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 promotes Expanded phosphorylation and int

5 CKI expression was also examined in fully confluent cult

6 CKI inhibition enhanced the recruitment of Fas-associate

7 CKI phosphorylates Ci at three clusters of serine residu

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

9 CKI phosphorylation sites act cooperatively to promote C

10 CKI-alpha-dependent hyperphosphorylation of NS5A plays a

11 CKI-gamma2 could further potentiate the ER corepressive

12 CKI-mediated Pah1 phosphorylation was also inhibited by

13 CKI-mediated phosphorylation of Pah1 stimulated both its

14 CKIs did not appreciably induce the apoptosis of LNCaP c

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

16 Here, we show that the Casein Kinase 1 (CKI) family is required for Expanded phosphorylation.

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

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

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

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

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

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

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

24 In addition, CKI directly phosphorylates Dsh in vitro.

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

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

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

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

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

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

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

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

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

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

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

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

37 rect link exists between DNA replication and CKI degradation.

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

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

40 Current FDA approved CKIs are also highlighted, in addition to a detailed ana

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

58 ho80 inhibited subsequent phosphorylation by CKI.

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

60 phosphorylated both in vivo and in vitro by CKI.

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

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

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

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

65 Conversely, CKI depletion in S2 cells impairs Expanded degradation d

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

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

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

69 In wing imaginal discs, CKI loss leads to elevated Expanded and Crumbs levels.

70 21, deletion of p18(INK4C) (p18), a distinct CKI, results in improved long-term engraftment, largely

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

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

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

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

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

76 Finally, CKI inhibitors that rescued dynein activity blocked phos

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

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

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

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

81 idues, Ser-475 and Ser-511 were specific for CKI, whereas the others were shared by casein kinase II

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

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

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

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

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

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

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

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

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

91 encodes a vacuolar membrane casein kinase I (CKI) homolog that nonredundantly functions in fusion reg

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

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

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

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

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

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

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

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

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

101 rylated by the YCK1-encoded casein kinase I (CKI), regulating Pah1 catalytic activity and phosphoryla

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

103 ing RNA helicase (FRH), and casein kinase I (CKI), which inhibits the activity of the clock's positiv

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

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

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

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

108 s the predominantly employed electrophile in CKI development, with its incorporation in the majority

109 tabilizes the ck-1a transcript, resulting in CKI protein levels sufficient for normal rhythmicity.

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

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

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

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

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

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

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

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

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

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

120 1/S transition by acting as a Cdk inhibitor (CKI), although the mechanisms remain unresolved.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

135 ing a promiscuous covalent kinase inhibitor (CKI) SM1-71 as a starting point, we developed covalent i

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

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

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

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

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

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

142 the past decade, covalent kinase inhibitors (CKI) have seen a resurgence in drug discovery.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

178 n homologous to the INK4 family of mammalian CKIs.

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

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

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

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

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

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

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

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

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

188 RCP binding and Ci processing independent of CKI.

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

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

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

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

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

194 fectively blocked by a specific inhibitor of CKI.

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

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

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

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

199 Ser-748, and Ser-774) as the target sites of CKI.

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

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

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

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

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

205 article provides a comprehensive overview of CKIs reported in the literature over a decade period, 20

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

207 The role of CKIs in inhibiting proliferation in corneal endothelium

208 ce of the Nonsense Mediated Decay pathway on CKI levels.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

231 ted kinases and that it also anchors an SXXS CKI phosphorylation motif ((328)SRFS(331)).

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

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

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

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

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

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

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

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

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

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

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

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

244 2, and provided new evidence to suggest that CKI-gamma2 phosphorylates and modulates the functions of

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

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

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

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

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

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

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

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

253 However, the CKI-mediated phosphorylation of Pah1 strongly inhibited

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

255 p2 abundance while diminishing levels of the CKI p27.

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

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

258 s coupled with phosphopeptide mapping of the CKI-phosphorylated Pah1 indicated that it is phosphoryla

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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