ライフサイエンスコーパス: CKI

1 CKI abrogated beta-catenin degradation in Xenopus egg ex

2 CKI activity was required for the expression and efficie

3 CKI alpha is associated with synaptic vesicles and phosp

4 CKI expression was also examined in fully confluent cult

5 CKI inhibition enhanced the recruitment of Fas-associate

6 CKI phosphorylates Ci at three clusters of serine residu

7 CKI phosphorylation of Ci confers binding to the F-box p

8 CKI phosphorylation sites act cooperatively to promote C

9 CKI-alpha-dependent hyperphosphorylation of NS5A plays a

10 CKI-gamma2 could further potentiate the ER corepressive

11 CKIs did not appreciably induce the apoptosis of LNCaP c

12 Two such regulators, casein kinase 1 (CKI) and F-box and leucine-rich repeat protein 3 (FBXL3)

13 eins, we identified casein kinase I-gamma 2 (CKI-gamma2, a ubiquitously expressed cytoplasmic kinase)

14 lularly and form a complex with Axin, GSK-3, CKI, and beta-catenin.

15 subsequently degraded by SCF(beta-TRCP) in a CKI-dependent manner.

16 ditis elegans studies, loss-of-function of a CKI isoform most similar to alpha produced the mom pheno

17 we show that deletion of p19(Ink4d) (p19), a CKI gene, in mice results in spontaneous development of

18 ion of DBT in Drosophila S2 cells produced a CKI-7-sensitive kinase activity which was reduced by bot

19 Thus, a CKI isoform is required for protein traffic through the

20 In addition, CKI directly phosphorylates Dsh in vitro.

21 d cyclin D1 protein levels without affecting CKI immunostaining suggesting CKI do not mediate the dev

22 alphavbeta3 heterodimer remains intact after CKI peptide treatment but is immediately dissociated fro

23 Small hairpin RNAs directed against CKI revealed that the CKIalpha isoform contributed signi

24 Casein kinase I-alpha (CKI-alpha) was identified as an NS5A-associated kinase i

25 Here we show that both CKI delta and CKI epsilon interacted directly with Dvl-1, and that CKI

26 PKA, GSK3, and CKI directly bind the N- and C-terminal regions of Cos2,

27 ounteracts phosphorylation by PKA, GSK3, and CKI to prevent Cubitus interruptus (Ci) processing throu

28 phosphorylate Ci and contain PKA, GSK3, and CKI.

29 phosphorylation and activation of LRP6, and CKI phosphorylation of Ci and mediation of Ci-Slimb/beta

30 a positive feedback loop involving mTOR and CKI-dependent turnover of its inhibitor, DEPTOR, suggest

31 hosphorylation of SMO, mainly by the PKA and CKI kinases.

32 We show that PKA and CKI phosphorylate Smo at several sites, and that phospho

33 s progressive Smo phosphorylation by PKA and CKI, leading to elevation of Smo cell-surface levels and

34 rect link exists between DNA replication and CKI degradation.

35 Here, we provide evidence that another CKI, p18/INK (p18), may also be a component of the timer

36 o CKIalpha, Star-PAP associates with another CKI isoform, CKIepsilon in the Star-PAP complex that pho

37 , and CGP74514A (collectively referred to as CKIs) induce the apoptosis of LNCaP and LNCaP-Rf cells,

38 motility mutants suggests that the axonemal CKI is located on the outer doublet microtubules.

39 the proteasome, but inhibition of GSK3 beta/CKI does not increase beta-catenin-mediated transcriptio

40 ferent APC functions and show that GSK3 beta/CKI phosphorylation regulates APC clusters and cell migr

41 cell migration and a scaffold for GSK3 beta/CKI-mediated phosphorylation and degradation of the Wnt

42 GSK3 beta/CKI-phosphorylated and -nonphosphorylated APC also local

43 GSK3 beta/CKI-phosphorylated APC and beta-catenin at clusters is d

44 Loss of GSK3 beta/CKI-phosphorylated APC from these clusters correlates wi

45 APC and a concomitant increase in GSK3 beta/CKI-phosphorylated APC in clusters.

46 ry endothelial cells, we show that GSK3 beta/CKI-phosphorylated APC localizes to microtubule-dependen

47 Wee1, suggesting that the antagonism between CKIs and Wee1 is evolutionarily conserved.

48 Here, we report that blocking CKI function inhibits embryonic morphogenesis and activa

49 Knockdown of both CKI isoforms (alpha and epsilon) resulted in the loss of

50 Here we show that both CKI delta and CKI epsilon interacted directly with Dvl-1

51 nhibitor compensates for the absence of both CKIs, and we identify this inhibitor as p130, a protein

52 ation events in HT29, HCT8, and JR1 cells by CKI-7 dramatically increased apoptosis after exposure to

53 We propose that phosphorylation of Ci by CKI creates multiple Slimb/beta-TRCP binding sites that

54 data suggest that phosphorylation of FADD by CKI is a crucial event during mitosis.

55 hat the SPOP/ERG interaction is modulated by CKI-mediated phosphorylation.

56 phosphorylated in vitro by CKII, but not by CKI.

57 at syntaxin-1A is phosphorylated in vitro by CKI on Thr21.

58 phosphorylated both in vivo and in vitro by CKI.

59 innermost spheroid fraction, including CDKs, CKIs, and cyclins.

60 The Saccharomyces cerevisiae CKI-encoded choline kinase is phosphorylated on a serine

61 The Kip/Cip CKIs, p27(Kip1) and p21(Cip1), are upregulated during ar

62 of GSK3beta (SB415286 and LiCl) or CK1alpha (CKI-7) resulted in dose- and time-dependent increases in

63 mer conformational switch, which coordinates CKI release for ETI signaling and reconfigures the selec

64 n clock genes (PER1, PER2, PER3, CRY1, CRY2, CKI, CLOCK, and BMAL1) of cancerous and noncancerous tis

65 regulatory subunit of PP2A, and kinase-dead CKI epsilon acted synergistically with B56 in inhibiting

66 21, deletion of p18(INK4C) (p18), a distinct CKI, results in improved long-term engraftment, largely

67 Inhibition of either CKI or FBXL3 leads to longer periods, and their effects

68 that promotes the degradation of C. elegans CKI-1 and human p21.

69 nscription, whereas inhibition of endogenous CKI catalytic activity with IC261 blocks only TGF-beta-s

70 f Drosophila PER by casein kinase I epsilon (CKI epsilon; doubletime protein or DBT) and CKII.

71 monstrated cyclin D1 within cells expressing CKI (p16(Ink4a), p21(Cip1),p27(Kip1)).

72 Finally, CKI inhibitors that rescued dynein activity blocked phos

73 While none of the other five CKI isoforms can substitute for CKIalpha in its inhibito

74 Western blots indicate that within flagella, CKI is anchored exclusively to the axoneme.

75 omplexity sequence I, which is important for CKI-alpha-mediated NS5A hyperphosphorylation.

76 -independent pathway and indicate a role for CKI during convergence extension in early vertebrate dev

77 ions as a potent transcription repressor for CKIs as well as D cyclins, was also significantly induce

78 onflicting reports regarding whether a given CKI family member functions as a positive or negative re

79 On the other hand, CKI and CKII progressively phosphorylate FRQ to promote

80 Recently, casein kinase I (CKI) and protein phosphatase 2A (PP2A) have emerged as p

81 y of the major clock kinase casein kinase I (CKI) epsilon is regulated by inhibitory autophosphorylat

82 ylation by PKA, GSK3, and a casein kinase I (CKI) family member(s).

83 Recent studies suggest that casein kinase I (CKI) family members play pivotal roles in the Wg/Wnt pat

84 Although members of the casein kinase I (CKI) family phosphorylate alphaSyn at S129, they attenua

85 disruption of a Neurospora casein kinase I (CKI) gene, ck-1b, showed that it is not required for clo

86 being hypophosphorylated by casein kinase I (CKI) in vitro.

87 at Ser45 phosphorylation by casein kinase I (CKI) initiates phosphorylation at Thr41, Ser37, and Ser3

88 were used to determine that casein kinase I (CKI) is physically anchored in the flagellar axoneme and

89 Casein kinase I (CKI) is required in both invertebrates and vertebrates t

90 ster, mutations affecting a casein kinase I (CKI) ortholog called doubletime (dbt) can produce short

91 including recent results on casein kinase I (CKI) phosphorylation and activation of LRP6, and CKI pho

92 Inhibition of casein kinase I (CKI) phosphorylation events in HT29, HCT8, and JR1 cells

93 We found that two casein kinase I (CKI) proteins, Yck1 and Yck2, previously identified as p

94 protein kinase A (PKA) and casein kinase I (CKI) regulate Smo cell-surface accumulation and activity

95 , and in collaboration with casein kinase I (CKI), generates a phosphodegron that binds betaTrCP.

96 widely studied mutation in casein kinase I (CKI), the CKIepsilon(tau) mutant, has been shown to caus

97 phorylation site within the casein kinase I (CKI)-binding domain of the human PER2 gene.

98 destruction of VEGFR2 in a casein kinase I (CKI)-dependent manner.

99 Casein kinases I (CKI) are serine/threonine protein kinases widely express

100 argeting host protein kinases, we identified CKI-alpha as an NS5A-associated kinase involved in NS5A

101 Amounts of p53 increased substantially in CKI-treated cells, whereas amounts of the endogenous cas

102 Multiple kinases, including CKI alpha and GSK3, are involved in beta-catenin phospho

103 s are lost in tumors, deletion of individual CKIs results in modest proliferation defects in murine m

104 ion, TGFbeta signaling is required to induce CKI expression and cellular senescence and suppress tumo

105 Upon ETI induction, CKIs are released from CPR5 to cause overactivation of a

106 via negative regulation of the CDK-inhibitor CKI-1.

107 ch subsequently rebounded, the MEK inhibitor CKI suppressed ERK signaling in a sustained manner by pr

108 The Cip/Kip CDK inhibitor (CKI) p21(Cip1/WAF1) has a critical role in the nucleus t

109 Moreover, we show that the CDK inhibitor (CKI) Sic1p protects bound Clb5p/Cdc28p complexes from ty

110 p27 is a CDK inhibitor (CKI) that binds to CDK2 to prevent premature activation

111 1/S transition by acting as a Cdk inhibitor (CKI), although the mechanisms remain unresolved.

112 Pho85; a cyclin, Pho80; and a CDK inhibitor (CKI), Pho81.

113 Pho85; a cyclin, Pho80; and a CDK inhibitor (CKI), Pho81.

114 lin/cyclin-dependent kinase (CDK) inhibitor (CKI) p21(Cip1/WAF1) and increases stability of the p21 p

115 the cyclin-dependent kinase (CDK) inhibitor (CKI)-CDK-retinoblastoma protein (Rb) pathway.

116 , a Cyclin-dependent kinase (CDK) inhibitor (CKI).

117 ase via a pheromone-activated Cdk-inhibitor (CKI) protein, Far1.

118 ip2)-like cyclin-dependent kinase inhibitor (CKI) Dacapo (Dap) as a key regulator of premeiotic S pha

119 (p21), a cyclin-dependent kinase inhibitor (CKI) in irradiated hosts.

120 t induced cyclin-dependent kinase inhibitor (CKI) p16(INK4a) protein expression and p21(WAF1/CIP1) pr

121 on of the cyclin-dependent kinase inhibitor (CKI) p16(INK4a), nor on changes in expression of the CKI

122 which the cyclin-dependent kinase inhibitor (CKI) p21(Waf1/Cip1/Sdi1) (p21), a known regulator of ste

123 on of the cyclin dependent kinase inhibitor (CKI) p21WAF1/ CIP1 in all cell lines, the level and kine

124 on of the cyclin-dependent kinase inhibitor (CKI) p27(Kip1), which induces growth arrest and apoptosi

125 that the cyclin-dependent kinase inhibitor (CKI) p27/Kip1 (p27) is a component of this TH-regulated

126 roles of cyclin-dependent kinase inhibitor (CKI) p57(KIP2), an important regulator of G1 phase, usin

127 f the p27 cyclin-dependent kinase inhibitor (CKI), and the associated inhibition of cyclin E-CDK2.

128 ip2)-like cyclin-dependent kinase inhibitor (CKI), Dacapo (Dap), promotes replication licensing durin

129 weakened cyclin-dependent kinase inhibitor (CKI)-cyclin-dependent kinase 2 positive-feedback loop, n

130 the cyclin-dependent kinase (CDK) inhibitors CKI-1 and p21(Cip1), respectively.

131 TGFbeta up-regulation of the Cdk inhibitors (CKI's) p27(Kip1) and p21(Cip1).

132 IP cyclin-dependent kinase (Cdk) inhibitors (CKI) activate pocket protein function by suppressing Cdk

133 Cyclin-dependent kinase inhibitors (CKI) have been identified as key effectors of cell cycle

134 n of the cyclin-dependent kinase inhibitors (CKI), p27(Kip1) and p57(Kip2).

135 F E3-ligase that targets the CDK inhibitors (CKIs) p21(Cip1), p27(Kip1), p57(Kip2), and p130 for degr

136 urther, the abundance of the Cdk inhibitors (CKIs) p21cip1/waf1 (p21cip1) and p27kip1 is substantiall

137 ependent kinases (CDKs), and CDK inhibitors (CKIs) regulate cycle progression.

138 pecifically, GPC1 suppressed CDK inhibitors (CKIs), including p21, p27, p16, and p19, and the D cycli

139 LMW isoforms to CDK2 and the CDK inhibitors (CKIs), p21 and p27, results in their functional hyperact

140 dependent kinases (CDKs) and CDK inhibitors (CKIs), the expression of which is often dysregulated in

141 amily of pocket proteins and CDK inhibitors (CKIs).

142 of cyclin-dependent kinase (CDK) inhibitors (CKIs) differs in monolayer versus spheroid cell culture.

143 by cyclin-dependent kinase (CDK) inhibitors (CKIs).

144 Cyclin-dependent kinase inhibitors (CKIs) and Notch receptor activation have been shown to i

145 evels of cyclin-dependent kinase inhibitors (CKIs) are associated with aggressive androgen-independen

146 Cyclin-dependent kinase inhibitors (CKIs) are important negative regulators of the cell cycl

147 that the cyclin-dependent kinase inhibitors (CKIs) are solely negative regulators of cyclin-dependent

148 The cyclin-dependent kinase inhibitors (CKIs) bind to and directly regulate the catalytic activi

149 n of the cyclin-dependent kinase inhibitors (CKIs) has been linked to the inhibition of cellular prol

150 The cyclin-dependent kinase inhibitors (CKIs) have different patterns of expression in vascular

151 questers cyclin-dependent kinase inhibitors (CKIs) involved in ETI signal transduction.

152 and pRB, cyclin-dependent kinase inhibitors (CKIs) p21 and p27, as well as cyclins D1 and E, in a coh

153 overexpression of cyclin kinase inhibitors (CKIs) p21 and p27.

154 n of the cyclin-dependent kinase inhibitors (CKIs) p21 and p27.

155 several cyclin-dependent kinase inhibitors (CKIs) via binding to Miz1; whether this interaction is i

156 Cip/Kip cyclin-dependent kinase inhibitors (CKIs), and CDH1, and upregulation of the pro-oncogenic p

157 posed by cyclin-dependent kinase inhibitors (CKIs), proteins that bind tightly to cyclin-CDK complexe

158 Cyclin-dependent kinase inhibitors (CKIs), such as p15 and p21, have been suggested to be cr

159 Cyclin-dependent kinase inhibitors (CKIs), such as p27kip1 and p15INK4b, help mediate mitoti

160 ion with cyclin-dependent kinase inhibitors (CKIs).

161 els, and cyclin dependent kinase inhibitors (CKIs).

162 Ks), and cyclin-dependent kinase inhibitors (CKIs).

163 amily of cyclin-dependent kinase inhibitors (CKIs).

164 The CKI inhibitors, CKI-7 and IC261, reduced Ser-1106 phosphorylation and de

165 ociated cell cycle kinases (CDK) inhibitory (CKI) synthetic peptides derived from p16(INK4a), p18(INK

166 for Cip/Kip class cyclin-kinase inhibitory (CKI) proteins in regulating this process during neurogen

167 In contrast, the Ink CKI, p16(Ink4), is not expressed in vascular lesions.

168 ex activity by recruiting the casein kinases CKI and CKII to phosphorylate the WC proteins, resulting

169 y, we show that all three identified Cip/Kip CKI proteins are expressed in both distinct and overlapp

170 n of interneurons, demonstrates that Cip/Kip CKI-independent factors initiate progenitor cell cycle e

171 n ligase as a conserved regulator of Cip/Kip CKIs that promotes the degradation of C. elegans CKI-1 a

172 that p19 is a tumor suppressor and the major CKI gene that controls pituitary AL cell proliferation.

173 marker Rab5 and co-localization of mammalian CKI with alphaSyn aggregates are observed in brain secti

174 n homologous to the INK4 family of mammalian CKIs.

175 mutant (GSK3beta inhibitors) or S45A mutant (CKI-7), demonstrating the specificity of the reporter.

176 Notably, CKI decreased, whereas inhibition of CKI increased, the

177 (LRR-1) complex negatively regulates nuclear CKI-1 levels to ensure G1-phase cell cycle progression i

178 The ability of CKI to induce secondary body axes in Xenopus embryos was

179 urther differentiated between the actions of CKI and FBXL3 by revealing opposite amplitude responses

180 In yeast cells, the combination of CKI binding and preferential phosphorylation/dephosphory

181 d cytochrome c accumulated in the cytosol of CKI-treated cells.

182 transcription factors promote expression of CKI-1, a member of the p27 family of cyclin-dependent ki

183 Our results suggest that the impact of CKI-alpha in the HCV life cycle is more profound on viri

184 RCP binding and Ci processing independent of CKI.

185 opment involves transcriptional induction of CKI-1 and transcriptional regulation through the Mediato

186 CKIdelta in T lymphocytes and inhibition of CKI in epithelial cells reduce microtubule growth.

187 Additionally, inhibition of CKI in vivo stabilized the beta-catenin degradation comp

188 otably, CKI decreased, whereas inhibition of CKI increased, the association of PP2A with the beta-cat

189 However, a pharmacological inhibition of CKI reset the circadian oscillator in a phase-dependent

190 fectively blocked by a specific inhibitor of CKI.

191 ver, genetic evidence for the involvement of CKI family members in physiological Wg/Wnt signaling eve

192 to spread on vitronectin in the presence of CKI peptides.

193 The cell type and the temporal profile of CKI expression during postnatal cerebellar development h

194 lex biological function, clarify the role of CKI in the clock, and demonstrate that a specific mutati

195 This argues against a primary role of CKI in the phase-shifting effects of SB 203580.

196 ese findings identified MTA1s as a target of CKI-gamma2, and provided new evidence to suggest that CK

197 of CDK2 and members of the CIP/KIP family of CKIs (p27Kip1, p57Kip2) were detected in developing rat

198 Induction of CKIs from separate families, as well as their associatio

199 ibited by c-Myc; therefore, the induction of CKIs was attributed to the ability of HIF to antagonize

200 vity of cyclin E/Cdk2 increases as levels of CKIs, particularly p21cip1, fall.

201 sion, at least in part through regulation of CKIs.

202 The role of CKIs in inhibiting proliferation in corneal endothelium

203 carcinoma cells with functional Rb) and one CKI-unresponsive cell line (SiHa human cervical cancer c

204 p16(Ink4a), p21(Waf1), and p27(Kip1) in one CKI-responsive cell line (A431 human vulvar epidermoid c

205 of Wnt action and suggest that more than one CKI isoform is capable of transducing Wnt signals in viv

206 However, p57Kip2 is the only CKI that is absolutely required for normal development.

207 beta-TRCP knockdown or CKI inhibition causes accumulation of VEGFR2, resulting

208 Blocking PKA or CKI activity in the Drosophila wing disc prevents Hh-ind

209 Overall, these studies identify the p27 CKI gene as a new target whereby c-Myc can control cell

210 phosites that enhance the effects of the PKA/CKI kinases on SMO accumulation, its localization at the

211 sidue at 321 to alanine, which is a possible CKI-gamma2 phopshorylation site in MTA1s, results in a s

212 By contrast, related CKI p27(KIP1) controlled IPC proliferation exclusively.

213 elective for p21 since silencing the related CKIs, p27(Kip1) and p18(INK4C), had no effect on HIV-1.

214 to Miz1 is continuously required to repress CKI expression and inhibit accumulation of trimethylated

215 eats is necessary and sufficient for Pho81's CKI function.

216 Second, CKI was unequivocally identified in salt extracts from i

217 a videomicroscopic motility assay, selective CKI inhibitors rescued dynein-driven microtubule sliding

218 eviously reported that a PI4,5P(2) sensitive CKI isoform, CKIalpha associates with and phosphorylates

219 Here we examine the roles of seven CKI family members in Wg signaling during Drosophila lim

220 s inhibitory role in the Wg pathway, several CKI isoforms including CG12147 exhibit a positive role b

221 Finally, we provide evidence that several CKI isoforms including CKIalpha and Gish/CKIgamma can ph

222 This novel pathway involving Notch/SKP2/CKIs connects a cell surface receptor with proximate med

223 Specific CKI activity inhibitors (IC261 and CKI7) block in vivo S

224 on of SKP2 in HSC and progenitors stabilized CKIs in vivo, particularly p27(Kip1), p57(Kip2), and p13

225 ependent manner and that estrogen stimulates CKI-gamma2 activity that could be effectively blocked by

226 hout affecting CKI immunostaining suggesting CKI do not mediate the developmental arrest.

227 Mice with targeted CKI gene deletions have only subtle proliferative abnorm

228 lon interacted directly with Dvl-1, and that CKI phosphorylated multiple components of the Wnt-regula

229 Our results demonstrate that CKI isoforms alpha and epsilon modulate Star-PAP activit

230 We also find that CKI (KIN-19) plays a role not only in the Wnt/beta-caten

231 Finally, we find that CKI is required in vivo for the Wnt-dependent phosphoryl

232 In addition, we found that CKI-gamma2 can phosphorylate MTA1s, but not ER, in an an

233 Our results indicate that CKI primarily regulates the accumulating phase of the PE

234 We propose that CKI is anchored on the outer doublet microtubules in pos

235 t protein receptor) complex, we propose that CKI may play a role in synaptic vesicle exocytosis.

236 Our findings reveal that CKI and PP2A phosphatase play antagonistic roles in SPS

237 nce confocal microscopy analyses showed that CKI-alpha-mediated hyperphosphorylation of NS5A contribu

238 Together, these results suggest that CKI and CKII, in addition to being the FRQ kinases, medi

239 These studies suggest that CKI might also act in the beta-catenin-independent pathw

240 The data suggest that CKI phosphorylates and destabilizes the beta-catenin deg

241 2, and provided new evidence to suggest that CKI-gamma2 phosphorylates and modulates the functions of

242 catenin degradation complex, suggesting that CKI actively destabilizes the complex in vivo.

243 orylated beta-catenin and axin suggests that CKI phosphorylates these proteins in vivo as well.

244 These findings show that CKIs induce the mitochondria-mediated apoptosis of prost

245 The CKI inhibitors, CKI-7 and IC261, reduced Ser-1106 phosph

246 All the CKI isoforms, with the exception of gamma, increase the

247 ed a functional inter-dependence between the CKI and the abundance of cyclin D1 in orchestrating grow

248 tand the functional relationship between the CKI-PER and FBXL3-CRY pathways, we generated robust mech

249 In addition to CKIepsilon, the CKI family includes several other isoforms (alpha, beta,

250 AIL-induced apoptosis in the presence of the CKI inhibitor.

251 p2 abundance while diminishing levels of the CKI p27.

252 , ALVA31 and PC-3, express low levels of the CKI, p21(CIP1), compared to the less-malignant, androgen

253 hree genes resulted in the expression of the CKI, p21, both in pRb- and pRb+ cells.

254 Perplexingly, none of the CKI-deficient mice reported thus far develop pituitary A

255 l- or cisplatin-mediated cytotoxicity on the CKI-responsive A431 cells but not on the CKI-unresponsiv

256 the CKI-responsive A431 cells but not on the CKI-unresponsive SiHa cells.

257 nscriptional repressors Whi5 and Stb1 or the CKI protein Sic1, whose metazoan analogues (Rb or p27) a

258 the dbt(S) and dbt(L) mutations reduced the CKI-7-sensitive kinase activity of an orthologous Xenopu

259 ess-induced by tBHQ treatment stimulates the CKI mediated phosphorylation of Star-PAP, which is criti

260 Together, our data suggest that the CKI Dap promotes the licensing of DNA replication origin

261 We showed previously that the CKI, p27, binds to Cdk2/cyclin A though a sequential mec

262 rocessing of Star-PAP targets similar to the CKI activity inhibitors.

263 p21 or p27, will directly substitute for the CKIs and restore normal CDK regulation by mitogens in ce

264 We report that expression of the CKIs p18(INK4c), p21(waf1/cip1), and p27(Kip1) all incre

265 (INK4a), nor on changes in expression of the CKIs p21(Cip1), p14(ARF), p27(Kip1) or p57(Kip2).

266 by p21 and p27, despite equal binding of the CKIs to the LMW complexes.

267 ances proteasome-mediated degradation of the CKIs, p27 Kip1 and p21 Cip1, and causes premature entry

268 relative protein and mRNA expression of the CKIs, p27kip1, and p15INK4b.

269 These results demonstrate that the CKIs are induced by differentiation cues in specific cel

270 s derived from these two cell lines when the CKIs were and were not induced.

271 specific cerebellar cell types in which the CKIs were expressed during post natal development by co-

272 These CKIs inhibit the G(1) to S-phase transition of the cell

273 ties of p21 and p27 while sequestering these CKIs from the full-length cyclin E.

274 etic mechanism to silence expression of this CKI in neural tumors.

275 difference, the relative expression of those CKIs and the kinetics of hyperphosphorylation of the ret

276 Of those CKIs, p16INK4a, p21WAF1/Cip1, and p27Kip1 are expressed

277 dy, we have examined the expression of three CKIs in EMT6 mouse mammary carcinoma and MEL28 human mel

278 the expression and localization of the three CKIs in corneal endothelium in situ.

279 is deregulated during ETI, probably through CKI-mediated hyperphosphorylation of retinoblastoma-rela

280 autophosphorylation sites do not conform to CKI substrate motifs identified in peptide substrates.

281 ated phosphorylation site was insensitive to CKI inhibition.

282 equence, although showing some similarity to CKI sequence.

283 PC3 cells readily apoptosed when exposed to CKIs or when depleted of XIAP by RNA interference.

284 Skp2 deletion leads to CKIs stabilization inducing cell-cycle delay or arrest,

285 drugs, topoisomerase inhibitors, can trigger CKI activation to restore the SPOP/DeltaERG interaction

286 nt signaling and find that all the wild-type CKI isoforms do so.

287 so regulates FRQ phosphorylation, but unlike CKI and CKII, PKA stabilizes FRQ, similar to the stabili

288 eport, we examine the ability of the various CKI isoforms to activate Wnt signaling and find that all

289 The vertebrate CKI p27(Kip1) similarly protects Cyclin A/Cdk2 complexes

290 te poly(ADP-ribose) polymerase occurred when CKI-7 and TRAIL were combined.

291 ment, CDK2 protein levels decreased, whereas CKI expression increased, suggesting that stimulatory an

292 to inhibit beta-catenin degradation, whereas CKI-7, an inhibitor of CK1epsilon, reduces the inhibitor

293 tion of PP2A, providing a mechanism by which CKI stabilizes beta-catenin and propagates the Wnt signa

294 In addition, TRAIL combined with CKI-7 promoted the release of cytochrome c, Smac/DIABLO,

295 We show that MTA1s interacts with CKI-gamma2 both in vitro and in vivo and colocalizes in

296 (i)-Metabolically labeled cells treated with CKI-7, a specific CK1 inhibitor, showed a reduction in C

297 n, normal rat kidney cells were treated with CKI-7, and Cx43 content was analyzed by Triton X-100 ext

298 ncurrent administration of chemotherapy with CKIs as chemoprotective agents for normal cells.

299 o-proteomic analysis of NS5A with or without CKI-alpha depletion identified peptide fragments that co

300 Thus, like the yeast CKIs Rum1 and Sic1, Drosophila Rux can reset G2 cells to