ライフサイエンスコーパス: p57(KIP2)

1 at least two other genes in this locus (IPL, p57(KIP2)).

2 is effect was not observed for either p15 or p57Kip2.

3 optosis, and it is located between hNAP2 and p57KIP2.

4 embers, including p21CiP1/WAF1, p27KIP1, and p57KIP2.

5 WS cell lines exhibited normal imprinting of p57KIP2.

6 proteins and resulted in phosphorylation of p57(Kip2).

7 ion of the cyclin-dependent kinase inhibitor p57(Kip2).

8 f the CKIs p21(Cip1), p14(ARF), p27(Kip1) or p57(Kip2).

9 increase levels of p21(CIP1), p27(KIP1), and p57(KIP2).

10 ncrease of apoptotic cells in the absence of p57(Kip2).

11 ndent kinase inhibitors (CKI), p27(Kip1) and p57(Kip2).

12 inhibitors includes p21(Cip1), p27(Kip1) and p57(Kip2).

13 By Western blot analysis, expression of p57(KIP2), a known marker of terminally differentiated f

14 dentified with loss-of-function mutations in p57(KIP2), a maternally expressed gene encoding a G(1) c

15 Expression of p57kip2, a BMP10-regulated cyclin-dependent kinase inhib

16 Here we report that p57Kip2, a cyclin-dependent kinase (CDK) inhibitor impli

17 rowth suppressor gene regulating IGF-II; (c) p57KIP2, a cyclin-dependent kinase inhibitor that causes

18 ssed from the paternal allele, while H19 and p57KIP2, a cyclin-dependent kinase inhibitor, are expres

19 d with decreased expression of PDGFRbeta and p57kip2, a cyclin-dependent kinase inhibitor, in these c

20 d/or methylation in 20% of BWS patients, and p57KIP2, a cyclin-dependent kinase inhibitor, which we f

21 found to co-occupy the promoter template of p57KIP2, a gene encoding a cyclin-dependent kinase inhib

22 t the CDK inhibitors p21(CIP), p27(KIP), and p57(KIP2) all promote the association of cdk4 with the D

23 ociation was observed between methylation of p57KIP2 alone and clinical-biologic characteristics stud

24 more centromeric domain including KVLQT1 and p57(KIP2), alterations in which are more common in BWS,

25 inted human genes on 11p15.5, IGF2, H19, and p57KIP2, although the latter gene is separated by 700 kb

26 le-mount antibody staining revealed that the p57Kip2 amacrine cells are evenly distributed across the

27 s of cyclin-dependent kinase inhibitor (CKI) p57(KIP2), an important regulator of G1 phase, using del

28 e display ectopic and elevated expression of p57(kip2) and a dramatic reduction in proliferative acti

29 e level of cyclin-dependent kinase inhibitor p57(KIP2) and an increase in the level of cyclin D3 as c

30 ture activation of p21(cip1), p27(kip1), and p57(kip2) and decreased myocyte proliferation.

31 for BWS that both harbors a null mutation in p57(Kip2) and displays loss of Igf2 imprinting.

32 p1) having the broadest expression, and both p57(Kip2) and p21(Cip1) showing transient expression in

33 In conclusion, our observations suggest that p57(KIP2) and p27(KIP1) control neuronal output for dist

34 re associated with its ability to upregulate p57(Kip2) and p27(Kip1) while downregulating Pax6 expres

35 R-92a in mice de-repressed the expression of p57(Kip2) and prevented glomerular injury in RPGN.

36 ggest that cyclin-dependent kinase inhibitor p57(Kip2) and vascular endothelial growth factor mRNAs a

37 at maintain normal heart functions (Myh6 and p57Kip2) and cnNfat3 counteracted their activation by Fo

38 me (BWS) have been mapped to 11p15.5 between p57KIP2 and IGF2, and all are derived from the maternal

39 at KVLQT1 spans much of the interval between p57KIP2 and IGF2, and that it is also imprinted.

40 The maternally expressed imprinted genes p57kip2 and M6P/Igf2r retard proliferation and reduce th

41 d it is located between two imprinted genes, p57KIP2 and TSSC3.

42 1 (Kvlqt1) and Cd81 (Tapa-1) between Cdkn1c (p57(Kip2)) and Mash2.

43 le regulators, such as p21(Cip1), p27(Kip1), p57(Kip2), and cyclin E.

44 luding p107, p130, p21(CIP1), p27(KIP1), and p57(KIP2), and is associated with cyclin.CDK complexes i

45 h depend on H19 for their imprinting, Mash2, p57(Kip2), and Kvlqt1 are unaffected by a deletion of th

46 CDK inhibitors (CKIs) p21(Cip1), p27(Kip1), p57(Kip2), and p130 for degradation.

47 ilized CKIs in vivo, particularly p27(Kip1), p57(Kip2), and p130.

48 cle checkpoint regulators such as p27(Kip1), p57(Kip2), and the aurora kinases through both an Akt-me

49 yclin-dependent kinase inhibitor 1C (CDKN1C; p57KIP2), and many polycomb-repressive complex 2 (PRC2)

50 n its expression pattern from IGF2, H19, and p57KIP2, and it shows biallelic expression in all tissue

51 associated cyclin-dependent kinase inhibitor p57kip2, and simultaneously suppresses the expression of

52 fiber cell differentiation, including Prox1, p57(KIP2), aquaporin 0 and beta-crystallins.

53 These studies demonstrate that p27(KIP1) and p57(KIP2) are critical terminal effectors of signal tran

54 ages of development, when both p27(Kip1) and p57(Kip2) are expressed in retinal progenitor cells, the

55 tigate if the tumor suppressor properties of p57KIP2 are dependent on its DNA methylation status, we

56 Our findings identify p57Kip2 as a functionally relevant target recruited by b

57 lly expressed genes, H19, Mash2, Kvlqt1, and p57(Kip2), as well as two paternally expressed genes, Ig

58 ipitation of CDK2 complex revealed increased p57Kip2 association with the kinase and concomitant redu

59 yzed the methylation levels of p73, p15, and p57(KIP2) at the time of initial remission in 199 patien

60 expression of the Cdkn1c gene (also known as p57(Kip2)) but does not interfere with maintenance of im

61 was considerably reduced after inhibition of p57(KIP2) by small interfering RNA, IEX-1 overexpression

62 cular mechanism underlying the regulation of p57(Kip2) by the Lhx genes, we combined chromatin immuno

63 Xic1) is a member of the p21(Cip1)/p27(Kip1)/p57(Kip2) CDK inhibitor family and inhibits CDK2-cyclin

64 s suggests that a key imprinting element for p57(Kip2) (Cdkn1c) also lies at a distance.

65 Only two of these genes, p57(KIP2) (CDKN1C) and IGF2, are likely to be functional

66 o evidence for allele-specific expression of p57(Kip2) (Cdkn1c) from our bacterial artificial chromos

67 hat key elements for expression of the mouse p57(Kip2) (Cdkn1c) gene also lie at a distance.

68 ntrol of Prox1, Jag1, p27(Kip1) (Cdkn1b) and p57(Kip2) (Cdkn1c) gene expression.

69 disruption of appropriate expression of the p57(KIP2) (CDKN1C) gene through mutations that occur at

70 ranscriptional profiling, we discovered that p57(Kip2) (Cdkn1c), encoding a cell cycle inhibitor, was

71 ecule, the cyclin-dependent kinase inhibitor p57(Kip2) (Cdkn1c).

72 OK (D11S4896E), Nup98, CARS, hNAP2 (NAP1L4), p57KIP2 (CDKN1C), KVLQT1 (KCNA9), TAPA-1, and ASCL2.

73 g the gene encoding the cell cycle inhibitor p57Kip2 (CDKN1C), which is silenced as a consequence of

74 We hypothesized that targeting p57Kip2 could stimulate adult human beta cell replicatio

75 We have found that the p57(Kip2) cyclin kinase inhibitor is upregulated during

76 We show that p57(Kip2) (cyclin-dependent kinase inhibitor protein 2)

77 By multivariate analysis, expression of p57Kip2, cytoplasmic p15, or a combination of p57Kip2 wi

78 Furthermore, p57(KIP2) deficiency markedly increased RGC and IPC divi

79 D-type and E cyclins was most evident in the p57(KIP2)-deficient lens wherein cyclin D overexpression

80 d for the inappropriate proliferation in the p57(Kip2)-deficient retinae to preserve the correct prop

81 ively regulates the cell cycle by inhibiting p57Kip2-dependent CDK2 activity in embryonic cortex.

82 vidence suggests that the inhibitory role of p57kip2 depends on specific interactions with binding pr

83 At this stage, p57(Kip2 )did not regulate proliferation.

84 tify a muscle-specific regulatory element of p57(kip2) directly activated by MRFs in myoblasts but re

85 CKIs (p15(Ink4b), p16(Ink4a), p21(Cip1), and p57(Kip2)) do not induce cleavage of cyclin A; other cyc

86 ression and imprinting of Mash2, Kvlqt1, and p57(Kip2) during development in embryonic and extraembry

87 e for the cyclin-dependent kinase inhibitor, p57KIP2, during the immortalization of cultured human ma

88 ctivities are integrated at the level of the p57(kip2) enhancer to regulate the decision between prog

89 Retinae from mice lacking p57(Kip2) exhibited inappropriate S-phase entry and apop

90 gnaling is required to repress p21(cip1) and p57(kip2) expression in muscle progenitor cells.

91 l in which Lhx6 and Lhx8 negatively regulate p57(Kip2) expression in the prospective palate area to a

92 luence myelopoiesis by transiently enhancing p57(KIP2) expression levels.

93 sposition to cancer, suggesting that loss of p57(KIP2) expression may play a role in the condition.

94 diabetes setting by regulating cyclin D3 and p57(KIP2) expression through the S1P signaling pathway.

95 Moreover, p27(KIP1) and p57(KIP2) expression were reduced, suggesting downregula

96 thesis and cyclin E, increased p27(KIP1) and p57(KIP2) expression, and prevented IGF-1-induced cyclin

97 f an element important for the regulation of p57(KIP2) expression.

98 ion in ES cells and generated mice devoid of p57(Kip2) expression.

99 which also exhibited increased p27(Kip1) and p57(Kip2) expression.

100 eration by maintaining Bmp10 and suppressing p57(kip2) expression.

101 D1 and E by 6 h, and decreased p27(KIP1) and p57(KIP2) expression.

102 We also examined p57KIP2 expression in the normal kidney and tongue of pa

103 protection assay to determine if changes in p57KIP2 expression play a role in WT.

104 Genotoxic stress induces p57Kip2 expression via the bone morphogenetic protein-Sm

105 e defects in cardiomyocyte proliferation and p57kip2 expression were rescued.

106 e of Id proteins, Id2 prevents activation of p57Kip2 expression, and the retinoblastoma tumor suppres

107 d in lens epithelium and directly suppresses p57Kip2 expression, providing a molecular link between N

108 pus p28Kix1, a member of the p21CIP1/p27KIP1/p57KIP2 family of cyclin-dependent kinase (Cdk) inhibito

109 e show that the Cdk inhibitors p27(KIP1) and p57(KIP2) function redundantly to control cell cycle exi

110 oliferation over that induced by the loss of p57(KIP2) function.

111 le of p57(Kip2) in vivo, we have ablated the p57(Kip2) gene by homologous recombination in ES cells a

112 The p57KIP2 gene encodes an inhibitor of cyclin-dependent ki

113 The p57kip2 gene encodes one such potent inhibitor of oligod

114 However, as the p57KIP2 gene is 500 kb centromeric to the gene encoding

115 We find that the p57KIP2 gene is imprinted, with preferential expression

116 chromosomal location, and imprinting of the p57KIP2 gene match the properties predicted for a tumor

117 We have previously shown that the p57KIP2 gene, which encodes a cyclin-dependent kinase in

118 These findings indicate that p57(Kip2) has an important role during mouse development

119 p57(Kip2) has been considered a candidate tumor suppress

120 p57(Kip2) has been linked to Beckwith-Wiedemann syndrome

121 Consequently, we propose that p57(Kip2) has two roles during retinal development, acti

122 sensitivity to doxorubicin, suggesting that p57Kip2 has a role in chemoresistance, which is consiste

123 d the gene encoding the cyclin-cdk inhibitor p57KIP2 has been a strong candidate.

124 ulatory proteins that includes p73, p15, and p57Kip2 has prognostic value in adult patients with ALL

125 Mice lacking the imprinted Cdk inhibitor p57(KIP2) have altered cell proliferation and differenti

126 Mutations in human p57(Kip2) have been implicated in Beckwith-Wiedemann syn

127 prenatal overgrowth, involves alterations in p57KIP2, IGF-II, H19, and KvLQT1; (c) we have found both

128 lts from this analysis demonstrated that the p57Kip2-immunoreactive amacrine cells are randomly organ

129 In addition, p57Kip2 immunoreactivity does not colocalize with any of

130 n 18 (9.5%) patients, p15 in 33 (17.4%), and p57(KIP2) in 7 (3.7%); 140 (74%) patients had methylatio

131 ogenitor cell cycle withdrawal that involves p57(Kip2) in a central role opposing latent Cyclin D1 an

132 uclei, where it associates with cyclin D and p57(Kip2) in active enzyme complexes.

133 We observed dramatic underexpression of p57(KIP2) in BiCHM, identical to that seen in complete H

134 Retroviral mediated overexpression of p57(Kip2) in embryonic retinal progenitor cells led to p

135 In addition, overexpression of p57(Kip2) in LNCaP cells inhibited tumor formation in nu

136 The specific functions of p57(Kip2) in lymphocytes have not yet been fully elucida

137 DK inhibitors p21(Waf1/Cip1), p27(Kip1), and p57(Kip2) in monkey kidney cells (CV-1).

138 n prostate cancer, and the overexpression of p57(Kip2) in prostate cancer cells significantly suppres

139 However, little is known about the role of p57(Kip2) in tumorigenesis and cancer progression.

140 To investigate the role of p57(Kip2) in vivo, we have ablated the p57(Kip2) gene by

141 in the imprinted gene CDKN1C (also known as P57KIP2) in two familial and four unrelated patients.

142 oding sequence and intron-exon boundaries of p57KIP2 in 40 unrelated BWS patients.

143 These findings place p57Kip2 in DDR and uncover molecular mechanisms by which

144 est that the tumor suppressive properties of p57KIP2 in leukemia may depend on the intrinsic promoter

145 Overexpression of p57KIP2 in p57KIP2 promoter methylated leukemic cell lin

146 In contrast, overexpression of p57KIP2 in partially methylated cells only resulted in a

147 Targeting p57Kip2 in primary rectal cancer cells and tumor models

148 However, one BWS patient did show LOI of p57KIP2 in skin fibroblasts.

149 concerning the absolute expression level of p57KIP2 in WT, we developed a sensitive and quantitative

150 Hh acts by inducing expression of cdkn1c (p57(Kip2)) in slow muscle precursor cells, but neither H

151 Consequently, loss of p57(KIP2) increased primarily layer 5-6 neuron productio

152 n of the cell cycle inhibitors p27(kip1) and p57(kip2), increased apoptosis and aberrant or reduced e

153 y, the deletion causes BWS with silencing of p57(KIP2), indicating deletion of an element important f

154 , and the cyclin dependent kinase inhibitor, p57Kip2, indicating a direct role for Notch signaling in

155 Elevated p57Kip2 induces G1/S phase cell cycle arrest but inhibit

156 activation of cdk6, the ultimate outcome of p57(Kip2) induction was a decrease in DNA synthesis and

157 f forced cyclin expression and/or of loss of p57(KIP2) inhibitor function in a cellular compartment t

158 of cyclins D and E and up-regulation of the p57(KIP2) inhibitor in the postmitotic lens fiber cell c

159 ibitor after PACAP exposure, suggesting that p57Kip2 interactions directly regulate CDK2 activity.

160 The CDK inhibitor p57(Kip2) is a major target of miR-92a that constitutive

161 p57(Kip2) is a paternally imprinted gene that encodes a

162 gulated very differently by DNA methylation; p57(Kip2) is activated, Kvlqt1 is silenced, and Mash2 is

163 erefore, these results strongly suggest that p57(Kip2) is an important gene in prostate cancer tumori

164 The results indicate that p57(Kip2) is involved in the regulation of several aspec

165 ptotic nuclei were found in the region where p57(Kip2) is normally expressed.

166 p57(Kip2) is primarily expressed in terminally different

167 Here, we show that the expression of p57(Kip2) is significantly decreased in human prostate c

168 p57(Kip2) is the first gene to be implicated as a regula

169 acking the cyclin-dependent kinase inhibitor p57(Kip2) is the opposite of the PTHrP-null phenotype, w

170 lin-dependent kinase inhibitor (CKI) CDKN1C (p57KIP2) is normally imprinted, with preferential expres

171 P57KIP2 is a cyclin-dependent kinase inhibitor silenced

172 ress the E protein E47 and Id2, we find that p57Kip2 is a target of E47.

173 p57Kip2 is also upregulated in stage I and II clinical r

174 In humans, p57KIP2 is expressed specifically in skeletal muscle, he

175 Our results indicate that p57KIP2 is frequently methylated in adult patients with

176 om the maternal grandfather, suggesting that p57KIP2 is not imprinted in at least some affected tissu

177 During brain development, expression of p57Kip2 is opposite that of Id2.

178 Thus, p57KIP2 is part of a domain of genes on 11p15 that show

179 ely reversed in cells in which expression of p57Kip2 is silenced by RNA interference.

180 However, p57Kip2 is the only CKI that is absolutely required for

181 e have found that a cyclin kinase inhibitor, p57Kip2, is expressed in a restricted group of amacrine

182 To probe further the function of p57(Kip2), Jurkat cells stably transfected with a plasmi

183 Furthermore, the prostates of p57(Kip2) knockout mice developed prostatic intraepithel

184 h contains the imprinted genes TSSC3, TSSC5, p57(KIP2), KVLQT1, ASCL2, IGF2 and H19.

185 2alpha, glucose transporter-like protein 1, p57(Kip2), La, BiP, and triose phosphate isomerase trans

186 Cs express similar levels of p57(Kip2), that p57(Kip2) levels increase over time in proliferating OPC

187 se over time in proliferating OPCs, and that p57(Kip2) levels regulate how many times an OPC can divi

188 Most notably, increased p57(Kip2) levels resulted in marked inhibition of both c

189 emonstrate a role for the p21(CIP)/p27(Kip1)/p57(Kip2)-like cyclin-dependent kinase inhibitor (cki) d

190 Here, we identify the p21(Cip1)/p27(Kip1)/p57(Kip2)-like cyclin-dependent kinase inhibitor (CKI) D

191 we demonstrate that the p21(cip1)/p27(kip1)/p57(kip2)-like cyclin-dependent kinase inhibitor (CKI),

192 The p57(Kip2) locus has been implicated in the Beckwith-Wied

193 nges in expression of marker genes including p57(KIP2), Maf and Prox1.

194 but not p21Cip1 or p27Kip1, suggesting that p57Kip2 mediates PACAP anti-mitogenic effects.

195 lacking p107 and p130, thus suggesting that p57(Kip2) might be an upstream regulator of these Rb-rel

196 known as p27KIP1) and Cdkn1c (also known as p57KIP2), misexpression of E-cadherin and inappropriate

197 Most p57(Kip2) mutant mice have short limbs, a defect attribu

198 Developmental defects of p57(Kip2) mutant mice include cleft palate and gastroint

199 bserved neoplastic development even in those p57(Kip2) mutant mice that have survived for >5 months o

200 The low frequency of p57KIP2 mutations, as well as our recent discovery of di

201 Aergic ACs that include all dopaminergic and p57Kip2(+) neurons as well as a simultaneous increase of

202 Prox1 and p57(KIP2), normally upregulated at the onset of fiber di

203 Most p57(Kip2) null mice die after birth and display severe d

204 regulatory pathway composed of p73, p15, and p57KIP2 occurred in 22% of Philadelphia chromosome (Ph)-

205 members) and negative regulators (p16Ink4a, p57Kip2) of the cell cycle.

206 n 11p15 and including infrequent mutation of p57(KIP2) or loss of imprinting of either of two imprint

207 tors (p15(INK4b), p21(CIP1/WAF1), p27(KIP1), p57(KIP2)) or to repress c-myc and Bcl-2 transcription.

208 d gene domains on 11p15: LIT1, which is near p57(KIP2), or H19/IGF2.

209 inhibitors, including p21(CIP1), p27(KIP1), p57(KIP2), p16(INK4a), and p18(INK4c), could block phosp

210 Analysis of p57(Kip2);p27(Kip1) double mutants, where p21 expression

211 CDK2, while blocked by CDK inhibition (i.e., p57KIP2 p27KIP1, p21CIP).

212 cells and microarray analysis, we identified p57KIP2 (p57) as the only cyclin-dependent kinase inhibi

213 ne in prostate cancer tumorigenesis, and the p57(Kip2) pathway may be a potential target for prostate

214 genes including H19 (H19 fetal liver mRNA), p57(Kip2), Peg3/Pw1 (paternally expressed gene 3), and Z

215 To determine whether the p57Kip2 population of amacrine cells is organized into a

216 ation of a pathway composed of p73, p15, and p57KIP2 predicts for poor prognosis in Ph-negative patie

217 timuli in leukemic cell lines with different p57KIP2 promoter DNA methylation levels.

218 Overexpression of p57KIP2 in p57KIP2 promoter methylated leukemic cell lines resulted

219 high-density culture or serum withdrawal in p57KIP2 promoter unmethylated cells but not in methylate

220 ex that facilitates their recruitment to the p57Kip2 promoter.

221 eins, it was shown in vitro that addition of p57(Kip2) protein to a mixture of cyclin D2 and cdk6 enh

222 e found that subcellular distribution of the p57kip2 protein changed during differentiation of rat, m

223 companied by a twofold increase in levels of p57Kip2 protein, but not p21Cip1 or p27Kip1, suggesting

224 In these cells, p57KIP2 reactivation required the use of a hypomethylati

225 p57KIP2 reactivation was observed after stimulation with

226 show that two Cdk inhibitors, p21(CIP1) and p57(KIP2), redundantly control differentiation of skelet

227 dynamics analyses in mutants indicated that p57(KIP2) regulates cell cycle length in both RGCs and I

228 ximal end of this BWS breakpoint cluster and p57KIP2, respectively.

229 Induction of p57(Kip2) resulted in increased association of cdk6 with

230 In contrast, nuclear accumulation of p57kip2 resulted in blocked oligodendroglial differentia

231 p53, p21(CIP1), p15(INK4b), p16(INK4a), and p57(KIP2) reveals altered expression in immortalized, no

232 Levels of p16(INK4a) and p57(KIP2) rise in HUCs during progressive passages, wher

233 cells expressing high levels of p57KIP2 with p57KIP2 short hairpin RNA resulted in increased cell pro

234 s late stage of development, animals lacking p57(Kip2) showed an alteration in amacrine subpopulation

235 DR and uncover molecular mechanisms by which p57Kip2 suppresses tumorigenesis and causes chemoresista

236 of a clone of OPCs express similar levels of p57(Kip2), that p57(Kip2) levels increase over time in p

237 es three distinct genes, p21, p27(Kip1), and p57(Kip2), that share a common N-terminal domain for bin

238 al for myogenic growth arrest (p21(cip1) and p57(kip2)), the Notch pathway and myogenic regulatory fa

239 Here we evaluate the expression of p57(KIP2), the product of CDKN1C, an imprinted, maternal

240 with cyclin E/CDK2 and antagonistically with p57(KIP2) to regulate the G1/S transition in a cell type

241 PAX3 nor FOXO1 share the ability to regulate p57Kip2 transcription.

242 ation because of an inability to up-regulate p57Kip2 transcription.

243 s stably transfected with a plasmid encoding p57(Kip2) under control of an inducible (tetracycline) p

244 ments indicated that LHX6 and LHX8 regulated p57(Kip2) via both direct and indirect mechanisms, with

245 Postnatally, p57(Kip2) was found to be expressed in a novel subpopula

246 Protein expression of p73, p15, and p57Kip2 was analyzed by immunohistochemistry using a tis

247 Nuclear export of p57kip2 was correlated with promoted myelin expression,

248 surrounding the transcription start site of p57KIP2 was found in acute lymphocytic leukemia (ALL)-de

249 Expression of p57KIP2 was found to be virtually absent in 21 of 21 WTs

250 P57KIP2 was methylated in 31 (50%) of 63 patients with n

251 Although LOI of p57KIP2 was observed in some WTs (approximately 10%), al

252 In addition, p57KIP2 was recently reported to show mutations in two o

253 Although p57KIP2 was undetectable in BWS tongue, similar results

254 tive expression, and chromosomal location of p57KIP2, we undertook the present study to search for po

255 tion approaches, we found that p27(Kip1) and p57(Kip2) were 2 target genes that were involved in miR-

256 ore, the cell cycle inhibitors p27(Kip1) and p57(Kip2) were selectively overexpressed in duodenal and

257 bers of the CIP/KIP family of CKIs (p27Kip1, p57Kip2) were detected in developing rat cortex from emb

258 While the CDK inhibitors p27Kip1 and p57Kip2 were present at equal levels in cells from both

259 In this study, it is shown that p57(Kip2), which is a member of the Cip/Kip family of cy

260 ough p53-dependent signals and (ii) inducing p57KIP2, while down-regulating c-IPA1 and IEX1 through a

261 e encoding cyclin-dependent kinase inhibitor p57KIP2, whose overexpression causes G1 phase arrest, wa

262 57Kip2, cytoplasmic p15, or a combination of p57Kip2 with either p15 or p73 was associated with a bet

263 unmethylated cells expressing high levels of p57KIP2 with p57KIP2 short hairpin RNA resulted in incre