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1 st through transcriptional activation of the cyclin-dependent kinase inhibitor p21.
2 antial increase in the protein levels of the cyclin-dependent kinase inhibitor p21.
3 to induce transcription of genes such as the cyclin-dependent kinase inhibitor p21.
4 cells by neutralizing the activities of the cyclin-dependent kinase inhibitor p21.
5 rvival through Akt-mediated induction of the cyclin-dependent kinase inhibitor p21.
6 e progression, as well as with the universal cyclin-dependent kinase inhibitor p21.
7 l cycle associated with the induction of the cyclin-dependent kinase inhibitor p21.
8 t of the failure to induce expression of the cyclin-dependent kinase inhibitor p21.
9 in-2, AR-specific coactivator ARA70, and the cyclin-dependent kinase inhibitor p21.
10 cretin gene as well as the gene encoding the cyclin-dependent kinase inhibitor p21.
11 capable of transcriptionally activating the cyclin-dependent kinase inhibitor p21.
12 for p53 in the promoter of the gene for the cyclin-dependent kinase inhibitor p21.
13 with a p53-independent up-regulation of the cyclin-dependent kinase inhibitor p21.
14 excision repair, and PCNA interacts with the cyclin-dependent kinase inhibitor p21.
15 d resulted in decreased transcription of the cyclin-dependent kinase inhibitor p21.
16 ession of proarrest gene targets such as the cyclin-dependent kinase inhibitor p21.
17 and one of its transcriptional targets, the cyclin-dependent kinase inhibitor p21.
18 d DNA synthesis through the induction of the cyclin-dependent kinase inhibitor p21.
19 decreased transcriptional activation of the cyclin-dependent kinase inhibitor p21.
20 nd E, the transcription factor E2F1, and the cyclin-dependent kinase inhibitor p21.
21 led to a large increase in the levels of the cyclin-dependent kinase inhibitor p21.
22 genes while up-regulating expression of the cyclin-dependent kinase inhibitor p21.
23 aglandin A2 (PGA2) induces expression of the cyclin-dependent kinase inhibitor p21.
24 in part through decreasing expression of the cyclin dependent kinase inhibitor, p21.
25 regulator p53 and a protein p53 induces, the cyclin dependent kinase inhibitor, p21.
26 icative senescence are all influenced by the cyclin-dependent kinase inhibitor, p21.
27 pathways that culminate in expression of the cyclin-dependent kinase inhibitor, p21.
28 r levels of specific proteins, including the cyclin-dependent kinase inhibitor, p21.
29 nd cycle accompanied by up-regulation of the cyclin-dependent kinase inhibitor, p21.
30 associated with precocious induction of the cyclin-dependent kinase inhibitor, p21.
31 s to localize the CDK2-binding domain of the cyclin-dependent kinase inhibitor, p21.
32 rin are mediated by protein kinase B and the cyclin-dependent kinase inhibitor, p21.
33 ng p53-induced protein with death domain and cyclin-dependent kinase inhibitor, p21.
35 rt that cellular mRNAs encoding the cellular cyclin-dependent kinase inhibitor p21, a key inducer of
38 hat fine-tuning the expression levels of the cyclin-dependent kinase inhibitor p21, a p53 target gene
40 structs expressing Fas ligand (Ad-FasL), the cyclin-dependent kinase inhibitor p21 (Ad-p21), or beta-
41 f HIV-1 coreceptors and up-regulation of the cyclin-dependent kinase inhibitor p21 (also known as cip
42 ith strong and selective upregulation of the cyclin-dependent kinase inhibitor p21 (also known as cip
43 ncreased transcription and expression of the cyclin-dependent kinase inhibitor p21 and consequent cel
44 ciated with HER2-induced accumulation of the cyclin-dependent kinase inhibitor p21 and decrease in th
45 rrest accompanied by increased expression of cyclin-dependent kinase inhibitor p21 and decreased expr
46 of PIAS1 induces p53-mediated expression of cyclin-dependent kinase inhibitor p21 and G(1) arrest of
47 ontained significantly reduced levels of the cyclin-dependent kinase inhibitor p21 and low levels of
48 this is correlated with an induction of the cyclin-dependent kinase inhibitor p21 and reduced cyclin
49 nally activated two of its target genes, the cyclin-dependent kinase inhibitor p21 and the mdm2 gene
50 arget genes, including those that encode the cyclin-dependent kinase inhibitor p21 and the proapoptot
52 growth factor-beta (TGF-beta)can induce the cyclin-dependent kinase inhibitors p21 and p15 in a vari
55 on of the Rb kinases, CDK4 and CDK6, and the cyclin-dependent kinase inhibitors p21 and p16 in senesc
58 le phase, and the expression of pAkt and the cyclin-dependent kinase inhibitors p21 and p27 was incre
60 for cdk2 and resistance to inhibition by the cyclin-dependent kinase inhibitors p21 and p27, (b) resi
61 ignificant increase in the expression of the cyclin-dependent kinase inhibitors p21 and p27, and a de
62 e/AKT signaling pathway, upregulation of the cyclin-dependent kinase inhibitors p21 and p27, antiprol
68 -dependent increase in the expression of the cyclin-dependent kinase inhibitors p21 and p27; we also
70 f the tumor suppressor protein, p53, and the cyclin-dependent kinase inhibitors, p21 and p27, as well
71 on factor, Zta, can induce expression of the cyclin-dependent kinase inhibitors, p21 and p27, the tum
74 induction of endogenous p21(WAF1/CIP1) (the cyclin-dependent kinase inhibitor p21) and growth arrest
75 tion, stabilization of p53, induction of the cyclin-dependent kinase inhibitor p21, and homologous re
76 9, it inhibits BMP-mediated induction of the cyclin-dependent kinase inhibitor p21, and it reverses B
78 ocodazole-treated adapted cells requires the cyclin-dependent kinase inhibitor p21, as p21-/- fibrobl
79 ed apoptosis is preceded by induction of the cyclin-dependent kinase inhibitor p21, associated with G
80 st cancer cells, increased expression of the cyclin-dependent kinase inhibitor p21 but had no effect
81 ally associated with induction of the potent cyclin-dependent kinase inhibitor p21, but not p27, and
84 r cells revealed increased expression of the cyclin-dependent kinase inhibitor, p21(CIP), independent
85 in the myogenic progenitor cell and that the cyclin-dependent kinase inhibitor, p21(CIP), may be a do
86 cancer cells led to increased levels of the cyclin-dependent kinase inhibitor p21 cip1/Waf1/Sdi1 and
88 rentiation of MLL-AF9 blasts, which requires cyclin-dependent kinase inhibitor p21(Cip1) (Cdkn1a) act
89 7-AAG blocked SAHA-mediated induction of the cyclin-dependent kinase inhibitor p21(CIP1) and resulted
91 vely lower in HTSF compared to NADF, and the cyclin-dependent kinase inhibitor p21(cip1) is upregulat
95 ding protein CksHs2 were induced whereas the cyclin-dependent kinase inhibitor p21(Cip1) was represse
96 ypoxia-inducible factor (HIF) 1alpha and the cyclin-dependent kinase inhibitor p21(CIP1), a surprisin
97 p53 to transcriptionally induce mdm2 and the cyclin-dependent kinase inhibitor p21(Cip1), and to arre
98 s exhibit selective pX-induced expression of cyclin-dependent kinase inhibitor p21(Cip1), tumor suppr
99 t manner by increasing the expression of the cyclin-dependent kinase inhibitor p21(CIP1), which leads
100 kinase pathway and in down-regulation of the cyclin-dependent kinase inhibitor p21(Cip1), which resul
103 on of the transcription factor Msx-2 and the cyclin-dependent kinase inhibitor p21(CIP1/WAF1) (p21).
104 ed marked elevation in the expression of the cyclin-dependent kinase inhibitor p21(cip1/waf1) accompa
105 t, differentiation-related activation of the cyclin-dependent kinase inhibitor p21(cip1/WAF1) gene is
107 K2AS treatment induced the expression of the cyclin-dependent kinase inhibitor p21(Cip1/Waf1) in pare
108 nstream-regulated gene 1 and upregulated the cyclin-dependent kinase inhibitor p21(CIP1/WAF1) while d
113 ibits proliferation through induction of the cyclin-dependent kinase inhibitor p21(Cip1/WAF1/Sdi1), w
114 , causing a decrease in the induction of the cyclin-dependent kinase inhibitor, p21(Cip1), and an inc
115 as a strong repressor of the promoter of the cyclin-dependent kinase inhibitor, p21(CIP1), while RUNX
116 iptional repression of TLX target genes, the cyclin-dependent kinase inhibitor, p21(CIP1/WAF1)(p21),
117 ectopic expression of p16(INK4a) and another cyclin-dependent kinase inhibitor, p21(CIP1/WAF1), induc
118 was associated with increased binding of the cyclin-dependent kinase inhibitor, p21(Cip1/WAF1), to th
120 cyclin D2 and cyclin E, and induction of the cyclin-dependent kinase inhibitors p21(Cip1) and p27(Kip
121 n the targets of GR's cytostatic action, the cyclin-dependent kinase inhibitors p21(Cip1) and p27(Kip
122 294002 resulted in the selective increase of cyclin-dependent kinase inhibitors p21(Cip1) or p27(Kip1
123 ve regulators of the cell cycle, such as the cyclin-dependent kinase inhibitors p21(Cip1), p27(Kip1),
124 has been proposed that the functions of the cyclin-dependent kinase inhibitors p21(Cip1/Waf1) and p2
125 egulation of cyclin D1, up-regulation of the cyclin-dependent kinase inhibitors, p21(cip1.) and p16(I
127 by hyperactivated NF-kappaB and mediated by cyclin-dependent kinase inhibitors, p21(CIP1/WAF1) and p
128 ggers a host senescence response mediated by cyclin-dependent kinase inhibitors: p21(CIP1/WAF1) (p21)
129 53 response, accompanied by induction of the cyclin-dependent kinase inhibitor p21/CIP1, which can be
130 phate (IP6) causes G(1) arrest and increases cyclin-dependent kinase inhibitors p21/Cip1 and p27/Kip1
132 damage response signaling pathway involving cyclin-dependent kinase inhibitor p21 expression and het
133 53-induced transcriptional activation of the cyclin-dependent kinase inhibitor p21 in G1 cell cycle a
134 ed expression of the key p53 target gene and cyclin-dependent kinase inhibitor p21 in HCT116 cells, p
135 Skp2-mediated proteasomal degradation of the cyclin-dependent kinase inhibitor p21 in mammalian cells
136 ulating the basal level of expression of the cyclin-dependent kinase inhibitor p21 in the absence of
137 hat directly regulates the expression of the cyclin-dependent kinase inhibitor p21, independently of
138 d cellular proteins, including c-jun and the cyclin-dependent kinase inhibitor p21, indicating that d
139 We found that PCBP4 expression decreases cyclin-dependent kinase inhibitor p21 induction in respo
147 usly, we demonstrated that expression of the cyclin-dependent kinase inhibitor p21 is reduced in syno
151 d at the promoters of the genes encoding the cyclin-dependent kinase inhibitor p21 or the transcripti
152 e to trigger an increase in the level of the cyclin-dependent kinase inhibitor p21 or to activate the
153 cyclin A expression, as co-expression of the cyclin-dependent kinase inhibitors p21 or p27, or a domi
154 xygenase-1, programmed cell death 4, and the cyclin-dependent kinase inhibitors p21, p27, and p57.
155 e inducible Src homology 2-containing genes, cyclin-dependent kinase inhibitors p21, p57, calmodulin
156 strongly suppress a phenotype caused by the cyclin-dependent kinase inhibitor p21, restoring S phase
157 dies indicate that myogenic induction of the cyclin-dependent kinase inhibitor p21 results in an inhi
158 an E3 ubiquitin ligase, CRL2(LRR1), for the cyclin-dependent kinase inhibitor p21 that specifically
159 ly that MDM2 promotes the degradation of the cyclin-dependent kinase inhibitor p21 through a ubiquiti
160 in D1, while it decreased the expressions of cyclin-dependent kinase inhibitor p21 (WAF-1/CIP1/MDA-6)
164 hemical expression patterns of the prototype cyclin-dependent kinase inhibitor p21 WAF1/CIP1 and the
165 niposide (VM-26) both increase levels of the cyclin dependent kinase inhibitor, p21(waf1/cip1) and pr
167 Inducible p53-independent regulation of the cyclin-dependent kinase inhibitor p21(waf1) transcriptio
168 a), IFN regulatory factor-1 (IRF-1), and the cyclin-dependent kinase inhibitor p21(WAF1) was found in
169 t transcription, increased expression of the cyclin-dependent kinase inhibitor p21(Waf1), and accumul
170 s resulted in an increased production of the cyclin-dependent kinase inhibitor p21(WAF1), whereas no
173 rminus deficiency promotes expression of the cyclin-dependent kinase inhibitor p21(Waf1/Cip1) (Cdkn1a
175 ll cycle arrest and apoptosis, including the cyclin-dependent kinase inhibitor p21(Waf1/Cip1) (p21).
176 liferation of ATC cells via induction of the cyclin-dependent kinase inhibitor p21(WAF1/CIP1) (p21).
177 t transcription of both IkappaBalpha and the cyclin-dependent kinase inhibitor p21(WAF1/CIP1) and ind
180 he rapid (within 30 minutes) increase of the cyclin-dependent kinase inhibitor p21(waf1/cip1) as well
181 cell cycle arrest through activation of the cyclin-dependent kinase inhibitor p21(WAF1/Cip1) gene.
182 epithelial (HOSE) cells via induction of the cyclin-dependent kinase inhibitor p21(WAF1/CIP1) has bee
184 tumorigenesis, targeted inactivation of the cyclin-dependent kinase inhibitor p21(WAF1/cip1) is high
186 etermine whether p53 and the p53 target gene cyclin-dependent kinase inhibitor p21(WAF1/CIP1) were in
187 residues with the PCNA-binding domain of the cyclin-dependent kinase inhibitor p21(Waf1/Cip1), and al
188 9 degrees C show increased expression of the cyclin-dependent kinase inhibitor p21(Waf1/Cip1), charac
189 ent increased protein and mRNA levels of the cyclin-dependent kinase inhibitor p21(WAF1/CIP1), increa
190 ntly increases transcription and activity of cyclin-dependent kinase inhibitor p21(WAF1/CIP1), leadin
191 on of manganese superoxide dismutase and the cyclin-dependent kinase inhibitor p21(Waf1/Cip1), protei
202 the ability to regulate transcription of the cyclin-dependent kinase inhibitor, p21(WAF1) (p21), one
203 with the p53-independent upregulation of the cyclin-dependent kinase inhibitor, p21(WAF1/Cip1) (p21).
204 th a homozygous deletion of the gene for the cyclin-dependent kinase inhibitor, p21(WAF1/CIP1), do no
205 ation of p27 than by inactivation of another cyclin-dependent kinase inhibitor, p21(WAF1/cip1), the n
208 density-arrested cells of high levels of the cyclin-dependent kinase inhibitors p21(WAF1) and p27(KIP
209 on of G(1)-S-phase regulators, including the cyclin-dependent kinase inhibitors p21(waf1) and p27(kip
210 retinoblastoma protein and induction of the cyclin-dependent kinase inhibitors p21(waf1/cip1) and p2
211 t at the G(1)-S checkpoint, and induction of cyclin-dependent kinase inhibitors p21(waf1/cip1) and p2
212 In this study, we investigated the role of cyclin-dependent kinase inhibitors, p21(WAF1/cip1) (p21)
215 he mechanism appeared to involve neither the cyclin-dependent kinase inhibitor, p21((waf1/cip1)) nor
216 ngs clearly demonstrate the up-regulation of cyclin-dependent kinase inhibitors p21((Waf1/Cip1)) and
217 xpression of p53 at 32 degrees C induced the cyclin-dependent kinase inhibitor p21/WAF1 and arrested
219 ess wild-type or mutant forms of p53, or the cyclin-dependent kinase inhibitor p21/WAF1, under a tetr
222 ntrol of proliferation and expression of the cyclin-dependent kinase inhibitor p21(WAFI/CIP1) seen in
223 These studies revealed that loss of the cyclin-dependent kinase inhibitor p21 was associated wit
226 m-2; present throughout the cell cycle), and cyclin-dependent kinase inhibitor p21, which inhibits G
227 evels of bone morphogenetic proteins and the cyclin-dependent kinase inhibitor p21, which might contr
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