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1 thway by which cortical tension inhibits the Rac protein.
2 o the putative second effector domain of the Rac protein.
3 suggested that CNF1 activated the Cdc42 and Rac proteins.
4 similar to those caused by activated Rho and Rac proteins.
5 xygenation injury requires the activation of rac proteins, and that inhibition of rac-dependent pathw
10 nstants (based on EC50 values) of the mutant Rac proteins for the oxidase are at least 13-25-fold hig
11 e, our biochemical analyses with recombinant Rac proteins found that EHT 1864 possesses high affinity
12 ulates intracellular ROS production and that rac proteins function as part of a redox-dependent signa
14 It is not known whether CrkII, Dock180, or Rac proteins have any role during engulfment in mammalia
17 Thus, FcgammaR signaling through the Vav and Rac proteins in neutrophils is critical for stimulating
20 rminus, a region of sequence disparity among Rac proteins, is essential for complementation of Rac2 f
21 poiesis are biochemically separable and that Rac proteins may be important molecular targets for stem
22 sults show that a pathway containing Vav and Rac proteins may negatively regulate Notch signaling dur
24 , regulated, in part, by GTP/GDP exchange on Rac, protein phosphorylation, and binding to lipid messe
25 PAKc preferentially binds the Dictyostelium Rac protein RacB, and point mutations in the conserved C
28 was largely normal, however, indicating that Rac proteins regulate inner ear morphogenesis without af
29 s controlling WASP activity, we identified a Rac protein that binds to the GTPase binding domain of W
32 is shown to be independent of the ability of rac proteins to activate the family of c-jun amino-termi
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