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1 4 (CDK4) and increased the expression of the CDK inhibitor p27.
2 ed CDK2 and CDK4 activity, and increased the CDK inhibitor p27.
3 RB and CDK inhibitor p21 but an increase in CDK inhibitor p27.
4 so, RA treatment increased expression of the cdk inhibitor p27 and decreased activity of cdk 2, cdk 4
6 CDK4 and CDK2, respectively) are suppressed, CDK inhibitor p27 and retinoblastoma protein are activat
7 or the ubiquitin-mediated degradation of the cdk-inhibitor p27 and is a bona fide proto-oncoprotein.
8 DK)-2 and CDK-4, increased expression of the CDK inhibitor p27, and shifted the retinoblastoma protei
9 hrough regulating cyclin D turnover, and the CDK inhibitor p27, as shown by depletion studies, functi
10 ential cofactor in the ubiquitination of the Cdk inhibitor p27 by the SCF(Skp2) ubiquitin ligase.
12 kp2 (SCF(SKP2)) complex is thought to be the Cdk inhibitor p27 during S phase, whereas the principal
13 ase-associated protein 2), which targets the CDK inhibitor p27 for degradation, reduces neuroblast pr
15 ent overexpression of p21 and/or the related Cdk inhibitor p27 in U937 cells in the absence of 1,25-d
16 e induced upon v-Abl activation; and (2) the CDK inhibitor p27 is decreased upon v-Abl activation.
17 show that a new biological function for the CDK inhibitor p27 is protection of cells from apoptosis
19 companied by an increase in the level of the Cdk inhibitor p27(Kip1) and a decrease in cyclin A expre
20 ells show a strong decrease in expression of Cdk inhibitor p27(Kip1) and increased expression of sele
21 yc(-/-) cells express elevated levels of the Cdk inhibitor p27(Kip1) and reduced levels of Cdk7, the
22 mediated transcription and expression of the cdk inhibitor p27(Kip1) impairs the proliferation of mel
25 tly lower, whereas the protein levels of the CDK inhibitor p27(Kip1) were higher in ROCK-inhibited ce
27 endent kinase (CDK) 2 and CDK4, induction of CDK inhibitor p27(KIP1), and retinoblastoma hypophosphor
28 T cells as evidenced by up-regulation of the CDK inhibitor p27(Kip1), loss of cyclin A, and reduced B
32 ulation or the down-regulation of the cyclin-cdk inhibitor p27 protein following c-Myc activation by
33 as also seen that was due to accumulation of Cdk inhibitor p27 which was an indirect effect of c-myc
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