ライフサイエンスコーパス: CK1

1 CK1 acts as a scaffolding protein for the assembly of th

2 CK1 and MBL were co-immunoprecipitated from hypoxic HUVE

3 CK1 associates with and phosphorylates REST at two neigh

4 CK1 exists with NFAT1 in a high-molecular-weight complex

5 CK1 family members are thought to be constitutively acti

6 CK1 interacts with MPO in vitro, even in the presence of

7 CK1 phosphorylates only the SRR-1 motif, the primary reg

8 CK1 was found on the external membrane of nonpermeabiliz

9 CK1-dependent phosphorylation of Ser-247 was induced by

10 CK1-mediated phosphorylation of Ser-247 also enhanced th

11 PAR) and, to a lesser extent, cytokeratin 1 (CK1) block FXII binding to HUVECs as determined by flow

12 vein endothelial cell (HUVEC) cytokeratin 1 (CK1) expression and activates the LCP via MBL binding to

13 Human cytokeratin 1 (CK1) in human umbilical vein endothelial cells (HUVEC) i

14 ilitates MPO internalization, cytokeratin 1 (CK1), identified using affinity chromatography and mass

15 ellular localization of human cytokeratin 1 (CK1), urokinase plasminogen activator receptor (uPAR), a

16 y that leads from mGluRs to casein kinase 1 (CK1) activation.

17 re blocked by disruption of casein kinase 1 (CK1) activity, and mass spectrometry and mutational anal

18 d by specific inhibitors of casein kinase 1 (CK1) and casein kinase 2 (CK2) (10 muM D4476, 100 muM CK

19 lation of clock proteins by casein kinase 1 (CK1) and glycogen synthase kinase 3 (GSK3), appear conse

20 ct NFAT kinases, among them casein kinase 1 (CK1) and glycogen synthase kinase 3 (GSK3).

21 pon dual phosphorylation by casein kinase 1 (CK1) and glycogen synthase kinase 3beta (GSK3beta) in a

22 he absence of a Wnt signal, casein kinase 1 (CK1) and glycogen synthase kinase-3beta (GSK-3beta) phos

23 cal conditions and identify Casein Kinase 1 (CK1) as an upstream effector that bidirectionally regula

24 both were inhibited by the casein kinase 1 (CK1) delta/epsilon inhibitor IC261.

25 An increase of casein kinase 1 (CK1) expression has been described in the human AD brain

26 d in vivo by members of the casein kinase 1 (CK1) family and by glycogen synthase kinase 3beta (GSK3b

27 Members of the casein kinase 1 (CK1) family are evolutionarily conserved eukaryotic prot

28 ases include members of the casein kinase 1 (CK1) family of phosphotransferases, which are highly ove

29 Ser-247 is a target of the casein kinase 1 (CK1) family of protein kinases.

30 Casein kinase 1 (CK1) has been implicated in a variety of cellular functi

31 Here, the casein kinase 1 (CK1) Hrr25 is shown to be an endocytic protein and to be

32 e have examined the role of casein kinase 1 (CK1) in connexin-43 (Cx43) gap junction assembly.

33 Casein kinase 1 (CK1) is a highly conserved serine/threonine kinase, pres

34 Casein kinase 1 (CK1) is one such enzyme; it stimulates p53 after transfo

35 The cDNA for casein kinase 1 (CK1) of Plasmodium falciparum was cloned, sequenced, and

36 ites or adjacent PKA-primed casein kinase 1 (CK1) sites are replaced by alanine residues.

37 Casein kinase 1 (CK1) was identified as the major kinase responsible for

38 by protein kinase A (PKA), casein kinase 1 (CK1), and glycogen synthase kinase 3 (GSK3), as well as

39 s Ser683 phosphorylation by casein kinase 1 (CK1), and these phosphorylation events elevate Smo activ

40 lation of the COPII coat by casein kinase 1 (CK1), Hrr25, contributes to the directional delivery of

41 ation by kinases, including casein kinase 1 (CK1), restores NFAT to its latent state in the cytoplasm

42 FZD3, FZD7, Dvl2, Dvl3, and casein kinase 1 (CK1)-epsilon are upregulated in B lymphocytes of patient

43 plasma membrane-associated casein kinase 1 (CK1).

44 hosphorylation at Ser(6) by casein kinase 1 (CK1).

45 5 by the nuclear isoform of casein kinase 1 (CK1).

46 ilaments are members of the casein kinase-1 (CK1) family of protein kinases.

47 , we determined the role of casein kinase-1 (CK1) in regulating NMDAR activity in the PVN.

48 recruited a TDP-43 kinase, casein kinase-1 (CK1), to GADD34.

49 combined activities of casein kinase 1delta (CK1 delta) and casein kinase 1epsilon (CK1epsilon) and w

50 se 3beta (GSK3beta) or casein kinase 1 or 2 (CK1/2) markedly slowed the decay of nuclear NFATc1-GFP a

51 tected when cells were treated with IC261, a CK1 inhibitor specific for delta or epsilon isoforms.

52 Together these results indicate that a CK1-Cdk5-DARPP-32 cascade may be involved in the regulat

53 r, these studies suggest that DHPG activates CK1(epsilon) via Ca(2+)-dependent stimulation of calcine

54 Autoactivation primes Fu for additional CK1-dependent phosphorylation, which further enhances ki

55 Furthermore, levels of all CK1 isoforms are elevated in the CA1 region of AD hippoc

56 Casein kinase 1 alpha (CK1 alpha) was shown to directly phosphorylate Ser(535)

57 Studies of Ci variants with altered CK1 and GSK3 sites suggest that the large number of phos

58 lation of Ci at the specific PKA, GSK-3, and CK1 sites required in vivo for partial proteolysis stimu

59 The major docking sites for calcineurin and CK1 are strongly conserved throughout vertebrate evoluti

60 onist for group I mGluRs, increased Cdk5 and CK1 activities in neostriatal slices, leading to the enh

61 Here we report that both Cdk5 and CK1 are regulated by metabotropic glutamate receptors (m

62 s (Bmal1, Clock, Per1, Per2, Cry1, Cry2, and CK1 epsilon ) was assayed by in situ hybridization in th

63 The CK1 inhibitors (DRB and CK1-7) and solubilization of CK1 restored microtubule sl

64 ibition of microtubule sliding in a DRB- and CK1-7-sensitive manner.

65 ase is activated by Smo and Cos2 via Fu- and CK1-dependent phosphorylation.

66 h the scaffold Axin and the kinases GSK3 and CK1 to target betacatenin for destruction.

67 ine-rich region 1 (SRR-1) motifs by GSK3 and CK1, respectively.

68 e subsequent phosphorylation by Sgg/GSK3 and CK1.

69 phosphorylation by the kinases Sgg/GSK3 and CK1.

70 uring muscle activity, and that GSK3beta and CK1/2 are responsible for phosphorylating NFATc1 in musc

71 Our results suggest that GSK3beta and CK1/2 are the major protein kinases that contribute to t

72 Simultaneous inhibition of GSK3beta and CK1/2 completely blocked the nuclear export of NFATc1-GF

73 destruction complex with Axin, GSK3beta, and CK1 that targets beta-catenin/Armadillo (beta-cat/Arm) f

74 pharmacological similarity between MDM2 and CK1 small molecule inhibitors and the fact that CK1 and

75 r741/Thr742, which is facilitated by PKA and CK1 phosphorylation at adjacent Ser residues.

76 mo aa625-753, which covers the three PKA and CK1 phosphorylation clusters.

77 over, we show that Hh regulates both PKA and CK1 phosphorylation of Smo.

78 at Smo containing acidic residues at PKA and CK1 sites can be stimulated further by Hh and acts throu

79 edback loop and acts downstream from PKA and CK1 to facilitate high-level Hh signaling by promoting t

80 Combined recombinant soluble uPAR and CK1 inhibit 80% FITC-FXII binding to HUVECs.

81 membrane sites/cell by (125)I-F(ab')(2) anti-CK1 antibody binding.

82 In competitive inhibition experiments, anti-CK1, anti-uPAR, or anti-gC1qR blocked both biotin-HK bin

83 Although intact dysbindin did not bind any CK1 isoform, deletion of its coiled-coil domain yielded

84 Ser(594), Thr(595), and Ser(597) of Dvl2 are CK1 targets.

85 se results firmly establish that an axonemal CK1 regulates dynein activity and flagellar motility.

86 -regulation and define a direct link between CK1 and translation initiation.

87 er prolonged arsenite exposure, GADD34-bound CK1 catalyzed TDP-43 phosphorylations at serines 409/410

88 proteins dictate prehair formation broadly, CK1-gamma/gish restricts nucleation to a single site.

89 acts of neostriatal slices, was abolished by CK1-7 and IC261.

90 G on both Thr-75 and Ser-137 were blocked by CK1-7 and IC261, specific inhibitors of CK1, suggesting

91 e levels of these proteins are controlled by CK1.

92 osphorylation of IFNAR1 within its degron by CK1 alpha.

93 ision cycle, exhibit period determination by CK1 and GSK3, and have peroxiredoxin over-oxidation cycl

94 the phosphorylation of human Dvl3 induced by CK1.

95 characteristic of CK1, such as inhibition by CK1-7, the ability to phosphorylate a highly specific pe

96 However, phosphorylation of PS by CK2 or by CK1/CK2 increased PS cofactor activity approximately 1.5

97 ion on site(s) that can be phosphorylated by CK1 in vitro.

98 Phosphorylation by CK1 thus targeted the protein for degradation.

99 a consensus sequence for phosphorylation by CK1, allowing it to phosphorylate Ser322, which in turn

100 r494, which primes Ser497 phosphorylation by CK1.

101 11-mediated vesicle trafficking regulated by CK1-gamma is required for PCP-directed processes.

102 Phosphorylation of ICP0 T67 by CK1 recruits RNF8 for degradation and thereby promotes v

103 an efficient substrate for PKA, PKG, CaMKII, CK1, CK2, MAPK, Cdk1, or Cdk5.

104 2, Akt1, PKCdelta, PKCepsilon, Cdk1/cyclinB, CK1, Cdc5, GSK3beta, Src and Abl.

105 DC-CK1 appears to act preferentially on naive mouse lymphoc

106 e, dendritic cell-derived CC chemokine 1 (DC-CK1), which is produced in humans and acts on naive lymp

107 CD14- surface Ag expression, and RelB and DC-CK1 gene expression.

108 P-1 alpha), CCL4 (MIP-1 beta), and CCL18 (DC-CK1/PARC/AMAC-1) are potent chemoattractants produced by

109 ow for the first time an in vivo role for DC-CK1 in the establishment of primary T cell responses and

110 oites, revealing an adjuvant activity for DC-CK1.

111 Kinase dead CK1-gamma2 could not repress estrogen-induced ER transac

112 In contrast, a purified "kinase-dead" CK1 failed to restore inhibition.

113 Diminished CK1 activity may contribute to potentiated glutamatergic

114 Conversely, three structurally dissimilar CK1-specific inhibitors significantly reduced endogenous

115 Like Dma1, CK1 accumulates at SPBs during a mitotic arrest and asso

116 In this paper, we show that Drosophila CK1-gamma/gilgamesh (gish) regulates the PCP-associated

117 by overexpression of PKA and the Drosophila CK1, Double-time, a regulator of circadian rhythms.

118 Co-immunoprecipitation of endogenous CK1 with MDM2 occurred in undamaged cells, indicating th

119 0% at saturation, suggesting that endogenous CK1 was the major source of basal phosphorylation activi

120 Our results establish CK1 as an integral component of a mitotic, ubiquitin-med

121 To examine CK1 function, normal rat kidney cells were treated with

122 ssing the bovine cardiac Na+-Ca2+ exchanger (CK1.4 cells) and vector-transfected control cells.

123 can co-localize with endogenously expressed CK1.

124 es with gC1qR, uPAR and, to a lesser extent, CK1 antigen.

125 novel and previously unappreciated role for CK1 as a brake on REST stability and abundance in adult

126 lta/epsilon inhibitor, suggesting a role for CK1 homologue(s) in Nematostella clock.

127 ch is consistent with an inhibitory role for CK1.

128 We identify a conserved docking site for CK1 in NFAT proteins and show that mutation of this site

129 es are likely to serve as a paradigm for how CK1 kinases act in membrane traffic.

130 On HUVECs, CK1 and uPAR, but not gC1qR, colocalized to be a multipr

131 plicated the protein kinase casein kinase I (CK1) in regulation of dynein.

132 To assess the role of casein kinase I (CK1) in the regulation of dopamine signaling, we generat

133 ynthase Kinase 3 (GSK3) and Casein Kinase I (CK1) sites.

134 Consistent with this idea, CK1-dependent phosphorylation of rpS6 promotes its assoc

135 This study identifies CK1 as a facilitator of MPO-mediated vascular responses

136 hemia in rats in vivo triggers a decrease in CK1 and an increase in REST in selectively vulnerable hi

137 ddition of extracellular Ca2+ was reduced in CK1.4 cells compared with control cells at physiological

138 Overexpression of Ckidelta increased CK1 enzyme activity and further raised tau phosphorylati

139 (24 hours, 1% O(2)) significantly increased CK1 mRNA (in situ hybridization) and membrane protein ex

140 t: 1) endothelial oxidative stress increases CK1 expression, MBL binding, and C3 deposition; 2) inhib

141 f PER2 stability, and how drugs that inhibit CK1 alter period.

142 Protein kinase CK1 (formerly termed casein kinase I) is ubiquitous in e

143 ort that the highly conserved protein kinase CK1 transmits the signal necessary to stall cytokinesis

144 of endothelial cells with the protein kinase CK1-specific inhibitor IC261 prevented the H(2)O(2)-stim

145 (kinase CK2 site, Ser97A), or Ser130 (kinase CK1 site, Ser130A).

146 Increased levels of casein kinase (CK1 and CK2), which are associated with TDP-43 phosphory

147 as phosphorylated in vitro by casein kinase (CK1); this process required the prior phosphorylation of

148 ngiectasia-mutated (ATM) and casein kinase1 (CK1) and casein kinase2 (CK2) positively and negatively

149 ochemical mechanisms whereby casein kinase1 (CK1) determines circadian period in mammals, we created

150 galectins as targets of the protein kinases CK1, CK2, and PKA.

151 rted action of at least 3 different kinases: CK1, GSK-3, and DYRK.

152 e of which showed strong identity with known CK1 isoforms.

153 lating IFNAR1 in vitro, human CK1alpha and L-CK1 produced by the protozoan Leishmania major were also

154 Expression of leishmania CK1 in mammalian cells stimulated the phosphorylation-de

155 M-CK1 encodes a protein of 381 amino acids and the M-CK2 c

156 M-CK1 has three alleles, M-CK1.1, M-CK1.2, and M-CK1.3, wh

157 M-CK1 has three alleles, M-CK1.1, M-CK1.2, and M-CK1.3, while M-CK2 has just one allele as d

158 M-CK1 has three alleles, M-CK1.1, M-CK1.2, and M-CK1.3, while M-CK2 has just one al

159 1 has three alleles, M-CK1.1, M-CK1.2, and M-CK1.3, while M-CK2 has just one allele as determined by

160 The M-CK1 gene was isolated, sequenced, and characterized and

161 nalysis indicated the existence of two major CK1 mRNAs, 2.4 and 3.2 kilobase pairs long, the levels o

162 The malarial CK1 appeared to be the one of the smallest and perhaps t

163 oscopy and transmission electron microscopy, CK1 and uPAR, but not gC1qR, colocalized on the cell sur

164 Moreover, CK1-gamma/gish works in parallel with the Fz/PCP effecto

165 in, in their intracellular regions, multiple CK1 consensus phosphorylation sites, many of which are c

166 In the neostriatum, CK1 has been found to phosphorylate Ser-137 of DARPP-32.

167 identified two heterocyclic molecules as new CK1-specific inhibitor compounds with favorable physicoc

168 ow that mutation of this site disrupts NFAT1-CK1 interaction and causes constitutive nuclear localiza

169 , Clock, Per1, Per2, Cry1, and Cry2, but not CK1 epsilon, were influenced by photoperiod.

170 xanthate compound D609 inhibited CK2 but not CK1 in vitro and had a very modest effect on P protein p

171 eted kinases was enhanced, while CK2 but not CK1 inhibitors reduced APC cofactor activity.

172 in the Dvl3 C terminus prevented ability of CK1 to induce electrophoretic mobility shift of Dvl3 and

173 tors, we present evidence that activation of CK1 decreases NMDA receptor activity in the striatum via

174 A, presumably through blocking activation of CK1.

175 ways, which also integrate the activities of CK1 and GSK3.

176 Yet given the constitutive activity of CK1 alpha, it remained unclear how this pathway is stimu

177 nzyme exhibited properties characteristic of CK1, such as inhibition by CK1-7, the ability to phospho

178 Depletion of CK1 using small interfering RNA or inhibition of CK1 usi

179 Deregulation of CK1 (casein kinase 1) activity can be involved in the de

180 uced squamous metaplasias, but expression of CK1 and CK6 was sporadic.

181 ous metaplasias and widespread expression of CK1 and CK6 were observed in DeltaE3 beta-catenin transg

182 d dynamically induced after co-expression of CK1, and surprisingly, phosphorylation of one cluster of

183 While many forms of CK1 were capable of phosphorylating IFNAR1 in vitro, hum

184 evented by betaTrCP silencing, inhibition of CK1 and MEK, or mutation of the Tiam1 degron site.

185 Indeed, inhibition of CK1 increases NMDA-mediated EPSCs in medium spiny striat

186 lts suggest that pharmacologic inhibition of CK1 may be a viable therapeutic option for the treatment

187 using small interfering RNA or inhibition of CK1 using the kinase inhibitor (D4476) activated p53 and

188 d by CK1-7 and IC261, specific inhibitors of CK1, suggesting that activation of Cdk5 by mGluRs requir

189 er-174 and Ser-175 by the nuclear isoform of CK1.

190 nce in adult neurons and reveal that loss of CK1 is causally related to ischemia-induced neuronal dea

191 Seven sequential 20 amino acid peptides of CK1 were prepared to cover the protein coded by exons 1-

192 ofluorescence experiments in the presence of CK1 inhibitor showed increases in Cx43 plasma membrane l

193 cytometry studies confirmed the presence of CK1, uPAR, and gC1qR on HUVECs.

194 binding motif generated by mutual priming of CK1 and GSK-3beta substrate sequences.

195 lts provide the first evidence for a role of CK1 in the regulation of synaptic transmission in the br

196 t and metazoans, but the biological roles of CK1 members in plants are not well understood.

197 bitors (DRB and CK1-7) and solubilization of CK1 restored microtubule sliding in pf17 axonemes, which

198 Through the use of CK1 inhibitors, we present evidence that activation of C

199 region of 20 amino acids coded by exon 1 on CK1 which is carboxyl-terminal to its glycine-rich amino

200 rmed to demonstrate the HK binding domain on CK1.

201 gh molecular weight kininogen (HK) reside on CK1 together or whether they compete for binding.

202 ere we characterized the contribution of one CK1 isoform, Ckidelta, to the phosphorylation of tau at

203 nt was eliminated by either butyrolactone or CK1-7 and was absent in DARPP-32 knockout mice.

204 rst messengers for the regulation of Cdk5 or CK1 have remained unknown.

205 Alteration of the GSK3 or CK1 sites prevents Ci-155 proteolysis and activates Ci i

206 deacetylases, calcium calmodulin kinase, or CK1.

207 Being compared to other CK1 isoforms, these compounds exhibited advanced isoform

208 CK1delta and CK1epsilon, but not with other CK1 isoforms.

209 We propose a role for mammalian and parasite CK1 enzymes in regulating IFNAR1 stability and type I IF

210 ng with elements of the fibrillar pathology, CK1 is found within the matrix of granulovacuolar degene

211 Treatment of cells with membrane permeable CK1 inhibitor 3-[(2,3,6-trimethoxyphenyl)methylidenyl]-i

212 ow that multiple successively phosphorylated CK1 sites on Ci create an atypical extended binding site

213 Gprk2/Smo interaction is facilitated by PKA/CK1-mediated phosphorylation of Smo C-tail.

214 Hh inhibits Smo ubiquitination via PKA/CK1-mediated phosphorylation of SAID, leading to Smo cel

215 ore, research interest in identifying potent CK1-specific inhibitors is still increasing.

216 tion site, and another disrupted a predicted CK1 phosphorylation site.

217 the smallest and perhaps the most primitive CK1 enzymes known, containing little sequence informatio

218 on; 2) inhibition of MBL attenuates purified CK1-induced complement activation; and 3) anti-human cyt

219 protein could be phosphorylated by purified CK1 at Ser(215) but this phosphorylation did not result

220 Phosphorylation of PS by purified CK1 did not affect its activated protein C (APC) cofacto

221 attenuated MBL and C3 deposition on purified CK1 (ELISA).

222 phosphorylation was confirmed using purified CK1/CK2.

223 Four overlapping recombinant (r) CK1 proteins were produced in Escherichia coli by a glut

224 Mutagenesis of recombinant CK1 defined important amino acid residues and their pote

225 depleted axonemes with purified, recombinant CK1 restored inhibition of microtubule sliding in a DRB-

226 nse to chronic oxidative stress and recruits CK1 and oxidized TDP-43 to facilitate its phosphorylatio

227 rified recombinant Chlamydomonas reinhardtii CK1, together with CK1-depleted axonemes from the paraly

228 g that activation of Cdk5 by mGluRs requires CK1 activity.

229 njection immediately after ischemia restores CK1 activity, suppresses REST expression, and rescues ne

230 ls (HUVECs) had 7.2 +/- 0.2 x 10(4) specific CK1 membrane sites/cell by (125)I-F(ab')(2) anti-CK1 ant

231 labeled cells treated with CKI-7, a specific CK1 inhibitor, showed a reduction in Cx43 phosphorylatio

232 um and epidermis, and the epidermis-specific CK1 and CK6 were used as differentiation markers.

233 pic glutamate receptors (mGluRs), stimulates CK1 and Cdk5 kinase activities in neostriatal neurons, l

234 HPG on the activity of transfected HA-tagged CK1(epsilon) was blocked by BAPTA/AM and cyclosporin A.

235 t that an Arabidopsis (Arabidopsis thaliana) CK1 member named casein kinase 1-like 6 (CKL6) associate

236 vel (i) support previous the assumption that CK1 acts via phosphorylation of distinct residues as the

237 of APP, it was possible to demonstrate that CK1 inhibitors act at the level of gamma-secretase cleav

238 small molecule inhibitors and the fact that CK1 and MDM2 form a stable complex suggest that the MDM2

239 CK1 phosphorylation reactions indicate that CK1 interacted with and phosphorylated Cx43, initially o

240 Our results indicate that CK1 represents a therapeutic target for prevention of Ab

241 hetamine or methylphenidate, indicating that CK1 activity has a profound effect on dopamine signaling

242 In the present study, we show that CK1 regulates fast synaptic transmission mediated by glu

243 beta-catenin signaling and (ii) suggest that CK1 acts on Dvl via different mechanism than Fzd5.

244 Our findings suggest that CK1 tonically suppresses NMDAR activity in the PVN by re

245 The CK1 docking motif is present in proteins of the Wnt, Hed

246 The CK1 inhibitor PF4800567 or PF670462 significantly increa

247 The CK1 inhibitors (DRB and CK1-7) and solubilization of CK1

248 tions of the phosphatase calcineurin and the CK1/GSK3beta protein kinases on the phosphodegron-depend

249 s, required for rescue, were retained in the CK1-depleted axonemes.

250 effects of thapsigargin on Ba2+ entry in the CK1.4 cells because Ba2+ is transported by the Na+-Ca2+

251 We conclude that in the CK1.4 cells, Ca2+ entry through store-operated channels

252 nly partially inhibited this response in the CK1.4 cells.

253 hen Li+ or NMDG was substituted for Na+, the CK1.4 cells showed a greater rise in [Ca2+]i than contro

254 Administration of the CK1 activator pyrvinium pamoate by in vivo injection imm

255 itogen kinases, GSK3beta, and members of the CK1 family.

256 constitutively active CK1epsilon, one of the CK1 isoforms expressed in brain, leads to an increase in

257 cking site to a high-affinity version or the CK1 docking site to a low-affinity version results in ge

258 osphorylate Ser322, which in turn primes the CK1-catalysed phosphorylation of Ser325.

259 ad similar pharmacological properties to the CK1 inhibitor D4476.

260 75 to alanine or treatment of cells with the CK1 inhibitor, D4476 inhibits nuclear export of eIF6 and

261 Here we report the distribution of three CK1 isoforms (Ckialpha, Ckidelta, and Ckiepsilon) in AD

262 alciparum by affinity chromatography through CK1-7 columns displayed identical properties.

263 lasminogen activation, whereas antibodies to CK1 only inhibited 24% of plasminogen activation.

264 Furthermore, HK binding to CK1 modulates PK activation on HUVEC.

265 ion and activates the LCP via MBL binding to CK1.

266 These findings point to CK1 as a potential therapeutic target for the ameliorati

267 ass of metabotropic glutamate receptors uses CK1 to inhibit NMDA-mediated synaptic currents.

268 immunoprecipitation experiments and in vitro CK1 phosphorylation reactions indicate that CK1 interact

269 of Drosophila, humans, and Neurospora, where CK1 and CK2 are emerging as the main protein kinases inv

270 We analyzed whether CK1 regulates p53 protein stability in unstressed condit

271 These findings support a model in which CK1-mediated phosphorylation of Rim8 contributes to sett

272 the NFAT1 SP-2 motif, and it synergizes with CK1 to regulate NFAT1 nuclear export.

273 Chlamydomonas reinhardtii CK1, together with CK1-depleted axonemes from the paralyzed flagellar mutan

274 476 suggested a critical role for the MDM2 x CK1 complex in maintaining E2F-1 anti-apoptotic signalin

275 orm a stable complex suggest that the MDM2 x CK1 complex is a component of a genetic pathway that co-

276 in level changes, indicating that the MDM2 x CK1 complex is both a negative regulator of p53 and a po