                 In contrast, Rho-associated kinase (ROCK) inhibition blocked MLC phos
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
79                                          The Rho-associated kinase (ROCK) inhibitor Y-27632 permits h
80 ays, impedance-based assays with a selective Rho-associated kinase (ROCK) inhibitor, Galpha12/13 knoc
81                           Activation of RhoA/Rho-associated kinase (ROCK) pathway and the associated
82 -I fiber orientation, inhibition of the RhoA/Rho-associated kinase (ROCK) pathway did not.
83  We investigated the involvement of the RhoA/Rho-associated kinase (ROCK) pathway in regulating ICAM-
84 s the thromboxane A2 receptor (TXAR) and the Rho-associated kinase (ROCK) pathway.
85                                Inhibition of Rho-associated kinase (ROCK) prevented cytoskeletal defe
86                                              Rho-associated kinase (ROCK) regulates neural cell migra
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
90                                              Rho-associated kinase (ROCK) signaling plays a fundament
91 ould be regulated by serotonin via serotonin-Rho-associated kinase (ROCK) signaling.
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
94                        Sustained blockade of Rho-associated kinase (ROCK) with Y-27632 down-regulates
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
98        Rho GTPase and its downstream target, Rho-associated kinase (ROCK), have been implicated in di
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
102       Its binding to Htt is regulated by the rho-associated kinase (ROCK), which phosphorylates profi
103 yosin cytoskeleton, through a Rho-GTPase and Rho-associated kinase (ROCK).
104 iven by myosin light chain kinase (MLCK) and Rho-associated kinase (ROCK).
105 nd actin cytoskeletal remodeling through the Rho-associated kinase (ROCK).
106 hibition of RhoA or its downstream effector, Rho-associated kinase (ROCK).
107                       Targeted inhibition of Rho-associated kinase (ROCK)2 downregulates the proinfla
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
110  activating RhoA and its downstream effector Rho-associated kinase (ROCK/Rho-kinase).
111                    Through these approaches, Rho-associated kinase ROCK1 emerged as a key molecule re
112                      In contrast, inhibiting Rho-associated kinase ROCK1/2 increased migration and sc
113                                          The Rho-associated kinases ROCK1 and ROCK2 are critical for
114  appears necessary for downregulation of the Rho-associated kinase (ROCK1) that occurs during myogeni
115                                              Rho-associated kinases (ROCK1 and ROCK2) regulate the ac
116                       We discovered that the Rho-associated kinase ROCK2 is required for CIE of MHCI
117 f inhibiting Rho or its downstream effector, Rho-associated kinase (ROCKII).
118                                              Rho-associated kinases (ROCKs) are critical molecules in
119 -induced STAT3 activation partly depended on Rho-associated kinase (ROK) and involved multiple effect
120          This synergy requires signaling via Rho-associated kinase (ROK) and p21-activated kinase (PA
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
123 hosphorylation of the targeting subunit at a Rho-associated kinase (ROK) phosphorylation site.
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
129                      Moreover, inhibition of rho-associated kinase was distinguished by abrogation of
130 over, dominant-negative RhoA or inhibitor of Rho-associated kinase (Y27632) substantially negated the

 
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