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1 a70kb) mice is prevented by treatment with a cyclin-dependent kinase inhibitor.
2 ell-cycle arrest and accumulation of the p27 cyclin-dependent kinase inhibitor.
3 Flavopiridol is a protein bound, cytotoxic, cyclin-dependent kinase inhibitor.
4 activity and the expression level of p16, a cyclin-dependent kinase inhibitor.
5 pecificity between a GHV cyclin and a single cyclin-dependent kinase inhibitor.
6 reased apoptosis and decreased expression of cyclin-dependent kinase inhibitors.
7 27(Kip1) , a member of the Kip/Cip family of cyclin-dependent kinase inhibitors.
8 , together with the induction of p21 and p27 cyclin-dependent kinase inhibitors.
9 Ecad- subpopulation through the induction of cyclin-dependent kinase inhibitors.
10 cyclin expression and elevated expression of cyclin-dependent kinase inhibitors.
11 way-directed agents such as flavopiridol and cyclin-dependent kinase inhibitors.
12 In the absence of Jdp2, a complex of the cyclin-dependent kinase inhibitor 1 (p21(Cip1)) and Nrf2
13 on of p53 target genes, most prominently the cyclin-dependent kinase inhibitor 1 encoding cell cycle
14 feration (miR20b, miR10b, and miR141 through cyclin-dependent kinase inhibitor 1 or CDK-interacting p
15 phase, and induces expression of p(21CIP1) (cyclin-dependent kinase inhibitor 1), and p(27KIP1) (cyc
16 logical functions of p21, the product of the cyclin-dependent kinase inhibitor 1A (CDKN1A) gene, with
17 The BRCA2 DNA repair associated (BRCA2) and cyclin-dependent kinase inhibitor 1A (CDKN1A) interactin
20 ed by short-term NEUROG3 expression required cyclin-dependent kinase inhibitor 1A (CDKN1A)/p21(CIP1)
21 re, we show that loss of the p53 target gene cyclin-dependent kinase inhibitor 1A (CDKN1A, also known
22 ecies and p38 MAPK-dependent upregulation of cyclin-dependent kinase inhibitor 1A (Cdkn1a, encoding f
23 l-cycle genes, and we identified the mRNA of cyclin-dependent kinase inhibitor 1A (Cdkn1a, p21) as a
25 R-34 family, TP53 gene, downstream effectors cyclin-dependent kinase inhibitor 1A (p21, Cip1) (CDKN1A
26 e stem cell (HFSC) homeostasis and find p21 (cyclin-dependent kinase inhibitor 1a, Cdkn1a), p57, and
27 pathways; and residual hepatocytes overcame cyclin-dependent kinase inhibitor 1A-induced cell growth
29 behavior through repression of two targets: cyclin dependent kinase inhibitor 1b (cdkn1b) and phosph
30 echanism was identified as downregulation of cyclin-dependent kinase inhibitor 1B (p27(Kip1)) via upr
31 e B-cell CLL/lymphoma 2 or xL (Bcl-2/xL) and cyclin-dependent kinase inhibitor 1B (P27) protein level
32 ependent kinase inhibitor 1), and p(27KIP1) (cyclin-dependent kinase inhibitor 1B) expression, key ce
33 ad markedly decreased quiescence and reduced cyclin-dependent kinase inhibitor 1b/c (Cdkn1b/1c) expre
34 is-derived transcript), the tumor suppressor cyclin-dependent kinase inhibitor 1C (CDKN1C; p57KIP2),
35 olutionarily conserved cell-cycle regulator, cyclin-dependent kinase inhibitor 1d (20 kDa protein, p2
36 genes phosphatase and tensin homolog (PTEN), cyclin dependent kinase inhibitor 2A (CDKN2A), LKB1, and
37 identifying the well-known tumor suppressor cyclin dependent kinase inhibitor 2A (Cdkn2a), whose alt
38 overexpression is concomitant with a loss of cyclin-dependent kinase inhibitor 2A (CDKN2A) locus (enc
39 tions of knockdowns of the tumor suppressors cyclin-dependent kinase inhibitor 2A (Cdkn2a), transform
41 BRAF(V600E)) in association with homozygous cyclin-dependent kinase inhibitor 2A (CDKN2A, encoding p
42 sistent microbial insult (e.g. LPSs) induces cyclin-dependent kinase inhibitor 2A (CDKN2A/p16(INK4a))
43 iral oncogene [Kras(G12V)] and disruption of cyclin-dependent kinase inhibitor 2A (CDKN2A; p16p19) in
45 d III transcription, and thyroxine decreased cyclin-dependent kinase inhibitor 2A (p16(ink4)) express
46 by a mechanism that involved suppression of cyclin-dependent kinase inhibitor 2A (p16INK4A) expressi
47 tivariate model, promoter methylation of the cyclin-dependent kinase inhibitor 2A gene p16, the H-cad
48 ers associated with repression of p16(INK4a)/cyclin-dependent kinase inhibitor 2A(CDKN2A), a critical
49 (hepatocyte growth factor receptor), CDKN2A (cyclin-dependent kinase inhibitor 2A) and CDKN2B (cyclin
50 essor genes RB1 (retinoblastoma) and CDKN2a (cyclin-dependent kinase inhibitor 2a) are critical cell-
52 d by another major POAG risk gene, p16INK4a (cyclin-dependent kinase inhibitor 2A, isoform INK4a).
53 tion and 3-fold hypomethylation of the human cyclin-dependent kinase inhibitor 2B (CDKN2B or p15) gen
54 at loss of one candidate gene at this locus, cyclin-dependent kinase inhibitor 2B (Cdkn2b), in mice p
55 factor beta (TGFbeta) signaling in cultured cyclin-dependent kinase inhibitor 2B (CDKN2B)-deficient
56 hypoxia inducible factor 1A antisense RNA 2, cyclin-dependent kinase inhibitor 2B antisense RNA 1 (AN
57 or STAT5, enhances expression of the Cdkn2b (cyclin-dependent kinase inhibitor 2B) gene and that STAT
58 n-dependent kinase inhibitor 2A) and CDKN2B (cyclin-dependent kinase inhibitor 2B), as well as many o
59 h Cyclin D1 and Cyclin D2, and the p27(Kip1) cyclin-dependent kinase inhibitor act downstream of Notc
60 be reversed by treatment with roscovitine, a cyclin-dependent kinase inhibitor and atypical L-type-ch
62 ociated with reduced levels of the p21(Cip1) cyclin-dependent kinase inhibitor and tumor suppressor p
64 w targets and associated therapeutic agents: cyclin-dependent kinase inhibitors and poly(adenosine di
65 of the cell cycle, decreasing expression of cyclin-dependent kinase inhibitors and upregulating pro-
66 AMPKalpha1 reduced the level of p27(Kip1), a cyclin-dependent kinase inhibitor, and increased the lev
67 specific upregulation of p57Kip2, a Cip/Kip cyclin-dependent kinase inhibitor, and we identified thi
69 cribed mechanisms involving the induction of cyclin-dependent kinase inhibitors but also by the recru
70 mechanisms, including YAP/TAZ signaling and cyclin-dependent kinase inhibitors, by blocking entry in
71 iferation, but the induction of TGF-beta and cyclin-dependent kinase inhibitors causes a cell cycle a
73 g a model of resistance to a pharmacological cyclin-dependent kinase inhibitor (CDKi), we show that t
74 inary efforts have led to the development of Cyclin-Dependent Kinase inhibitors (CDKi's) as small mol
77 ase 4 and 6, and increased the expression of cyclin dependent kinase inhibitors (CDKIs), p21 and p27.
79 on of its target protein-coding genes (i.e., cyclin-dependent kinase inhibitor [Cdkn]1b/p27, Cdkn1c/p
80 mediates GC formation through repression of cyclin-dependent kinase inhibitor CDKN1A (p21(Cip1)).
81 repressor, which leads to expression of the cyclin-dependent kinase inhibitor CDKN1A (p21(CIP1/WAF1)
86 its downstream targets, cJUN, ATF3, and the cyclin-dependent kinase inhibitors CDKN1A and CDKN2B.
87 lial marker expression, and late increase in cyclin-dependent kinase inhibitor CDKN1B (p27) protein-w
91 Hairy and Enhancer of Split 1 (HES1) and the cyclin-dependent kinase inhibitor CDKN1C/p57 as novel ta
92 cell-cycle transition through repression of cyclin-dependent kinase inhibitors Cdkn2a and Cdkn2b, an
93 e show that Hoxa9 represses the locus of the cyclin-dependent kinase inhibitors Cdkn2a/b in concert w
94 gnature correlates with the induction of the cyclin-dependent kinase inhibitors CDKN2D (p19(INK4d)) a
95 ty, and resulting in accumulation of p53 and cyclin-dependent kinase inhibitors, cell cycle arrest, a
96 a protein expression and increased levels of cyclin-dependent kinase inhibitors, CIP1 (p21) and KIP1
98 ntify the p21(Cip1)/p27(Kip1)/p57(Kip2)-like cyclin-dependent kinase inhibitor (CKI) Dacapo (Dap) as
101 e hypothesize that this is due to a weakened cyclin-dependent kinase inhibitor (CKI)-cyclin-dependent
102 ar access of signaling cargos and sequesters cyclin-dependent kinase inhibitors (CKIs) involved in ET
103 tein suppresses the transcription of several cyclin-dependent kinase inhibitors (CKIs) via binding to
104 lation of the tumor suppressors pRb, Cip/Kip cyclin-dependent kinase inhibitors (CKIs), and CDH1, and
106 Systemic administration of the selective cyclin-dependent kinase inhibitor CR8 after SCI signific
111 Here, we address how interactions between cyclin-dependent kinase inhibitors essential for myogeni
113 the redox-reactive thalidomide CPS49 and the cyclin-dependent kinase inhibitor flavopiridol as a sele
114 ase I (Topo I) poison CPT-11 followed by the cyclin-dependent kinase inhibitor flavopiridol in patien
115 matic mutations and deletions in CDKN1B, the cyclin-dependent kinase inhibitor gene, which encodes p2
116 associated with reduced aortic expression of cyclin-dependent kinase inhibitor genes p19Arf and p15In
117 the mRNA expression of osteoblast marker and cyclin-dependent kinase inhibitor genes were all reduced
121 s on the role of one RNA in silencing p15, a cyclin-dependent kinase inhibitor implicated in leukaemi
122 enetic inactivation of p16(ink4a) encoding a cyclin-dependent kinase inhibitor implicated in neuronal
123 reveals differential roles of two homologous cyclin-dependent kinase inhibitors in regulating cell-cy
124 viral cyclin has reduced sensitivity to host cyclin-dependent kinase inhibitors in vitro; however, th
125 to the down-regulation of p21(WAF1/cip1), a cyclin-dependent kinase inhibitor, in intestinal epithel
126 as its downstream target, the p21(Cip1/Waf1) cyclin-dependent kinase inhibitor, in the regulation of
132 liferation is due in part to derepression of cyclin-dependent kinase inhibitors Ink4a/b, while ineffe
133 Specifically, encapsulation of dinaciclib, a cyclin-dependent kinase inhibitor, into PD-L1-targeted L
134 We have found that the expression of p21, a cyclin-dependent kinase inhibitor involved in cell cycle
137 was reported to control the stability of the CYCLIN-DEPENDENT KINASE inhibitor KIP-RELATED PROTEIN (K
138 of FBL17 increases the stability of the CDK (CYCLIN-DEPENDENT KINASE) inhibitor KIP-RELATED PROTEIN2
139 ost inhibitors p27(Kip1) and p18(INK4c), two cyclin-dependent kinase inhibitors known to be important
140 nt of corneal transparency without affecting cyclin-dependent kinase inhibitor levels in Vim(-/-) mic
141 ly due to a failure in proliferation; p27, a cyclin dependent kinase inhibitor, normally undetectable
143 stically, this involved up-regulation of the cyclin-dependent kinase inhibitor p15 and the proapoptot
144 k genotype does not affect the activation of cyclin-dependent kinase inhibitors p15 and p16 by interf
145 senescence, accompanied by the induction of cyclin-dependent kinase inhibitors p15(INK4B), p16(INK4A
146 cytostatic program include activation of the cyclin-dependent kinase inhibitors, p15(Ink4B) and p21(W
147 xpression of two other cell cycle inhibitory cyclin-dependent kinase inhibitors, p15Ink4b (Cdkn2b) an
148 -->S cell cycle progression by targeting the cyclin-dependent kinase inhibitor p16(INK4a) (p16).
149 on of the Ink4a/Arf locus, which encodes the cyclin-dependent kinase inhibitor p16(INK4a) and tumor s
151 argeting the CDKN2A locus, which encodes the cyclin-dependent kinase inhibitor p16, decreased CDKN2A
154 l -74 C-to-T mutation in the promoter of the cyclin-dependent kinase inhibitor p18(Ink4c) (p18) gene
155 nalysis presents Cdkn2c, a gene encoding for cyclin-dependent kinase inhibitor p18(INK4c) (p18), as t
156 he expression of Cdkn2c, a gene encoding for cyclin-dependent kinase inhibitor p18(Ink4c) and located
157 cyclin functions specifically to bypass the cyclin-dependent kinase inhibitor p18(INK4c), revealing
158 the ATM inhibitor showed increased levels of cyclin-dependent kinase inhibitor p19(INK4D), reduced le
159 l cycle regulators cyclins D, A2, and B2 and cyclin-dependent kinase inhibitor p20 in brain tissue.
160 f HIV-1 coreceptors and up-regulation of the cyclin-dependent kinase inhibitor p21 (also known as cip
161 ith strong and selective upregulation of the cyclin-dependent kinase inhibitor p21 (also known as cip
162 ncreased transcription and expression of the cyclin-dependent kinase inhibitor p21 and consequent cel
163 ciated with HER2-induced accumulation of the cyclin-dependent kinase inhibitor p21 and decrease in th
164 rrest accompanied by increased expression of cyclin-dependent kinase inhibitor p21 and decreased expr
165 st cancer cells, increased expression of the cyclin-dependent kinase inhibitor p21 but had no effect
166 damage response signaling pathway involving cyclin-dependent kinase inhibitor p21 expression and het
167 ed expression of the key p53 target gene and cyclin-dependent kinase inhibitor p21 in HCT116 cells, p
168 We found that PCBP4 expression decreases cyclin-dependent kinase inhibitor p21 induction in respo
173 usly, we demonstrated that expression of the cyclin-dependent kinase inhibitor p21 is reduced in syno
174 d at the promoters of the genes encoding the cyclin-dependent kinase inhibitor p21 or the transcripti
175 an E3 ubiquitin ligase, CRL2(LRR1), for the cyclin-dependent kinase inhibitor p21 that specifically
178 rentiation of MLL-AF9 blasts, which requires cyclin-dependent kinase inhibitor p21(Cip1) (Cdkn1a) act
179 vely lower in HTSF compared to NADF, and the cyclin-dependent kinase inhibitor p21(cip1) is upregulat
182 nstream-regulated gene 1 and upregulated the cyclin-dependent kinase inhibitor p21(CIP1/WAF1) while d
184 rminus deficiency promotes expression of the cyclin-dependent kinase inhibitor p21(Waf1/Cip1) (Cdkn1a
185 liferation of ATC cells via induction of the cyclin-dependent kinase inhibitor p21(WAF1/CIP1) (p21).
186 t transcription of both IkappaBalpha and the cyclin-dependent kinase inhibitor p21(WAF1/CIP1) and ind
188 ntly increases transcription and activity of cyclin-dependent kinase inhibitor p21(WAF1/CIP1), leadin
190 rt that cellular mRNAs encoding the cellular cyclin-dependent kinase inhibitor p21, a key inducer of
191 hat fine-tuning the expression levels of the cyclin-dependent kinase inhibitor p21, a p53 target gene
192 tion, stabilization of p53, induction of the cyclin-dependent kinase inhibitor p21, and homologous re
193 9, it inhibits BMP-mediated induction of the cyclin-dependent kinase inhibitor p21, and it reverses B
194 hat directly regulates the expression of the cyclin-dependent kinase inhibitor p21, independently of
196 evels of bone morphogenetic proteins and the cyclin-dependent kinase inhibitor p21, which might contr
202 53 response, accompanied by induction of the cyclin-dependent kinase inhibitor p21/CIP1, which can be
204 le phase, and the expression of pAkt and the cyclin-dependent kinase inhibitors p21 and p27 was incre
205 ignificant increase in the expression of the cyclin-dependent kinase inhibitors p21 and p27, and a de
206 e/AKT signaling pathway, upregulation of the cyclin-dependent kinase inhibitors p21 and p27, antiprol
209 xygenase-1, programmed cell death 4, and the cyclin-dependent kinase inhibitors p21, p27, and p57.
210 e inducible Src homology 2-containing genes, cyclin-dependent kinase inhibitors p21, p57, calmodulin
211 phate (IP6) causes G(1) arrest and increases cyclin-dependent kinase inhibitors p21/Cip1 and p27/Kip1
213 ectopic expression of p16(INK4a) and another cyclin-dependent kinase inhibitor, p21(CIP1/WAF1), induc
214 with the p53-independent upregulation of the cyclin-dependent kinase inhibitor, p21(WAF1/Cip1) (p21).
217 egulation of cyclin D1, up-regulation of the cyclin-dependent kinase inhibitors, p21(cip1.) and p16(I
218 by hyperactivated NF-kappaB and mediated by cyclin-dependent kinase inhibitors, p21(CIP1/WAF1) and p
219 ggers a host senescence response mediated by cyclin-dependent kinase inhibitors: p21(CIP1/WAF1) (p21)
224 is likely due to increased expression of the cyclin-dependent kinase inhibitors p21Cip1/Waf1 and p19I
225 plexes bind a promoter motif and repress the cyclin-dependent kinase inhibitor p21WAF1 in both human
226 an increase in the tumor protein p53 and the cyclin-dependent kinase inhibitor p21WAF1/CIP1, which ar
227 C-mediated transcriptional inhibition of the cyclin-dependent kinase inhibitors p21WAF1 and p27KIP2,
228 ng the receptors EGFR, ERBB3 (HER3), and the cyclin-dependent kinase inhibitor p27 (CDKN1B) was found
229 1 and E1 while suppressing the expression of cyclin-dependent kinase inhibitor p27 (CDKN1B), each con
230 rapamycin, mTOR) and altered activity of the cyclin-dependent kinase inhibitor p27 (p27(kip1)) and ex
231 ell proliferation and elevated expression of cyclin-dependent kinase inhibitor P27 (P27KIP1) in a GEF
233 C/C(Cdh1)), resulting in accumulation of the cyclin-dependent kinase inhibitor p27 and a concomitant
235 kdown results in the nuclear localization of cyclin-dependent kinase inhibitor p27 and prevents the p
237 d with rapamycin produced an increase in the cyclin-dependent kinase inhibitor p27(Kip), through a de
238 s generated an adenovirus that expresses the cyclin-dependent kinase inhibitor p27(Kip1) (p27) and be
240 l endothelial cells (rCECs) by degrading the cyclin-dependent kinase inhibitor p27(Kip1) (p27) throug
241 used an adenoviral (Ad) vector that encodes cyclin-dependent kinase inhibitor p27(Kip1) (p27) with t
243 tating translation of mRNAs encoding for the cyclin-dependent kinase inhibitor p27(Kip1) and antiapop
244 ors of cell proliferation and migration, the cyclin-dependent kinase inhibitor p27(Kip1) and the micr
245 EFs leads to an increase in the level of the cyclin-dependent kinase inhibitor p27(Kip1) and to rapid
247 ion and hyperproliferation by downregulating cyclin-dependent kinase inhibitor p27(kip1) in a proteas
248 colleagues (3121-3134) demonstrate that the cyclin-dependent kinase inhibitor p27(Kip1) is ubiquityl
250 that HINT1 regulates cellular levels of the cyclin-dependent kinase inhibitor p27(KIP1) through mult
251 g for the proliferation marker Ki-67 and the cyclin-dependent kinase inhibitor p27(Kip1) were perform
252 orroborated in this study by coexpression of cyclin-dependent kinase inhibitor p27(Kip1)), we hypothe
253 s are actively cycling, but some express the cyclin-dependent kinase inhibitor p27(Kip1), and are pre
254 s T-cell proliferation by the destruction of cyclin-dependent kinase inhibitor p27(kip1), and deletio
255 One of these, miR-221, a regulator of the cyclin-dependent kinase inhibitor p27(kip1), displayed r
256 ivation, and cytoplasmic localization of the cyclin-dependent kinase inhibitor p27(Kip1), which has b
261 re, attributed to elevated expression of the cyclin-dependent kinase inhibitor p27, a Siah2 substrate
262 osol, which causes hyper-accumulation of the cyclin-dependent kinase inhibitor p27, leading to mitoti
266 differentiation by modulating expression of cyclin-dependent kinase inhibitor p27/p57 and E3 ubiquit
268 jugating E3 ligase Skp2 and up-regulation of cyclin-dependent kinase inhibitors p27(Kip1) and p21(Cip
269 and (3) an increase in the expression of the cyclin-dependent kinase inhibitors p27(kip1) and p21(cip
271 ors of cell proliferation and migration, the cyclin-dependent kinase inhibitor p27Kip1 and the microt
274 bited a significant decrease in the level of cyclin-dependent kinase inhibitor p57(KIP2) and an incre
277 s the expression of the beta-cell-associated cyclin-dependent kinase inhibitor p57kip2, and simultane
278 gnaling reduced expression of N-cad, and the cyclin dependent kinase inhibitor, p57Kip2, indicating a
280 rest mediated by the ROS-activated SMR5/SMR7 cyclin-dependent kinase inhibitors pathway in the intera
282 associated with reduced expression of p21, a cyclin-dependent kinase inhibitor previously implicated
283 TX-1 and benzamil up-regulated expression of cyclin-dependent kinase inhibitor proteins p21(Cip1) and
284 e, we show that polymersomes can deliver the cyclin-dependent kinase inhibitor (R)-roscovitine into h
285 F-box protein) recognizes its substrate, the cyclin-dependent kinase inhibitor Sic1, in a multisite p
286 iquitinylates many substrates, including the cyclin-dependent kinase inhibitor Sic1, targeting it for
287 his study, we show that dinaciclib, a potent cyclin dependent kinase inhibitor, significantly increas
290 oRNAs, and represses expression of Cdkn1a, a cyclin-dependent kinase inhibitor that negatively regula
292 ctor of tumor suppressors and functions as a cyclin-dependent kinase inhibitor to block cellular prol
293 ore rearrangement and release of sequestered cyclin-dependent kinase inhibitors to elicit immunity an
294 Senescent cells often express p16(INK4a), a cyclin-dependent kinase inhibitor, tumor suppressor, and
295 Expression of p57kip2, a BMP10-regulated cyclin-dependent kinase inhibitor, was induced in Myocd-
296 e SIAMESE/SIAMESE-RELATED (SIM/SMR) class of cyclin-dependent kinase inhibitors were discovered that
299 lation of the Skp2-degradation target p27, a cyclin-dependent kinase inhibitor, which was confirmed a
300 e switching, the Xenopus laevis Cip/Kip-type cyclin-dependent kinase inhibitor Xic1 associates with t