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1 ants of v-Crk, results in hyperactivation of p160ROCK.
2 y for actin stress fiber assembly induced by p160ROCK.
3 tions through the biochemical pathway of Rho-p160ROCK.
4               Here, we provide evidence that p160ROCK, a Rho-associate serine/threonine kinase, assoc
5                     We also demonstrate that p160ROCK, a serine/threonine kinase effector of RhoA, is
6                                              p160ROCK, a serine/threonine protein kinase, is a direct
7      These results suggest that Aurora-A and p160ROCK act in a common genetic pathway that promotes a
8 icle, we report that the absence of RhoA and p160ROCK activity in fibroblastic NIH 3T3 cells and its
9                    Inhibition of Rho kinase (p160ROCK) also suppressed stretch-induced ERK activation
10                      These findings identify p160ROCK as an upstream, possibly direct, activator of N
11 mulated by expression of mutationally active p160ROCK, but not by mutationally active protein kinase
12  by the dominant-negative mutants of Rho and p160ROCK, but not by the dominant-negative mutant of Cdc
13 n of a second genetic lesion, suppression of p160ROCK by RNA interference, can rescue abnormal mitoti
14  that blocking RhoA or its downstream target p160(ROCK), by the expression of dominant-negative mutan
15   The inhibition of a Rho-associated kinase, p160ROCK, decreased the traction force and migration spe
16 2, an inhibitor of the Rho-associated kinase p160ROCK, diminished polyglutamine protein aggregation (
17 ical residues in NHE1 were phosphorylated by p160ROCK in vivo and in vitro.
18         Expression of a dominant interfering p160ROCK inhibited RhoA-, but not Cdc42- or Rac-activati
19 shape change was completely inhibited by the p160(ROCK) inhibitor, Y-27632.
20 ion of Rho and a downstream effector of Rho, p160ROCK, inhibits neurite outgrowth.
21 ide evidence that signaling through RhoA and p160ROCK is important in TGF-beta inhibition of cell pro
22 at Rho is activated by stretch, and that Rho/p160ROCK mediates stretch-induced ERK activation and vas
23 ive mutant of Cdc42, indicating that the Rho-p160ROCK pathway regulates the cytoskeletal reorganizati
24             Furthermore, mutationally active p160ROCK phosphorylated an NHE1 C-terminal fusion protei
25 was seen when using selective inhibitors for p160(ROCK), PKC, or MEKK1.
26 cological inhibition of its effector kinase, p160ROCK, restores normal Rac1 and Cdc42 activity and re
27  which was partly dependent on activation of p160(ROCK) (Rho-kinase).
28 n of 293T cells with expression plasmids for p160ROCK (Rho-associated coiled-coil-containing kinase)
29 n, Y-27632, an inhibitor of the Rho effector p160ROCK/Rho kinase, decreased thrombin-stimulated DNA s
30                        Finally, we find that p160ROCK signaling negatively regulates integrin adhesio
31                             In addition, the p160ROCK-specific inhibitor Y-27632 inhibited increases
32 vidence is presented for TGF-beta-stimulated p160ROCK translocation to the nucleus and inhibitory pho
33      Here, stress fiber formation induced by p160ROCK was inhibited by the addition of a specific NHE
34 vation of RhoA or the RhoA-associated kinase p160ROCK with a dominant-negative mutant of RhoA or the
35 transferase and inhibition of the Rho-kinase p160ROCK with the pyridine derivative Y-27632 completely
36                                Inhibition of p160ROCK with Y-27632 also promotes neurite outgrowth on

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