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1 alignancies; and KIP1, the gene encoding the cyclin-dependent kinase inhibitor p27.
2 ar localization relies on its binding to the cyclin-dependent kinase inhibitor p27.
3 IRES) in the 5'-UTR of the mRNA encoding the cyclin-dependent kinase inhibitor p27.
4 n D protein levels while down-regulating the cyclin-dependent kinase inhibitor p27.
5 to target certain substrates, including the Cyclin-dependent kinase inhibitor p27.
6 g II)-induced Rac1-mediated, upregulation of cyclin-dependent kinase inhibitor p27.
7 st partially through the upregulation of the cyclin-dependent kinase inhibitor p27.
8 activator, is involved in degradation of the cyclin-dependent kinase inhibitor p27.
9 ls arrest in G1 with increased levels of the cyclin-dependent kinase inhibitor p27.
12 of TGFbeta, plus reduction in levels of the cyclin-dependent kinase inhibitor p27, allows transducti
14 C/C(Cdh1)), resulting in accumulation of the cyclin-dependent kinase inhibitor p27 and a concomitant
16 of cell cycle regulation: suppression of the cyclin-dependent kinase inhibitor p27 and induction of t
17 kdown results in the nuclear localization of cyclin-dependent kinase inhibitor p27 and prevents the p
20 d by a growth arrest and the upregulation of cyclin-dependent kinase inhibitors, p27 and p57, as well
21 toma protein levels, a rapid increase in the cyclin-dependent kinase inhibitor p27, and accelerated G
22 on of D-type cyclins, down-regulation of the cyclin-dependent kinase inhibitor p27, and, therefore, i
23 a reduced binding of cytoplasmic RhoA to the cyclin-dependent kinase inhibitor p27 both contributed t
25 ng the receptors EGFR, ERBB3 (HER3), and the cyclin-dependent kinase inhibitor p27 (CDKN1B) was found
26 1 and E1 while suppressing the expression of cyclin-dependent kinase inhibitor p27 (CDKN1B), each con
27 ted in a dose-dependent up-regulation of the cyclin-dependent kinase inhibitor p27, down-regulation o
28 , a calcium-activated protease, degrades the cyclin-dependent kinase inhibitor, p27, during the mitot
36 d with rapamycin produced an increase in the cyclin-dependent kinase inhibitor p27(Kip), through a de
41 s shown to regulate the transcription of the cyclin-dependent kinase inhibitor p27 Kip1 gene directly
42 that its oncogenic signals down-regulate the cyclin-dependent kinase inhibitor p27 Kip1, which is def
44 o changes in the ability to downregulate the cyclin-dependent kinase inhibitor p27(Kip1) (also known
45 s generated an adenovirus that expresses the cyclin-dependent kinase inhibitor p27(Kip1) (p27) and be
47 In addition, we show that the levels of the cyclin-dependent kinase inhibitor p27(Kip1) (p27) rise f
48 l endothelial cells (rCECs) by degrading the cyclin-dependent kinase inhibitor p27(Kip1) (p27) throug
49 rein results in lack of up-regulation of the cyclin-dependent kinase inhibitor p27(Kip1) (p27) to arr
50 used an adenoviral (Ad) vector that encodes cyclin-dependent kinase inhibitor p27(Kip1) (p27) with t
54 associated with increased expression of the cyclin-dependent kinase inhibitor p27(Kip1) and a reduce
55 tating translation of mRNAs encoding for the cyclin-dependent kinase inhibitor p27(Kip1) and antiapop
56 ls is preceded by elevated expression of the cyclin-dependent kinase inhibitor p27(Kip1) and cell cyc
57 was associated with the up-regulation of the cyclin-dependent kinase inhibitor p27(Kip1) and down-reg
58 ciated with a selective up-regulation of the cyclin-dependent kinase inhibitor P27(KIP1) and inductio
59 ated protein kinase, increases the levels of cyclin-dependent kinase inhibitor p27(kip1) and reduces
60 ors of cell proliferation and migration, the cyclin-dependent kinase inhibitor p27(Kip1) and the micr
61 EFs leads to an increase in the level of the cyclin-dependent kinase inhibitor p27(Kip1) and to rapid
66 targeted inactivation of both alleles of the cyclin-dependent kinase inhibitor p27(kip1) developed bo
67 ion and hyperproliferation by downregulating cyclin-dependent kinase inhibitor p27(kip1) in a proteas
68 cyclin E displayed an increase in the cyclin/cyclin-dependent kinase inhibitor p27(Kip1) in both asyn
69 f c-Myc and cyclin E and upregulation of the cyclin-dependent kinase inhibitor p27(Kip1) in both the
70 atment with NaBT increased expression of the cyclin-dependent kinase inhibitor p27(kip1) in HT29 cell
71 hibits ubiquitination and degradation of the cyclin-dependent kinase inhibitor p27(kip1) in vitro.
76 colleagues (3121-3134) demonstrate that the cyclin-dependent kinase inhibitor p27(Kip1) is ubiquityl
80 es a posttranscriptional accumulation of the cyclin-dependent kinase inhibitor p27(KIP1) that is acco
81 that HINT1 regulates cellular levels of the cyclin-dependent kinase inhibitor p27(KIP1) through mult
82 t is not clear whether 14-3-3sigma regulates cyclin-dependent kinase inhibitor p27(Kip1) to negativel
85 g for the proliferation marker Ki-67 and the cyclin-dependent kinase inhibitor p27(Kip1) were perform
86 orroborated in this study by coexpression of cyclin-dependent kinase inhibitor p27(Kip1)), we hypothe
87 ein Skp2 as well as by downregulation of the cyclin-dependent kinase inhibitor p27(Kip1), a principal
88 s are actively cycling, but some express the cyclin-dependent kinase inhibitor p27(Kip1), and are pre
89 s T-cell proliferation by the destruction of cyclin-dependent kinase inhibitor p27(kip1), and deletio
90 One of these, miR-221, a regulator of the cyclin-dependent kinase inhibitor p27(kip1), displayed r
91 ivation, and cytoplasmic localization of the cyclin-dependent kinase inhibitor p27(Kip1), which has b
106 te oligodeoxynucleotide (S-ON) targeting the cyclin-dependent kinase inhibitor, p27(kip1), enhanced a
107 a candidate to regulate the abundance of the cyclin-dependent kinase inhibitor, p27(KIP1), in human l
109 rrelate with modulation of the expression of cyclin-dependent kinase inhibitors (p27(Kip1) and p21(Wa
110 polarization also caused accumulation of the cyclin-dependent kinase inhibitors p27(Kip1) and p21(CIP
111 jugating E3 ligase Skp2 and up-regulation of cyclin-dependent kinase inhibitors p27(Kip1) and p21(Cip
112 and (3) an increase in the expression of the cyclin-dependent kinase inhibitors p27(kip1) and p21(cip
113 r agonist kainate caused accumulation of the cyclin-dependent kinase inhibitors p27(Kip1)and p21(CIP1
114 e complex, and promotes the stability of the cyclin-dependent kinase-inhibitor p27(Kip1) through an u
117 osol, which causes hyper-accumulation of the cyclin-dependent kinase inhibitor p27, leading to mitoti
119 rapamycin, mTOR) and altered activity of the cyclin-dependent kinase inhibitor p27 (p27(kip1)) and ex
120 differentiation by modulating expression of cyclin-dependent kinase inhibitor p27/p57 and E3 ubiquit
122 mmunocytochemical analysis of the cell cycle cyclin-dependent kinase inhibitor p27 showed that treatm
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