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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 ct with various isoforms of casein kinase 1 (CK1) and keratins and to mediate organization of keratin
24 cal conditions and identify Casein Kinase 1 (CK1) as an upstream effector that bidirectionally regula
25  both were inhibited by the casein kinase 1 (CK1) delta/epsilon inhibitor IC261.
26              An increase of casein kinase 1 (CK1) expression has been described in the human AD brain
27 d in vivo by members of the casein kinase 1 (CK1) family and by glycogen synthase kinase 3beta (GSK3b
28              Members of the casein kinase 1 (CK1) family are evolutionarily conserved eukaryotic prot
29 ases include members of the casein kinase 1 (CK1) family of phosphotransferases, which are highly ove
30  Ser-247 is a target of the casein kinase 1 (CK1) family of protein kinases.
31                             Casein kinase 1 (CK1) has been implicated in a variety of cellular functi
32                   Here, the casein kinase 1 (CK1) Hrr25 is shown to be an endocytic protein and to be
33 e have examined the role of casein kinase 1 (CK1) in connexin-43 (Cx43) gap junction assembly.
34                             Casein kinase 1 (CK1) is a highly conserved serine/threonine kinase, pres
35                             Casein kinase 1 (CK1) is one such enzyme; it stimulates p53 after transfo
36 luding the serine-threonine casein kinase 1 (CK1) isoforms CK1d/e, regulate the timing of the circadi
37                             Casein kinase 1 (CK1) isoforms epsilon and delta, key circadian regulator
38                The cDNA for casein kinase 1 (CK1) of Plasmodium falciparum was cloned, sequenced, and
39 A (PKA) sites and secondary casein kinase 1 (CK1) or glycogen synthase kinase 3 (GSK3) sites was care
40 ites or adjacent PKA-primed casein kinase 1 (CK1) sites are replaced by alanine residues.
41 (PKC) site Cx43(S368A), the casein kinase 1 (CK1) sites Cx43(S325A/328Y/330A), and the mitogen-activa
42                             Casein kinase 1 (CK1) was identified as the major kinase responsible for
43  by protein kinase A (PKA), casein kinase 1 (CK1), and glycogen synthase kinase 3 (GSK3), as well as
44 s Ser683 phosphorylation by casein kinase 1 (CK1), and these phosphorylation events elevate Smo activ
45 lation of the COPII coat by casein kinase 1 (CK1), Hrr25, contributes to the directional delivery of
46 ation by kinases, including casein kinase 1 (CK1), restores NFAT to its latent state in the cytoplasm
47 FZD3, FZD7, Dvl2, Dvl3, and casein kinase 1 (CK1)-epsilon are upregulated in B lymphocytes of patient
48                             Casein kinase 1 (CK1)-mediated phosphorylation of Cx43 promotes gap junct
49 5 by the nuclear isoform of casein kinase 1 (CK1).
50 hosphorylation at Ser(6) by casein kinase 1 (CK1).
51  plasma membrane-associated casein kinase 1 (CK1).
52 ilaments are members of the casein kinase-1 (CK1) family of protein kinases.
53 , we determined the role of casein kinase-1 (CK1) in regulating NMDAR activity in the PVN.
54  recruited a TDP-43 kinase, casein kinase-1 (CK1), to GADD34.
55 combined activities of casein kinase 1delta (CK1 delta) and casein kinase 1epsilon (CK1epsilon) and w
56 locus is controlled by Casein Kinase 1delta (CK1 delta)-dependent phosphorylation during GCP prolifer
57 se 3beta (GSK3beta) or casein kinase 1 or 2 (CK1/2) markedly slowed the decay of nuclear NFATc1-GFP a
58 tected when cells were treated with IC261, a CK1 inhibitor specific for delta or epsilon isoforms.
59       Together these results indicate that a CK1-Cdk5-DARPP-32 cascade may be involved in the regulat
60 s can be modulated pharmacologically using a CK1 epsilon/delta inhibitor, suggesting a role of this k
61 r, these studies suggest that DHPG activates CK1(epsilon) via Ca(2+)-dependent stimulation of calcine
62      Autoactivation primes Fu for additional CK1-dependent phosphorylation, which further enhances ki
63                   Furthermore, levels of all CK1 isoforms are elevated in the CA1 region of AD hippoc
64                       Casein kinase 1 alpha (CK1 alpha) was shown to directly phosphorylate Ser(535)
65          Studies of Ci variants with altered CK1 and GSK3 sites suggest that the large number of phos
66 lation of Ci at the specific PKA, GSK-3, and CK1 sites required in vivo for partial proteolysis stimu
67  The major docking sites for calcineurin and CK1 are strongly conserved throughout vertebrate evoluti
68 onist for group I mGluRs, increased Cdk5 and CK1 activities in neostriatal slices, leading to the enh
69            Here we report that both Cdk5 and CK1 are regulated by metabotropic glutamate receptors (m
70 s (Bmal1, Clock, Per1, Per2, Cry1, Cry2, and CK1 epsilon ) was assayed by in situ hybridization in th
71                  The CK1 inhibitors (DRB and CK1-7) and solubilization of CK1 restored microtubule sl
72 ibition of microtubule sliding in a DRB- and CK1-7-sensitive manner.
73 ase is activated by Smo and Cos2 via Fu- and CK1-dependent phosphorylation.
74 h the scaffold Axin and the kinases GSK3 and CK1 to target betacatenin for destruction.
75 ine-rich region 1 (SRR-1) motifs by GSK3 and CK1, respectively.
76 e subsequent phosphorylation by Sgg/GSK3 and CK1.
77  phosphorylation by the kinases Sgg/GSK3 and CK1.
78 truction complex that scaffolds GSK3beta and CK1 to earmark beta-catenin for proteosomal degradation.
79 uring muscle activity, and that GSK3beta and CK1/2 are responsible for phosphorylating NFATc1 in musc
80        Our results suggest that GSK3beta and CK1/2 are the major protein kinases that contribute to t
81      Simultaneous inhibition of GSK3beta and CK1/2 completely blocked the nuclear export of NFATc1-GF
82 destruction complex with Axin, GSK3beta, and CK1 that targets beta-catenin/Armadillo (beta-cat/Arm) f
83  pharmacological similarity between MDM2 and CK1 small molecule inhibitors and the fact that CK1 and
84 r741/Thr742, which is facilitated by PKA and CK1 phosphorylation at adjacent Ser residues.
85 mo aa625-753, which covers the three PKA and CK1 phosphorylation clusters.
86 over, we show that Hh regulates both PKA and CK1 phosphorylation of Smo.
87 at Smo containing acidic residues at PKA and CK1 sites can be stimulated further by Hh and acts throu
88 edback loop and acts downstream from PKA and CK1 to facilitate high-level Hh signaling by promoting t
89  a stable complex between clock proteins and CK1 is a conserved feature in eukaryotic circadian mecha
90        Combined recombinant soluble uPAR and CK1 inhibit 80% FITC-FXII binding to HUVECs.
91 membrane sites/cell by (125)I-F(ab')(2) anti-CK1 antibody binding.
92  In competitive inhibition experiments, anti-CK1, anti-uPAR, or anti-gC1qR blocked both biotin-HK bin
93   Although intact dysbindin did not bind any CK1 isoform, deletion of its coiled-coil domain yielded
94                                  Arabidopsis CK1 family member MUT9-LIKE KINASEs, such as MLK1 and ML
95 Ser(594), Thr(595), and Ser(597) of Dvl2 are CK1 targets.
96 se results firmly establish that an axonemal CK1 regulates dynein activity and flagellar motility.
97 -regulation and define a direct link between CK1 and translation initiation.
98 er prolonged arsenite exposure, GADD34-bound CK1 catalyzed TDP-43 phosphorylations at serines 409/410
99  proteins dictate prehair formation broadly, CK1-gamma/gish restricts nucleation to a single site.
100 acts of neostriatal slices, was abolished by CK1-7 and IC261.
101 G on both Thr-75 and Ser-137 were blocked by CK1-7 and IC261, specific inhibitors of CK1, suggesting
102 e levels of these proteins are controlled by CK1.
103 osphorylation of IFNAR1 within its degron by CK1 alpha.
104 ision cycle, exhibit period determination by CK1 and GSK3, and have peroxiredoxin over-oxidation cycl
105 the phosphorylation of human Dvl3 induced by CK1.
106 characteristic of CK1, such as inhibition by CK1-7, the ability to phosphorylate a highly specific pe
107  However, phosphorylation of PS by CK2 or by CK1/CK2 increased PS cofactor activity approximately 1.5
108 ion on site(s) that can be phosphorylated by CK1 in vitro.
109  feeds back to reduce FRQ phosphorylation by CK1 at higher temperatures.
110  which primes its further phosphorylation by CK1 on adjacent sties.
111                           Phosphorylation by CK1 thus targeted the protein for degradation.
112  a consensus sequence for phosphorylation by CK1, allowing it to phosphorylate Ser322, which in turn
113 r494, which primes Ser497 phosphorylation by CK1.
114 11-mediated vesicle trafficking regulated by CK1-gamma is required for PCP-directed processes.
115               Phosphorylation of ICP0 T67 by CK1 recruits RNF8 for degradation and thereby promotes v
116 an efficient substrate for PKA, PKG, CaMKII, CK1, CK2, MAPK, Cdk1, or Cdk5.
117 2, Akt1, PKCdelta, PKCepsilon, Cdk1/cyclinB, CK1, Cdc5, GSK3beta, Src and Abl.
118                                           DC-CK1 appears to act preferentially on naive mouse lymphoc
119 e, dendritic cell-derived CC chemokine 1 (DC-CK1), which is produced in humans and acts on naive lymp
120 CD14- surface Ag expression, and RelB and DC-CK1 gene expression.
121 P-1 alpha), CCL4 (MIP-1 beta), and CCL18 (DC-CK1/PARC/AMAC-1) are potent chemoattractants produced by
122 ow for the first time an in vivo role for DC-CK1 in the establishment of primary T cell responses and
123 oites, revealing an adjuvant activity for DC-CK1.
124                                  Kinase dead CK1-gamma2 could not repress estrogen-induced ER transac
125        In contrast, a purified "kinase-dead" CK1 failed to restore inhibition.
126                                   Diminished CK1 activity may contribute to potentiated glutamatergic
127    Conversely, three structurally dissimilar CK1-specific inhibitors significantly reduced endogenous
128                                   Like Dma1, CK1 accumulates at SPBs during a mitotic arrest and asso
129       In this paper, we show that Drosophila CK1-gamma/gilgamesh (gish) regulates the PCP-associated
130  by overexpression of PKA and the Drosophila CK1, Double-time, a regulator of circadian rhythms.
131         Co-immunoprecipitation of endogenous CK1 with MDM2 occurred in undamaged cells, indicating th
132 0% at saturation, suggesting that endogenous CK1 was the major source of basal phosphorylation activi
133 ability by Casein Kinase 1delta and epsilon (CK1) plays a key regulatory role in metazoan circadian r
134                        Our results establish CK1 as an integral component of a mitotic, ubiquitin-med
135                                   To examine CK1 function, normal rat kidney cells were treated with
136 ssing the bovine cardiac Na+-Ca2+ exchanger (CK1.4 cells) and vector-transfected control cells.
137  can co-localize with endogenously expressed CK1.
138 es with gC1qR, uPAR and, to a lesser extent, CK1 antigen.
139  novel and previously unappreciated role for CK1 as a brake on REST stability and abundance in adult
140 lta/epsilon inhibitor, suggesting a role for CK1 homologue(s) in Nematostella clock.
141 ch is consistent with an inhibitory role for CK1.
142     We identify a conserved docking site for CK1 in NFAT proteins and show that mutation of this site
143                                      The FRQ-CK1 interaction has two roles in the circadian negative
144 Together, these results suggest that the FRQ-CK1 interaction is a major rate-limiting step in circadi
145   Mutations that specifically affect the FRQ-CK1 interaction lead to severe alterations in circadian
146                    Here we show that the FRQ-CK1 interaction, but not FRQ stability, correlates with
147 es are likely to serve as a paradigm for how CK1 kinases act in membrane traffic.
148                                   On HUVECs, CK1 and uPAR, but not gC1qR, colocalized to be a multipr
149 plicated the protein kinase casein kinase I (CK1) in regulation of dynein.
150       To assess the role of casein kinase I (CK1) in the regulation of dopamine signaling, we generat
151 ynthase Kinase 3 (GSK3) and Casein Kinase I (CK1) sites.
152                   Consistent with this idea, CK1-dependent phosphorylation of rpS6 promotes its assoc
153                        This study identifies CK1 as a facilitator of MPO-mediated vascular responses
154 hemia in rats in vivo triggers a decrease in CK1 and an increase in REST in selectively vulnerable hi
155 ddition of extracellular Ca2+ was reduced in CK1.4 cells compared with control cells at physiological
156 ing a highly conserved anion binding site in CK1.
157         Overexpression of Ckidelta increased CK1 enzyme activity and further raised tau phosphorylati
158  (24 hours, 1% O(2)) significantly increased CK1 mRNA (in situ hybridization) and membrane protein ex
159 t: 1) endothelial oxidative stress increases CK1 expression, MBL binding, and C3 deposition; 2) inhib
160 f PER2 stability, and how drugs that inhibit CK1 alter period.
161                               Protein kinase CK1 (formerly termed casein kinase I) is ubiquitous in e
162 ort that the highly conserved protein kinase CK1 transmits the signal necessary to stall cytokinesis
163 of endothelial cells with the protein kinase CK1-specific inhibitor IC261 prevented the H(2)O(2)-stim
164 (kinase CK2 site, Ser97A), or Ser130 (kinase CK1 site, Ser130A).
165           Increased levels of casein kinase (CK1 and CK2), which are associated with TDP-43 phosphory
166 as phosphorylated in vitro by casein kinase (CK1); this process required the prior phosphorylation of
167 ngiectasia-mutated (ATM) and casein kinase1 (CK1) and casein kinase2 (CK2) positively and negatively
168 ochemical mechanisms whereby casein kinase1 (CK1) determines circadian period in mammals, we created
169  galectins as targets of the protein kinases CK1, CK2, and PKA.
170 rted action of at least 3 different kinases: CK1, GSK-3, and DYRK.
171 e of which showed strong identity with known CK1 isoforms.
172 lating IFNAR1 in vitro, human CK1alpha and L-CK1 produced by the protozoan Leishmania major were also
173                     Expression of leishmania CK1 in mammalian cells stimulated the phosphorylation-de
174                                            M-CK1 encodes a protein of 381 amino acids and the M-CK2 c
175                                            M-CK1 has three alleles, M-CK1.1, M-CK1.2, and M-CK1.3, wh
176          M-CK1 has three alleles, M-CK1.1, M-CK1.2, and M-CK1.3, while M-CK2 has just one allele as d
177                   M-CK1 has three alleles, M-CK1.1, M-CK1.2, and M-CK1.3, while M-CK2 has just one al
178 1 has three alleles, M-CK1.1, M-CK1.2, and M-CK1.3, while M-CK2 has just one allele as determined by
179                                        The M-CK1 gene was isolated, sequenced, and characterized and
180 nalysis indicated the existence of two major CK1 mRNAs, 2.4 and 3.2 kilobase pairs long, the levels o
181                                 The malarial CK1 appeared to be the one of the smallest and perhaps t
182 ndation to understand and further manipulate CK1 regulation of circadian rhythms.
183 oscopy and transmission electron microscopy, CK1 and uPAR, but not gC1qR, colocalized on the cell sur
184                                    Moreover, CK1-gamma/gish works in parallel with the Fz/PCP effecto
185 in, in their intracellular regions, multiple CK1 consensus phosphorylation sites, many of which are c
186                          In the neostriatum, CK1 has been found to phosphorylate Ser-137 of DARPP-32.
187 identified two heterocyclic molecules as new CK1-specific inhibitor compounds with favorable physicoc
188 ow that mutation of this site disrupts NFAT1-CK1 interaction and causes constitutive nuclear localiza
189 , Clock, Per1, Per2, Cry1, and Cry2, but not CK1 epsilon, were influenced by photoperiod.
190 xanthate compound D609 inhibited CK2 but not CK1 in vitro and had a very modest effect on P protein p
191 eted kinases was enhanced, while CK2 but not CK1 inhibitors reduced APC cofactor activity.
192  in the Dvl3 C terminus prevented ability of CK1 to induce electrophoretic mobility shift of Dvl3 and
193 tors, we present evidence that activation of CK1 decreases NMDA receptor activity in the striatum via
194 A, presumably through blocking activation of CK1.
195 ways, which also integrate the activities of CK1 and GSK3.
196       Yet given the constitutive activity of CK1 alpha, it remained unclear how this pathway is stimu
197 nzyme exhibited properties characteristic of CK1, such as inhibition by CK1-7, the ability to phospho
198 espite the deep evolutionary conservation of CK1 in eukaryotes, little is known about its regulation
199                                 Depletion of CK1 using small interfering RNA or inhibition of CK1 usi
200                              Deregulation of CK1 (casein kinase 1) activity can be involved in the de
201 uced squamous metaplasias, but expression of CK1 and CK6 was sporadic.
202 ous metaplasias and widespread expression of CK1 and CK6 were observed in DeltaE3 beta-catenin transg
203 d dynamically induced after co-expression of CK1, and surprisingly, phosphorylation of one cluster of
204                          While many forms of CK1 were capable of phosphorylating IFNAR1 in vitro, hum
205 evented by betaTrCP silencing, inhibition of CK1 and MEK, or mutation of the Tiam1 degron site.
206                        Indeed, inhibition of CK1 increases NMDA-mediated EPSCs in medium spiny striat
207 lts suggest that pharmacologic inhibition of CK1 may be a viable therapeutic option for the treatment
208 using small interfering RNA or inhibition of CK1 using the kinase inhibitor (D4476) activated p53 and
209 d by CK1-7 and IC261, specific inhibitors of CK1, suggesting that activation of Cdk5 by mGluRs requir
210 er-174 and Ser-175 by the nuclear isoform of CK1.
211 nce in adult neurons and reveal that loss of CK1 is causally related to ischemia-induced neuronal dea
212   Seven sequential 20 amino acid peptides of CK1 were prepared to cover the protein coded by exons 1-
213 ofluorescence experiments in the presence of CK1 inhibitor showed increases in Cx43 plasma membrane l
214  cytometry studies confirmed the presence of CK1, uPAR, and gC1qR on HUVECs.
215 binding motif generated by mutual priming of CK1 and GSK-3beta substrate sequences.
216 lts provide the first evidence for a role of CK1 in the regulation of synaptic transmission in the br
217 t and metazoans, but the biological roles of CK1 members in plants are not well understood.
218 bitors (DRB and CK1-7) and solubilization of CK1 restored microtubule sliding in pf17 axonemes, which
219                           Through the use of CK1 inhibitors, we present evidence that activation of C
220  region of 20 amino acids coded by exon 1 on CK1 which is carboxyl-terminal to its glycine-rich amino
221 rmed to demonstrate the HK binding domain on CK1.
222 gh molecular weight kininogen (HK) reside on CK1 together or whether they compete for binding.
223 ere we characterized the contribution of one CK1 isoform, Ckidelta, to the phosphorylation of tau at
224 nt was eliminated by either butyrolactone or CK1-7 and was absent in DARPP-32 knockout mice.
225 rst messengers for the regulation of Cdk5 or CK1 have remained unknown.
226                    Alteration of the GSK3 or CK1 sites prevents Ci-155 proteolysis and activates Ci i
227  deacetylases, calcium calmodulin kinase, or CK1.
228                      Being compared to other CK1 isoforms, these compounds exhibited advanced isoform
229  CK1delta and CK1epsilon, but not with other CK1 isoforms.
230 We propose a role for mammalian and parasite CK1 enzymes in regulating IFNAR1 stability and type I IF
231 ng with elements of the fibrillar pathology, CK1 is found within the matrix of granulovacuolar degene
232   Treatment of cells with membrane permeable CK1 inhibitor 3-[(2,3,6-trimethoxyphenyl)methylidenyl]-i
233 ow that multiple successively phosphorylated CK1 sites on Ci create an atypical extended binding site
234 idues present in many kinases including PIM, CK1, DAPK, and CLK.
235  Gprk2/Smo interaction is facilitated by PKA/CK1-mediated phosphorylation of Smo C-tail.
236       Hh inhibits Smo ubiquitination via PKA/CK1-mediated phosphorylation of SAID, leading to Smo cel
237 ore, research interest in identifying potent CK1-specific inhibitors is still increasing.
238 tion site, and another disrupted a predicted CK1 phosphorylation site.
239  the smallest and perhaps the most primitive CK1 enzymes known, containing little sequence informatio
240 on; 2) inhibition of MBL attenuates purified CK1-induced complement activation; and 3) anti-human cyt
241  protein could be phosphorylated by purified CK1 at Ser(215) but this phosphorylation did not result
242            Phosphorylation of PS by purified CK1 did not affect its activated protein C (APC) cofacto
243 attenuated MBL and C3 deposition on purified CK1 (ELISA).
244 phosphorylation was confirmed using purified CK1/CK2.
245             Four overlapping recombinant (r) CK1 proteins were produced in Escherichia coli by a glut
246                   Mutagenesis of recombinant CK1 defined important amino acid residues and their pote
247 depleted axonemes with purified, recombinant CK1 restored inhibition of microtubule sliding in a DRB-
248 nse to chronic oxidative stress and recruits CK1 and oxidized TDP-43 to facilitate its phosphorylatio
249 rified recombinant Chlamydomonas reinhardtii CK1, together with CK1-depleted axonemes from the paraly
250 g that activation of Cdk5 by mGluRs requires CK1 activity.
251 njection immediately after ischemia restores CK1 activity, suppresses REST expression, and rescues ne
252 ls (HUVECs) had 7.2 +/- 0.2 x 10(4) specific CK1 membrane sites/cell by (125)I-F(ab')(2) anti-CK1 ant
253 labeled cells treated with CKI-7, a specific CK1 inhibitor, showed a reduction in Cx43 phosphorylatio
254 um and epidermis, and the epidermis-specific CK1 and CK6 were used as differentiation markers.
255 pic glutamate receptors (mGluRs), stimulates CK1 and Cdk5 kinase activities in neostriatal neurons, l
256 HPG on the activity of transfected HA-tagged CK1(epsilon) was blocked by BAPTA/AM and cyclosporin A.
257 t that an Arabidopsis (Arabidopsis thaliana) CK1 member named casein kinase 1-like 6 (CKL6) associate
258 vel (i) support previous the assumption that CK1 acts via phosphorylation of distinct residues as the
259  of APP, it was possible to demonstrate that CK1 inhibitors act at the level of gamma-secretase cleav
260  small molecule inhibitors and the fact that CK1 and MDM2 form a stable complex suggest that the MDM2
261  CK1 phosphorylation reactions indicate that CK1 interacted with and phosphorylated Cx43, initially o
262                    Our results indicate that CK1 represents a therapeutic target for prevention of Ab
263 hetamine or methylphenidate, indicating that CK1 activity has a profound effect on dopamine signaling
264           In the present study, we show that CK1 regulates fast synaptic transmission mediated by glu
265 beta-catenin signaling and (ii) suggest that CK1 acts on Dvl via different mechanism than Fzd5.
266                    Our findings suggest that CK1 tonically suppresses NMDAR activity in the PVN by re
267                                          The CK1 docking motif is present in proteins of the Wnt, Hed
268                                          The CK1 inhibitor PF4800567 or PF670462 significantly increa
269                                          The CK1 inhibitors (DRB and CK1-7) and solubilization of CK1
270 tions of the phosphatase calcineurin and the CK1/GSK3beta protein kinases on the phosphodegron-depend
271 s, required for rescue, were retained in the CK1-depleted axonemes.
272 effects of thapsigargin on Ba2+ entry in the CK1.4 cells because Ba2+ is transported by the Na+-Ca2+
273                      We conclude that in the CK1.4 cells, Ca2+ entry through store-operated channels
274 nly partially inhibited this response in the CK1.4 cells.
275 hen Li+ or NMDG was substituted for Na+, the CK1.4 cells showed a greater rise in [Ca2+]i than contro
276                        Administration of the CK1 activator pyrvinium pamoate by in vivo injection imm
277 itogen kinases, GSK3beta, and members of the CK1 family.
278 constitutively active CK1epsilon, one of the CK1 isoforms expressed in brain, leads to an increase in
279 on assays, we show here that mutation of the CK1 phosphorylation sites in Cx43 reduces the levels of
280 cking site to a high-affinity version or the CK1 docking site to a low-affinity version results in ge
281 osphorylate Ser322, which in turn primes the CK1-catalysed phosphorylation of Ser325.
282 ad similar pharmacological properties to the CK1 inhibitor D4476.
283 75 to alanine or treatment of cells with the CK1 inhibitor, D4476 inhibits nuclear export of eIF6 and
284     Here we report the distribution of three CK1 isoforms (Ckialpha, Ckidelta, and Ckiepsilon) in AD
285 alciparum by affinity chromatography through CK1-7 columns displayed identical properties.
286 lasminogen activation, whereas antibodies to CK1 only inhibited 24% of plasminogen activation.
287                   Furthermore, HK binding to CK1 modulates PK activation on HUVEC.
288 ion and activates the LCP via MBL binding to CK1.
289                      These findings point to CK1 as a potential therapeutic target for the ameliorati
290                   Applying our principles to CK1.2 we identified four new substrates, BBP59, LRRP1, C
291 ass of metabotropic glutamate receptors uses CK1 to inhibit NMDA-mediated synaptic currents.
292 immunoprecipitation experiments and in vitro CK1 phosphorylation reactions indicate that CK1 interact
293 of Drosophila, humans, and Neurospora, where CK1 and CK2 are emerging as the main protein kinases inv
294                          We analyzed whether CK1 regulates p53 protein stability in unstressed condit
295      These findings support a model in which CK1-mediated phosphorylation of Rim8 contributes to sett
296 the NFAT1 SP-2 motif, and it synergizes with CK1 to regulate NFAT1 nuclear export.
297 Chlamydomonas reinhardtii CK1, together with CK1-depleted axonemes from the paralyzed flagellar mutan
298 476 suggested a critical role for the MDM2 x CK1 complex in maintaining E2F-1 anti-apoptotic signalin
299 orm a stable complex suggest that the MDM2 x CK1 complex is a component of a genetic pathway that co-
300 in level changes, indicating that the MDM2 x CK1 complex is both a negative regulator of p53 and a po

 
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