ライフサイエンスコーパス: cyclin-dependent kinase inhibitor

1 ell-cycle arrest and accumulation of the p27 cyclin-dependent kinase inhibitor.

2 Flavopiridol is a protein bound, cytotoxic, cyclin-dependent kinase inhibitor.

3 activity and the expression level of p16, a cyclin-dependent kinase inhibitor.

4 e consequence of sporadic loss of p27kip1, a cyclin-dependent kinase inhibitor.

5 pecificity between a GHV cyclin and a single cyclin-dependent kinase inhibitor.

6 a70kb) mice is prevented by treatment with a cyclin-dependent kinase inhibitor.

7 , together with the induction of p21 and p27 cyclin-dependent kinase inhibitors.

8 Ecad- subpopulation through the induction of cyclin-dependent kinase inhibitors.

9 cyclin expression and elevated expression of cyclin-dependent kinase inhibitors.

10 way-directed agents such as flavopiridol and cyclin-dependent kinase inhibitors.

11 reased apoptosis and decreased expression of cyclin-dependent kinase inhibitors.

12 27(Kip1) , a member of the Kip/Cip family of cyclin-dependent kinase inhibitors.

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 logical functions of p21, the product of the cyclin-dependent kinase inhibitor 1A (CDKN1A) gene, with

16 dramatically up-regulated the mRNA encoding cyclin-dependent kinase inhibitor 1a (Cdkn1a).

17 re, we show that loss of the p53 target gene cyclin-dependent kinase inhibitor 1A (CDKN1A, also known

18 l-cycle genes, and we identified the mRNA of cyclin-dependent kinase inhibitor 1A (Cdkn1a, p21) as a

19 Among the tested miR-17 targets, the cyclin-dependent kinase inhibitor 1A (p21) was up-regula

20 R-34 family, TP53 gene, downstream effectors cyclin-dependent kinase inhibitor 1A (p21, Cip1) (CDKN1A

21 e stem cell (HFSC) homeostasis and find p21 (cyclin-dependent kinase inhibitor 1a, Cdkn1a), p57, and

22 pathways; and residual hepatocytes overcame cyclin-dependent kinase inhibitor 1A-induced cell growth

23 is led to liver cell growth arrest involving cyclin-dependent kinase inhibitor 1A.

24 behavior through repression of two targets: cyclin dependent kinase inhibitor 1b (cdkn1b) and phosph

25 e B-cell CLL/lymphoma 2 or xL (Bcl-2/xL) and cyclin-dependent kinase inhibitor 1B (P27) protein level

26 ad markedly decreased quiescence and reduced cyclin-dependent kinase inhibitor 1b/c (Cdkn1b/1c) expre

27 is-derived transcript), the tumor suppressor cyclin-dependent kinase inhibitor 1C (CDKN1C; p57KIP2),

28 olutionarily conserved cell-cycle regulator, cyclin-dependent kinase inhibitor 1d (20 kDa protein, p2

29 genes phosphatase and tensin homolog (PTEN), cyclin dependent kinase inhibitor 2A (CDKN2A), LKB1, and

30 overexpression is concomitant with a loss of cyclin-dependent kinase inhibitor 2A (CDKN2A) locus (enc

31 tions of knockdowns of the tumor suppressors cyclin-dependent kinase inhibitor 2A (Cdkn2a), transform

32 Furthermore, T-box (TBX) genes and cyclin-dependent kinase inhibitor 2A (CDKN2A), which are

33 BRAF(V600E)) in association with homozygous cyclin-dependent kinase inhibitor 2A (CDKN2A, encoding p

34 sistent microbial insult (e.g. LPSs) induces cyclin-dependent kinase inhibitor 2A (CDKN2A/p16(INK4a))

35 iral oncogene [Kras(G12V)] and disruption of cyclin-dependent kinase inhibitor 2A (CDKN2A; p16p19) in

36 on through derepression of the gene encoding cyclin-dependent kinase inhibitor 2a (INK4a).

37 d III transcription, and thyroxine decreased cyclin-dependent kinase inhibitor 2A (p16(ink4)) express

38 by a mechanism that involved suppression of cyclin-dependent kinase inhibitor 2A (p16INK4A) expressi

39 tivariate model, promoter methylation of the cyclin-dependent kinase inhibitor 2A gene p16, the H-cad

40 ers associated with repression of p16(INK4a)/cyclin-dependent kinase inhibitor 2A(CDKN2A), a critical

41 (hepatocyte growth factor receptor), CDKN2A (cyclin-dependent kinase inhibitor 2A) and CDKN2B (cyclin

42 d by another major POAG risk gene, p16INK4a (cyclin-dependent kinase inhibitor 2A, isoform INK4a).

43 at loss of one candidate gene at this locus, cyclin-dependent kinase inhibitor 2B (Cdkn2b), in mice p

44 factor beta (TGFbeta) signaling in cultured cyclin-dependent kinase inhibitor 2B (CDKN2B)-deficient

45 hypoxia inducible factor 1A antisense RNA 2, cyclin-dependent kinase inhibitor 2B antisense RNA 1 (AN

46 or STAT5, enhances expression of the Cdkn2b (cyclin-dependent kinase inhibitor 2B) gene and that STAT

47 n-dependent kinase inhibitor 2A) and CDKN2B (cyclin-dependent kinase inhibitor 2B), as well as many o

48 Edg1/S1P(1), beta(7) integrin, CD52, Cdkn2d (cyclin-dependent kinase inhibitor 2D), s100a4, and IL10R

49 h Cyclin D1 and Cyclin D2, and the p27(Kip1) cyclin-dependent kinase inhibitor act downstream of Notc

50 p27(kip1) is a cyclin-dependent kinase inhibitor and a tumor suppressor

51 be reversed by treatment with roscovitine, a cyclin-dependent kinase inhibitor and atypical L-type-ch

52 CDKN1C is a cyclin-dependent kinase inhibitor and is a candidate tum

53 This was accompanied by upregulation of cyclin-dependent kinase inhibitors and a significant cel

54 w targets and associated therapeutic agents: cyclin-dependent kinase inhibitors and poly(adenosine di

55 AMPKalpha1 reduced the level of p27(Kip1), a cyclin-dependent kinase inhibitor, and increased the lev

56 he SAM, suggesting that the effects of these cyclin-dependent kinase inhibitors are context dependent

57 cribed mechanisms involving the induction of cyclin-dependent kinase inhibitors but also by the recru

58 iferation, but the induction of TGF-beta and cyclin-dependent kinase inhibitors causes a cell cycle a

59 These include the cyclin-dependent kinase inhibitor (CDKI) p18INK4c, the m

60 g a model of resistance to a pharmacological cyclin-dependent kinase inhibitor (CDKi), we show that t

61 Previous studies showed that cyclin-dependent kinase inhibitors (CDKI) induce autopha

62 ich normally regulates cell cycle inhibitory cyclin-dependent kinase inhibitors (cdki).

63 ase 4 and 6, and increased the expression of cyclin dependent kinase inhibitors (CDKIs), p21 and p27.

64 Cyclin-dependent kinase inhibitors (CDKis) are known inh

65 on of its target protein-coding genes (i.e., cyclin-dependent kinase inhibitor [Cdkn]1b/p27, Cdkn1c/p

66 mediates GC formation through repression of cyclin-dependent kinase inhibitor CDKN1A (p21(Cip1)).

67 repressor, which leads to expression of the cyclin-dependent kinase inhibitor CDKN1A (p21(CIP1/WAF1)

68 Runx1 deletion resulted in cyclin-dependent kinase inhibitor Cdkn1a (p21) upregulat

69 In particular, we found that the cyclin-dependent kinase inhibitor CDKN1A (p21) was overe

70 inogenesis that depends, in part, on loss of cyclin-dependent kinase inhibitor CDKN1A.

71 Its KD results in accumulation of the cyclin-dependent kinase inhibitors CDKN1A and CDKN1B, G(

72 its downstream targets, cJUN, ATF3, and the cyclin-dependent kinase inhibitors CDKN1A and CDKN2B.

73 lial marker expression, and late increase in cyclin-dependent kinase inhibitor CDKN1B (p27) protein-w

74 Here we increase levels of the cyclin-dependent kinase inhibitor Cdkn1b (p27kip1) in ad

75 We identified the cyclin-dependent kinase inhibitor Cdkn1c (p57) as a key

76 cell-cycle transition through repression of cyclin-dependent kinase inhibitors Cdkn2a and Cdkn2b, an

77 e show that Hoxa9 represses the locus of the cyclin-dependent kinase inhibitors Cdkn2a/b in concert w

78 gnature correlates with the induction of the cyclin-dependent kinase inhibitors CDKN2D (p19(INK4d)) a

79 ty, and resulting in accumulation of p53 and cyclin-dependent kinase inhibitors, cell cycle arrest, a

80 a protein expression and increased levels of cyclin-dependent kinase inhibitors, CIP1 (p21) and KIP1

81 G1 arrest in part through regulation of the cyclin-dependent kinase inhibitor cki-1.

82 ntify the p21(Cip1)/p27(Kip1)/p57(Kip2)-like cyclin-dependent kinase inhibitor (CKI) Dacapo (Dap) as

83 Peptide treatment induced cyclin-dependent kinase inhibitor (CKI) p16(INK4a) prote

84 re, we report a novel mechanism by which the cyclin-dependent kinase inhibitor (CKI) p21(Waf1/Cip1/Sd

85 Here, we defined the roles of cyclin-dependent kinase inhibitor (CKI) p57(KIP2), an im

86 that the p21(cip1)/p27(kip1)/p57(kip2)-like cyclin-dependent kinase inhibitor (CKI), Dacapo (Dap), p

87 e hypothesize that this is due to a weakened cyclin-dependent kinase inhibitor (CKI)-cyclin-dependent

88 of cyclin D1 and increased expression of the cyclin-dependent kinase inhibitors (CKI), p27(Kip1) and

89 ar access of signaling cargos and sequesters cyclin-dependent kinase inhibitors (CKIs) involved in ET

90 tein suppresses the transcription of several cyclin-dependent kinase inhibitors (CKIs) via binding to

91 lation of the tumor suppressors pRb, Cip/Kip cyclin-dependent kinase inhibitors (CKIs), and CDH1, and

92 ated PCD through a physical interaction with cyclin-dependent kinase inhibitors (CKIs).

93 Systemic administration of the selective cyclin-dependent kinase inhibitor CR8 after SCI signific

94 The cyclin-dependent kinase inhibitor Dacapo (Dap), a p21/p2

95 Using the cyclin-dependent kinase inhibitor dinaciclib, which down

96 lation and indicate that modulating a single cyclin-dependent kinase inhibitor does not disrupt cell

97 Furthermore p21, a cyclin-dependent kinase inhibitor downstream of S100/A11

98 Here, we address how interactions between cyclin-dependent kinase inhibitors essential for myogeni

99 oma cation channel complex, had no effect on cyclin-dependent kinase inhibitor expression.

100 the redox-reactive thalidomide CPS49 and the cyclin-dependent kinase inhibitor flavopiridol as a sele

101 ase I (Topo I) poison CPT-11 followed by the cyclin-dependent kinase inhibitor flavopiridol in patien

102 matic mutations and deletions in CDKN1B, the cyclin-dependent kinase inhibitor gene, which encodes p2

103 associated with reduced aortic expression of cyclin-dependent kinase inhibitor genes p19Arf and p15In

104 the mRNA expression of osteoblast marker and cyclin-dependent kinase inhibitor genes were all reduced

105 was selectively restricted by expressing two cyclin-dependent kinase inhibitor genes, KRP1/ICK1 and K

106 Two homologous cyclin-dependent kinase inhibitor genes, SIAMESE (SIM) a

107 However, whether cyclin-dependent kinase inhibitor I induction by IP6 pla

108 CDKN1C/P57 is a cyclin-dependent kinase inhibitor implicated in differen

109 s on the role of one RNA in silencing p15, a cyclin-dependent kinase inhibitor implicated in leukaemi

110 enetic inactivation of p16(ink4a) encoding a cyclin-dependent kinase inhibitor implicated in neuronal

111 Our data, in addition to identifying cyclin-dependent kinase inhibitors important in cell cyc

112 reveals differential roles of two homologous cyclin-dependent kinase inhibitors in regulating cell-cy

113 viral cyclin has reduced sensitivity to host cyclin-dependent kinase inhibitors in vitro; however, th

114 to the down-regulation of p21(WAF1/cip1), a cyclin-dependent kinase inhibitor, in intestinal epithel

115 as its downstream target, the p21(Cip1/Waf1) cyclin-dependent kinase inhibitor, in the regulation of

116 eased expression of PDGFRbeta and p57kip2, a cyclin-dependent kinase inhibitor, in these cells.

117 Hdac3 overexpression inhibits several cyclin-dependent kinase inhibitors, including Cdkn1a, Cd

118 Cyclin-dependent kinase inhibitors, including p21Cip1, a

119 Messenger RNA levels of cyclin-dependent kinase inhibitors increased progressive

120 from an alternative reading frame of the p16 cyclin-dependent kinase inhibitor INK4a/ARF gene.

121 liferation is due in part to derepression of cyclin-dependent kinase inhibitors Ink4a/b, while ineffe

122 We have found that the expression of p21, a cyclin-dependent kinase inhibitor involved in cell cycle

123 The stability of p21, a cyclin-dependent kinase inhibitor, is highly regulated b

124 p21, a cyclin-dependent kinase inhibitor, is necessary for prop

125 of FBL17 increases the stability of the CDK (CYCLIN-DEPENDENT KINASE) inhibitor KIP-RELATED PROTEIN2

126 ost inhibitors p27(Kip1) and p18(INK4c), two cyclin-dependent kinase inhibitors known to be important

127 nt of corneal transparency without affecting cyclin-dependent kinase inhibitor levels in Vim(-/-) mic

128 ly due to a failure in proliferation; p27, a cyclin dependent kinase inhibitor, normally undetectable

129 wt cells, which also correlated with p27/p21 cyclin-dependent kinase inhibitor over-expression.

130 stically, this involved up-regulation of the cyclin-dependent kinase inhibitor p15 and the proapoptot

131 k genotype does not affect the activation of cyclin-dependent kinase inhibitors p15 and p16 by interf

132 senescence, accompanied by the induction of cyclin-dependent kinase inhibitors p15(INK4B), p16(INK4A

133 cytostatic program include activation of the cyclin-dependent kinase inhibitors, p15(Ink4B) and p21(W

134 xpression of two other cell cycle inhibitory cyclin-dependent kinase inhibitors, p15Ink4b (Cdkn2b) an

135 -->S cell cycle progression by targeting the cyclin-dependent kinase inhibitor p16(INK4a) (p16).

136 on of the Ink4a/Arf locus, which encodes the cyclin-dependent kinase inhibitor p16(INK4a) and tumor s

137 Mutations or deletions in the cyclin-dependent kinase inhibitor p16(INK4A) are associa

138 argeting the CDKN2A locus, which encodes the cyclin-dependent kinase inhibitor p16, decreased CDKN2A

139 (stasis) associated with elevated levels of cyclin-dependent kinase inhibitors p16 and/or p21.

140 Restored expression of the cyclin-dependent kinase inhibitor p16INK4a abrogated the

141 l -74 C-to-T mutation in the promoter of the cyclin-dependent kinase inhibitor p18(Ink4c) (p18) gene

142 nalysis presents Cdkn2c, a gene encoding for cyclin-dependent kinase inhibitor p18(INK4c) (p18), as t

143 he expression of Cdkn2c, a gene encoding for cyclin-dependent kinase inhibitor p18(Ink4c) and located

144 cyclin functions specifically to bypass the cyclin-dependent kinase inhibitor p18(INK4c), revealing

145 the ATM inhibitor showed increased levels of cyclin-dependent kinase inhibitor p19(INK4D), reduced le

146 l cycle regulators cyclins D, A2, and B2 and cyclin-dependent kinase inhibitor p20 in brain tissue.

147 f HIV-1 coreceptors and up-regulation of the cyclin-dependent kinase inhibitor p21 (also known as cip

148 ith strong and selective upregulation of the cyclin-dependent kinase inhibitor p21 (also known as cip

149 ncreased transcription and expression of the cyclin-dependent kinase inhibitor p21 and consequent cel

150 ciated with HER2-induced accumulation of the cyclin-dependent kinase inhibitor p21 and decrease in th

151 rrest accompanied by increased expression of cyclin-dependent kinase inhibitor p21 and decreased expr

152 st cancer cells, increased expression of the cyclin-dependent kinase inhibitor p21 but had no effect

153 damage response signaling pathway involving cyclin-dependent kinase inhibitor p21 expression and het

154 ed expression of the key p53 target gene and cyclin-dependent kinase inhibitor p21 in HCT116 cells, p

155 We found that PCBP4 expression decreases cyclin-dependent kinase inhibitor p21 induction in respo

156 We have previously shown that the cyclin-dependent kinase inhibitor p21 inhibits the repli

157 The cyclin-dependent kinase inhibitor p21 is an important pl

158 The cyclin-dependent kinase inhibitor p21 is an important tr

159 Here, we demonstrate that the cyclin-dependent kinase inhibitor p21 is both necessary

160 usly, we demonstrated that expression of the cyclin-dependent kinase inhibitor p21 is reduced in syno

161 d at the promoters of the genes encoding the cyclin-dependent kinase inhibitor p21 or the transcripti

162 an E3 ubiquitin ligase, CRL2(LRR1), for the cyclin-dependent kinase inhibitor p21 that specifically

163 These studies revealed that loss of the cyclin-dependent kinase inhibitor p21 was associated wit

164 sed expression of proapoptotic genes and the cyclin-dependent kinase inhibitor p21 was seen.

165 OS) and by maintaining the expression of the cyclin-dependent kinase inhibitor p21(CDKN1A).

166 rentiation of MLL-AF9 blasts, which requires cyclin-dependent kinase inhibitor p21(Cip1) (Cdkn1a) act

167 vely lower in HTSF compared to NADF, and the cyclin-dependent kinase inhibitor p21(cip1) is upregulat

168 The cyclin-dependent kinase inhibitor p21(Cip1) plays an imp

169 The cyclin-dependent kinase inhibitor p21(Cip1) regulates mu

170 stoma suppressor protein pRb, as well as the cyclin-dependent kinase inhibitor p21(Cip1).

171 nstream-regulated gene 1 and upregulated the cyclin-dependent kinase inhibitor p21(CIP1/WAF1) while d

172 ited cell proliferation and up-regulated the cyclin-dependent kinase inhibitor p21(CIP1/WAF1).

173 rminus deficiency promotes expression of the cyclin-dependent kinase inhibitor p21(Waf1/Cip1) (Cdkn1a

174 liferation of ATC cells via induction of the cyclin-dependent kinase inhibitor p21(WAF1/CIP1) (p21).

175 t transcription of both IkappaBalpha and the cyclin-dependent kinase inhibitor p21(WAF1/CIP1) and ind

176 The cyclin-dependent kinase inhibitor p21(Waf1/Cip1) is a ma

177 ntly increases transcription and activity of cyclin-dependent kinase inhibitor p21(WAF1/CIP1), leadin

178 the nitric oxide-dependent induction of the cyclin-dependent kinase inhibitor p21(Waf1/Cip1).

179 rt that cellular mRNAs encoding the cellular cyclin-dependent kinase inhibitor p21, a key inducer of

180 hat fine-tuning the expression levels of the cyclin-dependent kinase inhibitor p21, a p53 target gene

181 tion, stabilization of p53, induction of the cyclin-dependent kinase inhibitor p21, and homologous re

182 9, it inhibits BMP-mediated induction of the cyclin-dependent kinase inhibitor p21, and it reverses B

183 hat directly regulates the expression of the cyclin-dependent kinase inhibitor p21, independently of

184 A key target of PC1, the cyclin-dependent kinase inhibitor p21, is also up-regula

185 evels of bone morphogenetic proteins and the cyclin-dependent kinase inhibitor p21, which might contr

186 d resulted in decreased transcription of the cyclin-dependent kinase inhibitor p21.

187 ession of proarrest gene targets such as the cyclin-dependent kinase inhibitor p21.

188 and one of its transcriptional targets, the cyclin-dependent kinase inhibitor p21.

189 d DNA synthesis through the induction of the cyclin-dependent kinase inhibitor p21.

190 decreased transcriptional activation of the cyclin-dependent kinase inhibitor p21.

191 ultiple targets of the family, including the cyclin-dependent kinase inhibitor p21/CDKN1A.

192 53 response, accompanied by induction of the cyclin-dependent kinase inhibitor p21/CIP1, which can be

193 endent on increased expression of the cyclin/cyclin-dependent kinase inhibitor p21/WAF1/CIP1.

194 le phase, and the expression of pAkt and the cyclin-dependent kinase inhibitors p21 and p27 was incre

195 ignificant increase in the expression of the cyclin-dependent kinase inhibitors p21 and p27, and a de

196 e/AKT signaling pathway, upregulation of the cyclin-dependent kinase inhibitors p21 and p27, antiprol

197 bited proliferation through induction of the cyclin-dependent kinase inhibitors p21 and p27.

198 fect was mediated through decreased level of cyclin-dependent kinase inhibitors p21 and p27.

199 xygenase-1, programmed cell death 4, and the cyclin-dependent kinase inhibitors p21, p27, and p57.

200 e inducible Src homology 2-containing genes, cyclin-dependent kinase inhibitors p21, p57, calmodulin

201 phate (IP6) causes G(1) arrest and increases cyclin-dependent kinase inhibitors p21/Cip1 and p27/Kip1

202 in part through decreasing expression of the cyclin dependent kinase inhibitor, p21.

203 iptional repression of TLX target genes, the cyclin-dependent kinase inhibitor, p21(CIP1/WAF1)(p21),

204 ectopic expression of p16(INK4a) and another cyclin-dependent kinase inhibitor, p21(CIP1/WAF1), induc

205 with the p53-independent upregulation of the cyclin-dependent kinase inhibitor, p21(WAF1/Cip1) (p21).

206 r senescence by repressing the expression of cyclin-dependent kinase inhibitor, p21(Waf1/Cip1).

207 ng p53-induced protein with death domain and cyclin-dependent kinase inhibitor, p21.

208 egulation of cyclin D1, up-regulation of the cyclin-dependent kinase inhibitors, p21(cip1.) and p16(I

209 by hyperactivated NF-kappaB and mediated by cyclin-dependent kinase inhibitors, p21(CIP1/WAF1) and p

210 ggers a host senescence response mediated by cyclin-dependent kinase inhibitors: p21(CIP1/WAF1) (p21)

211 o a partial G1/S arrest and induction of the cyclin-dependent kinase inhibitor, p21cip/CDKN1A.

212 We found that the expression of cyclin-dependent kinase inhibitor p21cip1 was impaired i

213 ers led to compensatory up-regulation of the cyclin-dependent kinase inhibitor p21Cip1.

214 , processes also under the regulation of the cyclin-dependent kinase inhibitor p21Cip1.

215 is likely due to increased expression of the cyclin-dependent kinase inhibitors p21Cip1/Waf1 and p19I

216 plexes bind a promoter motif and repress the cyclin-dependent kinase inhibitor p21WAF1 in both human

217 C-mediated transcriptional inhibition of the cyclin-dependent kinase inhibitors p21WAF1 and p27KIP2,

218 ng the receptors EGFR, ERBB3 (HER3), and the cyclin-dependent kinase inhibitor p27 (CDKN1B) was found

219 1 and E1 while suppressing the expression of cyclin-dependent kinase inhibitor p27 (CDKN1B), each con

220 rapamycin, mTOR) and altered activity of the cyclin-dependent kinase inhibitor p27 (p27(kip1)) and ex

221 Down-regulation of the cyclin-dependent kinase inhibitor p27 alone significantl

222 C/C(Cdh1)), resulting in accumulation of the cyclin-dependent kinase inhibitor p27 and a concomitant

223 LMP1 decreases expression of the cyclin-dependent kinase inhibitor p27 and increases the

224 kdown results in the nuclear localization of cyclin-dependent kinase inhibitor p27 and prevents the p

225 a reduced binding of cytoplasmic RhoA to the cyclin-dependent kinase inhibitor p27 both contributed t

226 The cyclin-dependent kinase inhibitor p27 is a key regulator

227 d with rapamycin produced an increase in the cyclin-dependent kinase inhibitor p27(Kip), through a de

228 s generated an adenovirus that expresses the cyclin-dependent kinase inhibitor p27(Kip1) (p27) and be

229 Cyclin-dependent kinase inhibitor p27(kip1) (p27) has re

230 l endothelial cells (rCECs) by degrading the cyclin-dependent kinase inhibitor p27(Kip1) (p27) throug

231 rein results in lack of up-regulation of the cyclin-dependent kinase inhibitor p27(Kip1) (p27) to arr

232 used an adenoviral (Ad) vector that encodes cyclin-dependent kinase inhibitor p27(Kip1) (p27) with t

233 which is cytoplasmic mislocalization of the cyclin-dependent kinase inhibitor p27(Kip1) (p27).

234 tating translation of mRNAs encoding for the cyclin-dependent kinase inhibitor p27(Kip1) and antiapop

235 ciated with a selective up-regulation of the cyclin-dependent kinase inhibitor P27(KIP1) and inductio

236 ors of cell proliferation and migration, the cyclin-dependent kinase inhibitor p27(Kip1) and the micr

237 EFs leads to an increase in the level of the cyclin-dependent kinase inhibitor p27(Kip1) and to rapid

238 The cyclin-dependent kinase inhibitor p27(Kip1) arrests cell

239 Here, we have identified the cyclin-dependent kinase inhibitor p27(Kip1) as a critica

240 Reduced levels of the cyclin-dependent kinase inhibitor p27(Kip1) connote poor

241 ion and hyperproliferation by downregulating cyclin-dependent kinase inhibitor p27(kip1) in a proteas

242 atment with NaBT increased expression of the cyclin-dependent kinase inhibitor p27(kip1) in HT29 cell

243 colleagues (3121-3134) demonstrate that the cyclin-dependent kinase inhibitor p27(Kip1) is ubiquityl

244 The cyclin-dependent kinase inhibitor p27(Kip1) plays a crit

245 that HINT1 regulates cellular levels of the cyclin-dependent kinase inhibitor p27(KIP1) through mult

246 g for the proliferation marker Ki-67 and the cyclin-dependent kinase inhibitor p27(Kip1) were perform

247 orroborated in this study by coexpression of cyclin-dependent kinase inhibitor p27(Kip1)), we hypothe

248 s are actively cycling, but some express the cyclin-dependent kinase inhibitor p27(Kip1), and are pre

249 s T-cell proliferation by the destruction of cyclin-dependent kinase inhibitor p27(kip1), and deletio

250 One of these, miR-221, a regulator of the cyclin-dependent kinase inhibitor p27(kip1), displayed r

251 ivation, and cytoplasmic localization of the cyclin-dependent kinase inhibitor p27(Kip1), which has b

252 possess significantly reduced levels of the cyclin-dependent kinase inhibitor p27(kip1).

253 ion in part through the up-regulation of the cyclin-dependent kinase inhibitor p27(kip1).

254 t ultimately involves destabilization of the cyclin-dependent kinase inhibitor p27(Kip1).

255 endogenous expression of the E2F1-regulated cyclin-dependent kinase inhibitor p27(Kip1).

256 osol, which causes hyper-accumulation of the cyclin-dependent kinase inhibitor p27, leading to mitoti

257 ar localization relies on its binding to the cyclin-dependent kinase inhibitor p27.

258 IRES) in the 5'-UTR of the mRNA encoding the cyclin-dependent kinase inhibitor p27.

259 n D protein levels while down-regulating the cyclin-dependent kinase inhibitor p27.

260 regulation of c-Myc and stabilization of the cyclin-dependent kinase inhibitor p27/KIP1.

261 lls were proliferative, most coexpressed the cyclin-dependent kinase inhibitor p27/Kip1.

262 differentiation by modulating expression of cyclin-dependent kinase inhibitor p27/p57 and E3 ubiquit

263 dicted to target the cell growth suppressive cyclin-dependent kinase inhibitors p27 and p57.

264 jugating E3 ligase Skp2 and up-regulation of cyclin-dependent kinase inhibitors p27(Kip1) and p21(Cip

265 and (3) an increase in the expression of the cyclin-dependent kinase inhibitors p27(kip1) and p21(cip

266 n by causing a decrease in expression of the cyclin dependent-kinase inhibitor p27Kip1.

267 ors of cell proliferation and migration, the cyclin-dependent kinase inhibitor p27Kip1 and the microt

268 N-myc represses the expression of the cyclin-dependent kinase inhibitor p27Kip1 but acts indep

269 eading to the induction of FOXO3a and target cyclin-dependent kinase inhibitor p27Kip1 levels.

270 problem by reporting phosphorylation of the cyclin-dependent kinase inhibitor p27Kip1 on a tyrosine

271 The cyclin-dependent kinase inhibitor p57 is highly expresse

272 bited a significant decrease in the level of cyclin-dependent kinase inhibitor p57(KIP2) and an incre

273 In addition, our data suggest that cyclin-dependent kinase inhibitor p57(Kip2) and vascular

274 s the expression of the beta-cell-associated cyclin-dependent kinase inhibitor p57kip2, and simultane

275 gnaling reduced expression of N-cad, and the cyclin dependent kinase inhibitor, p57Kip2, indicating a

276 -line endocrine therapy, with or without the cyclin-dependent kinase inhibitor palbociclib.

277 rest mediated by the ROS-activated SMR5/SMR7 cyclin-dependent kinase inhibitors pathway in the intera

278 ls and fungi, a group of proteins called the cyclin-dependent kinase inhibitors play a key role in ce

279 P21, a cyclin-dependent kinase inhibitor, plays a pivotal role

280 associated with reduced expression of p21, a cyclin-dependent kinase inhibitor previously implicated

281 TX-1 and benzamil up-regulated expression of cyclin-dependent kinase inhibitor proteins p21(Cip1) and

282 e, we show that polymersomes can deliver the cyclin-dependent kinase inhibitor (R)-roscovitine into h

283 at p15(INK4b), rather than p27(KIP1), is the cyclin-dependent kinase inhibitor responsible for G0/G1

284 ase is sensitive to serum deprivation or the cyclin-dependent kinase inhibitor roscovatine.

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 The p16INK4a protein is a principal cyclin-dependent kinase inhibitor that decelerates the c

288 p21(Waf1/Cip1/Sdi1) is a cyclin-dependent kinase inhibitor that mediates cell cyc

289 oRNAs, and represses expression of Cdkn1a, a cyclin-dependent kinase inhibitor that negatively regula

290 Among cyclin-dependent kinase inhibitors that control the G1 p

291 ctor of tumor suppressors and functions as a cyclin-dependent kinase inhibitor to block cellular prol

292 ore rearrangement and release of sequestered cyclin-dependent kinase inhibitors to elicit immunity an

293 Senescent cells often express p16(INK4a), a cyclin-dependent kinase inhibitor, tumor suppressor, and

294 Cyclin-dependent kinase inhibitor type 2A (CDKN2A) has b

295 ed that the senescence pathway involving p21 cyclin-dependent kinase inhibitor was up-regulated in PG

296 Expression of p57kip2, a BMP10-regulated cyclin-dependent kinase inhibitor, was induced in Myocd-

297 e SIAMESE/SIAMESE-RELATED (SIM/SMR) class of cyclin-dependent kinase inhibitors were discovered that

298 Levels of p21 (Cip1/WAF1), a cyclin-dependent kinase inhibitor, were decreased in aff

299 The p16(INK4a) (p16) is a cyclin-dependent kinase inhibitor, which has been evalua

300 e switching, the Xenopus laevis Cip/Kip-type cyclin-dependent kinase inhibitor Xic1 associates with t