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

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

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

12 ndent kinase inhibitors (CKI), 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 ors resulted in the specific upregulation of p57Kip2, a Cip/Kip cyclin-dependent kinase inhibitor, an

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

43 1 (Kvlqt1) and Cd81 (Tapa-1) between Cdkn1c (p57(Kip2)) and Mash2.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

61 Together, CD38/cADPR/Ca2+/c-Fos/p57Kip2 axis maintains HSC dormancy.

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

63 s critical; shRNA-mediated downregulation of p57Kip2, but not the related p27Kip1, significantly atte

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

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

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

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

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

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

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

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

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

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

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

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

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

77 We show here that the cell cycle inhibitor p57Kip2/Cdkn1c limits the number of emerging HSCs by res

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

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

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

81 Levels of p21(Cip1/Waf1), p57(Kip2), cyclin A and cyclin E, all of which are also

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

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

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

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

86 ctivation following MEKi withdrawal drives a p57(KIP2)-dependent G1 cell cycle arrest and senescence

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

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

89 nt kinase inhibitor Dacapo (Dap; ortholog of p57(KIP2)) determines whether NSCs enter G(0) or G(2) qu

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

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

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

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

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

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

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

97 ortantly, this not only defined the relevant p57Kip2-expressing SNS progenitor stage but also reveale

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

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

100 p57(KIP2) expression is required for loss of BRAF(V600E)

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

117 resistance was associated with dysregulated p57Kip2 expression.

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

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

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

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

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

123 The p57kip2 gene encodes one such potent inhibitor of oligod

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

155 n contrast to the cell-intrinsic function of p57Kip2 in maintaining adult HSCs, highlighting profound

156 Overexpression of p57KIP2 in p57KIP2 promoter methylated leukemic cell lin

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

158 Targeting p57Kip2 in primary rectal cancer cells and tumor models

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

175 The cyclin-dependent kinase inhibitor p57(kip2) is encoded by an imprinted gene Cdkn1c, with t

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

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

178 p57(Kip2) is primarily expressed in terminally different

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

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

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

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

183 P57KIP2 is a cyclin-dependent kinase inhibitor silenced

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

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

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

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

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

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

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

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

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

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

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

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

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

197 2alpha, glucose transporter-like protein 1, p57(Kip2), La, BiP, and triose phosphate isomerase trans

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

224 Here, we identified p57(Kip2) (p57) as a molecular switch for the reserve st

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

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

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

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

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

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

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

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

233 ex that facilitates their recruitment to the p57Kip2 promoter.

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

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

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

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

238 p57KIP2 reactivation was observed after stimulation with

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

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

241 ntiation by directly targeting p27(Kip1) and p57(Kip2), respectively.

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

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

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

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

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

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

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

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

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

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

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

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

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

255 s the expression of the cell cycle inhibitor p57Kip2 to drive HSC dormancy.

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

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

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

259 o suggest that loss of Cdkn1c imprinting and p57(KIP2) upregulation alters the cellular composition o

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

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

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

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

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

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

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

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

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

269 Although p57KIP2 was undetectable in BWS tongue, similar results

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

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

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

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

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

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

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

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

278 57Kip2, cytoplasmic p15, or a combination of p57Kip2 with either p15 or p73 was associated with a bet

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