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1                                              PLK1 (polo-like kinase 1) is a key mitotic kinase and a
2                                              PLK1 activity continually accumulates from initial level
3                                              PLK1 inhibition by BI-2536 or siRNA-mediated knockdown s
4                                              PLK1 inhibition is a promising therapeutic strategy and
5                                              PLK1 inhibition prevented medulloblastoma cell prolifera
6                                              PLK1 is a proviral host factor that could be envisaged a
7                                              PLK1 knockdown or use of PLK1 inhibitor can mitigate onc
8                                              PLK1 mediates invasion via vimentin and beta1 integrin,
9                                              PLK1 phosphorylates NDR1 at three putative threonine res
10                                              PLK1-mediated phosphorylation of FoxM1b abrogates the in
11 higher cyclin B/CDK1 and Polo-like kinase 1 (PLK1) activities in an S-phase-enriched population that
12 our transforming gene 1, Polo-like kinase 1 (PLK1) and Caveolin-2.
13 tified a central role of Polo-like kinase 1 (PLK1) and known PLK1 targets.
14  serine/threonine kinase Polo-like kinase 1 (PLK1) as a host kinase that phosphorylates P and have fo
15 vious studies identified polo-like kinase 1 (PLK1) as a major regulator of FoxM1b.
16 ellular serine/threonine Polo-like-kinase 1 (PLK1) as a positive effector of HBV replication.
17 g 720 kinases identified Polo-like kinase 1 (PLK1) as one of the top genes whose downregulation resul
18 sistent up-regulation of polo-like kinase 1 (PLK1) as well as other genes controlling the G(2)/M tran
19                          Polo-like kinase 1 (PLK1) has important functions in maintaining genome stab
20 a site phosphorylated by Polo-like kinase 1 (PLK1) in the GRASP65 N-terminal domain for which mutatio
21                          Polo-like kinase 1 (PLK1) is a key cell cycle regulator implicated in the de
22                          Polo-like kinase 1 (PLK1) is an evolutionarily conserved serine/threonine ki
23                          Polo-like kinase 1 (PLK1) is an oncogenic kinase that controls cell cycle an
24 phosphorylation requires polo-like kinase 1 (PLK1) rather than DNA-PKcs, that SAF-A interacts with PL
25 Here, we report that the polo-like kinase 1 (PLK1) regulates BMI1 expression, and that its inhibition
26 C-protein kinase A (PKA)-polo-like kinase 1 (PLK1) signaling loop in cells.
27 arrest via inhibition of polo-like kinase 1 (PLK1) signalling pathway and down-modulation of Aurora k
28                          Polo-like kinase 1 (PLK1) was found to be significantly overexpressed in TNB
29 riggering proteolysis of polo-like kinase 1 (PLK1), a tumor suppressor and multitasking mitotic kinas
30                          Polo-like kinase 1 (PLK1), an essential regulator of cell division, is curre
31  when compared with AKT, polo-like kinase 1 (PLK1), CDK activating kinase (CAK), CAMKIIalpha, and thr
32 ed genes, in particular, Polo-like kinase 1 (PLK1), were associated with disease aggressiveness.
33 er-4, a site shared with polo-like kinase 1 (PLK1).
34  of potent inhibitors of Polo-like kinase 1 (PLK1).
35 parently by antagonizing polo-like kinase 1 (PLK1).
36 ytokinesis 1 (PRC1), and polo-like kinase 1 (PLK1).
37 ivation by overexpressed Polo-like kinase 1 (PLK1).
38 mammalian MYPT1 binds to polo-like kinase 1 (PLK1).
39  of G2/M kinases such as polo-like kinase 1 (PLK1).
40 g mechanism dependent on polo-like kinase-1 (PLK1) activity underlies this heterogeneity.
41                          Polo-like kinase-1 (PLK1) plays a major role in driving mitotic events, incl
42 hibitors for one target, Polo-like kinase-1 (PLK1), are already in clinical trials for other malignan
43 beta-TrCP, Aurora A, and Polo-like kinase-1 (PLK1).
44 iferation genes CCNA1, CCND2, IGFII, MCM4-6, PLK1, RPA2, and TYMS.
45 nd activity, we utilized photokinetics and a PLK1 activity biosensor.
46 his respect, our studies identified HBc as a PLK1 substrate in vitro, and mapped PLK1 phosphorylation
47 1 depletion requires PLK1 activity because a PLK1 inhibitor, BI-2536, blocked precocious segregation.
48 n errors, with a specific focus on Gravin, a PLK1 scaffold.
49  discover that HMMR acts at centrosomes in a PLK1-dependent pathway that locates active Ran and modul
50 demonstrate that HBV core protein (HBc) is a PLK1 substrate.
51 o maximally effective doses of paclitaxel, a PLK1 inhibitor, or cisplatin.
52    In support of this idea, treatment with a PLK1 inhibitor potently induced G(2)-M growth arrest and
53            Knockdown of MLL5 caused aberrant PLK1 aggregation that led to acentrosomal microtubule-or
54                                       Active PLK1, in turn, phosphorylates MCAK at Ser715 which promo
55  and overexpression of constitutively active PLK1 (PLK1(CA) ).
56 action, causing the redistribution of active PLK1, which leads to increased defocusing and phosphoryl
57  examine whether the loss of Gravin affected PLK1 distribution and activity, we utilized photokinetic
58                       Levels of Aurora A and PLK1 as well as phosphorylated PLK1 at threonine 210, a
59 ents) using NanoString nCounter analysis and PLK1 mRNA was assessed.
60  cells this process is controlled by ATR and PLK1, and that in the absence of FANCM, stalled replicat
61 c-myc bitransgenic livers, whereas BAMBI and PLK1 were overexpressed in hepatic tumors from X/c-myc b
62              Combined inhibition of BRAF and PLK1 resulted in significantly greater antiproliferative
63  causes premature inactivation of Cdc25C and PLK1, leading to faster mitotic exit.
64 yperactivation of Cdc25C, cyclin B/CDK1, and PLK1 in a G(2)-M-enriched population, LMW-E overexpressi
65             NPM1 phosphorylation by GRK5 and PLK1 correlates with the sensitivity of cells to undergo
66 ty are regulated by associating with JLP and PLK1.
67 dentify a novel interaction between MLL5 and PLK1 in the cytosol that is crucial for sustaining spind
68       We found that codepletion of MYPT1 and PLK1 reinstates gamma-tubulin at the centrosomes, rescui
69 at sequential MYC phosphorylation by PKA and PLK1 protects MYC from proteasome-mediated degradation.
70 ffold protein SLX4, suggesting that RNF4 and PLK1 either help activate the SLX4 complex or make DNA r
71 ynthetic lethal interaction between TP53 and PLK1, other potential synthetic lethal interactions with
72 iminated the NO. effect on both p21/Waf1 and PLK1 gene expression.
73  MYPT1 in regulating mitosis by antagonizing PLK1.
74 romoter regions of several oncogenes such as PLK1 (Polo-like kinase 1), C-MYC, serine-threonine kinas
75 gical inhibition of APC-CDH1 targets such as PLK1 and Aurora kinases.
76 implications for current approaches aimed at PLK1 inhibition for cancer therapy.
77 ey spindle assembly regulators (i.e., AURKA, PLK1, and gamma-tubulin) to the microtubule-organizing c
78 itin ligase RNF4 and activation of the AURKA-PLK1 pathway.
79 scribe a novel pathway involving an Aurora B-PLK1 axis for regulation of MCAK activity in mitosis.
80                  We reason that the Aurora B-PLK1 signaling at the kinetochore orchestrates MCAK acti
81                                      Because PLK1 is up-regulated in many invasive carcinomas, we ask
82 mation, but a mutant Gravin that cannot bind PLK1 did not.
83     Mechanistically, TOPBP1 physically binds PLK1 and promotes PLK1 kinase-mediated phosphorylation o
84 y serine 59 of SAF-A as a new target of both PLK1 and PP2A in mitosis and reveal that both phosphoryl
85          NO. was shown to down-regulate both PLK1 mRNA and protein.
86 ) cells, prompting our investigation of BRAF/PLK1 combination treatment effects in an orthotopic GBM
87  and dephosphorylation of SAF-A serine 59 by PLK1 and PP2A, respectively, are required for accurate a
88 al modification of FoxM1b was antagonized by PLK1-mediated phosphorylation.
89 bition and overcomes senescence induction by PLK1 inhibitors.
90 of phosphoinhibition as direct inhibition by PLK1 of the PDZ ligand underlying the GRASP65 self-inter
91  and have found that phosphorylation of P by PLK1 is enhanced by NP.
92 er-189) that in GRASP65 is phosphorylated by PLK1, causing a block in membrane tethering and Golgi ri
93 2 along chromosome arms is phosphorylated by PLK1, leading to SA2 dissociation at chromosome arms.
94 sults indicate that JLP is phospho-primed by PLK1 on Thr-351, which is recognized by the Polo box dom
95 n which NDR1 kinase activity is regulated by PLK1 in mitosis.
96             These effects were replicated by PLK1 insufficiency, indicating that PLK1 is responsible
97 , DLGAP5, CENPF, CENPE, MKI67, PTTG1, CDC20, PLK1, HMMR, and CCNB1) and decreased dependence upon and
98 trated that HBV infection activated cellular PLK1 in PHHs and differentiated HepaRG cells.
99 volasertib, a small-molecule ATP-competitive PLK1 inhibitor, decreased LTED cell growth, ER transcrip
100 +) cells, suggesting the need for concurrent PLK1 inhibition to improve antitumor activity against a
101                                Consistently, PLK1 downregulation in metastatic prostate cancer cells
102 he other is myosin phosphatase counteracting PLK1.
103 dle bipolarity through maintaining cytosolic PLK1 in a nonaggregated form.
104 kinome siRNA and small molecules, we defined PLK1 as an upstream-acting regulator.
105 rved cellular effects of PLK1 involve direct PLK1-dependent phosphorylation of CRAF with subsequent s
106  distinguish the C1 subtype with key drivers PLK1 and ECT2, whereas the C2 subtype is linked to obesi
107 icient cells is caused, in part, by elevated PLK1 kinase-mediated phosphorylation of FANCM, constitut
108 83 and T407) at mitotic entry, which elicits PLK1-dependent suppression of NDR1 activity and ensures
109                                       First, PLK1 triggers a decondensation of the MTOC structure.
110 nd -4 and an expanded consensus sequence for PLK1, which we use to design an optimal peptide substrat
111                                     We found PLK1 to be also highly expressed in preinvasive in situ
112  lung maturation and was regulated by FOXM1, PLK1, chromobox, and high mobility group families of tra
113 ion of specific intracellular kinases (e.g., PLK1) can significantly enhance non-viral transgene expr
114 findings suggest that disruption of a Gravin-PLK1 interface leads to inappropriate PLK1 activity cont
115                                         High PLK1 expression was confirmed by reverse phase protein a
116                                         High PLK1 mRNA and protein correlated with a high Ki-67 score
117 of human aRMS tumor biopsies documented high PLK1 expression to offer prognostic significance for bot
118 ppressed the self-renewal of cells with high PLK1 but not low PLK1 expression.
119     Taken together, these findings highlight PLK1 as a rational therapeutic target for ccRCC.
120                           Here we identified PLK1 (Polo-like kinase 1) as a novel interaction partner
121  LC-MS/MS analysis was performed to identify PLK1-dependent JLP-interacting proteins.
122 se with defects that parallel those found in PLK1(Delta/Delta) cells.
123         Expression of either kinase-inactive PLK1/K82M or the C-terminal plk1 Delta N induced a pre-a
124 Gravin-PLK1 interface leads to inappropriate PLK1 activity contributing to chromosome segregation err
125    Gravin depletion resulted in an increased PLK1 mobile fraction, causing the redistribution of acti
126  lines at concentrations required to inhibit PLK1 kinase activity, and sustained inhibition of PLK1 b
127                        Dacominitib inhibited PLK1-FOXM1 signalling pathway and its down-stream target
128 lly potent inhibitor of the polo-like kinase PLK1.
129 propose to understand how the mitotic kinase PLK1 drives chromosome segregation errors, with a specif
130 cribe a pathway involving the mitotic kinase PLK1, the anaphase-promoting complex/cyclosome, and the
131 ERF2(TRF2)-TERF2IP(RAP1), the protein kinase PLK1 and the uncharacterized protein C20orf94.
132 , specifically the cell cycle related kinase PLK1, has been shown have an effect in cells that harbor
133                            Polo-like kinase (PLK1) is identified as being an additional cellular part
134 he optimal activation of the mitotic kinases PLK1 and Aurora B and thereby the proper kinetochore loc
135                     Whereas several kinases (PLK1, HK1) were equally vulnerable in epithelial cells,
136  role of Polo-like kinase 1 (PLK1) and known PLK1 targets.
137 -renewal of cells with high PLK1 but not low PLK1 expression.
138 HBc as a PLK1 substrate in vitro, and mapped PLK1 phosphorylation sites on this protein.
139                             Mechanistically, PLK1 interacted with and phosphorylated PAX3-FOXO1 at th
140                             Mechanistically, PLK1-mediated phosphorylation protects the binding of Mo
141 les of p38 MAPK and p21/Waf1 in NO.-mediated PLK1 repression were investigated using differentiated U
142 In triple-negative cell lines, RNAi-mediated PLK1 depletion or inhibition of PLK1 activity with a sma
143                                    Moreover, PLK1 activity is important for FOXC2 protein stability,
144 reporter and quantitative analysis of native PLK1 substrate phosphorylation.
145 gnaling by cyclopamine reduced PLK2, but not PLK1 or PLK3, messenger RNA and protein expression in ve
146                                     Notably, PLK1 inhibition led to elevated ubiquitination and rapid
147 2 as a kinase that phosphorylates Ser-137 of PLK1, which is sufficient to mediate this survival signa
148                       The proviral action of PLK1 is associated with the biogenesis of the nucleocaps
149 as a mitosis regulator through activation of PLK1 and also suggested metadherin as a putative TBK1 do
150                           The association of PLK1 in both disease aggression and in vitro growth prom
151 tion, pairwise and three-way combinations of PLK1 inhibitors with the histone deacetylase-1 (HDAC-1)
152                 Thus, homeostatic control of PLK1 by the dynamic opposition between checkpoint signal
153 n part by promoting the dephosphorylation of PLK1 at Thr210.
154                                 Depletion of PLK1 by small interfering RNAs is known to result in los
155                    Premitotic destruction of PLK1 disrupts centrosome separation, causing mitotic spi
156 hich is recognized by the Polo box domain of PLK1 leading to phosphorylation of JLP at additional sit
157 the binding motif for the polo box domain of PLK1.
158 as used to determine the antiviral effect of PLK1 inhibitor BI-2536 on HBV infection in vivo.
159 pression mitigates anti-oncogenic effects of PLK1 inhibition and overcomes senescence induction by PL
160  underlying the observed cellular effects of PLK1 involve direct PLK1-dependent phosphorylation of CR
161 s highlight novel non-canonical functions of PLK1 as a key regulator of EMT and cell motility in norm
162                    However, the functions of PLK1 beyond cell cycle regulation remain poorly characte
163 d antagonizes essential mitotic functions of PLK1, at least in part by promoting the dephosphorylatio
164  our results suggest that hyperactivation of PLK1 caused by MYPT1 reduction could override the counte
165 NAi-mediated PLK1 depletion or inhibition of PLK1 activity with a small molecule (BI-2536) induced an
166 kinase activity, and sustained inhibition of PLK1 by BI 2536 led to dramatic regression of ccRCC xeno
167                   Importantly, inhibition of PLK1 kinase activity or expression of a non-phosphorylat
168                  Pharmacologic inhibition of PLK1 with volasertib, a small-molecule ATP-competitive P
169 rug perturbations, such as the inhibition of PLK1, which is verified experimentally.
170 ks was enhanced by concomitant inhibition of PLK1.
171 produced an orally bioavailable inhibitor of PLK1 (12c, MLN0905).
172 the effects of a small-molecule inhibitor of PLK1, BI 2536, in ccRCC cell lines.
173 significant protection against inhibitors of PLK1, but the events underpinning this effect are not kn
174 esults support a role for the involvement of PLK1 in the invasion process and point to this pathway a
175                       Moreover, knockdown of PLK1 affected the interaction between JLP and FOXK1.
176      As expected, RNAi-mediated knockdown of PLK1 and other cell-cycle kinases was sufficient to supp
177                   RNAi-mediated knockdown of PLK1 inhibited ER expression, estrogen-independent growt
178                    We show that knockdown of PLK1, PLK3, and PLK4, as well as inhibition of PLK kinas
179 th medulloblastoma expressing high levels of PLK1 are at elevated risk.
180  DNA biosynthesis, whereas overexpression of PLK1(CA) increased it, suggesting that the PLK1 effects
181 s revealed that the polo-box domain (PBD) of PLK1 interacted with a binding motif on MLL5 (Thr887-Ser
182 MYPT1 depletion increases phosphorylation of PLK1 at its activating site (Thr210) in vivo, explaining
183  of TBK1 impaired mitotic phosphorylation of PLK1 in TBK1-sensitive lung cancer cells.
184 kinase-1 (PDK1) to induce phosphorylation of PLK1, which in turn induces c-MYC transcription.
185 ecificity and pharmacological relatedness of PLK1, -2, -3, and -4 that together comprise a conserved
186 tor, prevented transcriptional repression of PLK1 by NO..
187  uncovers a previously unanticipated role of PLK1 as a potent activator of MAPK signaling.
188        These data support a critical role of PLK1 in acquired hormone-independent growth of ER(+) hum
189 tudy was to demonstrate the proviral role of PLK1 in HBV biosynthesis and validate PLK1 inhibition a
190 hough recent work has identified the role of PLK1 in spindle orientation, the mechanisms underlying P
191                     PLK1 knockdown or use of PLK1 inhibitor can mitigate oncogenic function of SUB1 i
192  has therapeutic implications for the use of PLK1 inhibitors in the clinic.
193 , we embarked on a preclinical validation of PLK1 as a target in a xenograft mouse model of aRMS, whe
194 f stressed cells without WT TP53 depended on PLK1.
195 udies demonstrated that the effect of NO. on PLK1 expression was associated with decreased transcript
196 ally reduced the regulatory effect of NO. on PLK1.
197      However, suppression of RNF4, AURKA, or PLK1 returned the reinitiation of replication in Atr-del
198 tations that selectively disrupt the STAT or PLK1 interaction site have no effects on Nipah virus P p
199                        Aurora B-orchestrated PLK1 kinase activity was examined in real-time mitosis u
200  a previously unrecognised link between p53, PLK1 and centrosome separation that has therapeutic impl
201 wnregulation of PRC1 and its docking partner PLK1 suggests that miR-143 inhibits cytokinesis in these
202 78 acts as an upstream regulator of the PDK1/PLK1 signaling axis to modulate c-MYC transcription and
203 paRG cells in conjunction with pharmacologic PLK1 inhibitors, small interfering RNA (siRNA)-mediated
204  Aurora A and PLK1 as well as phosphorylated PLK1 at threonine 210, a prerequisite for DNA damage che
205   We found that TBK1 directly phosphorylated PLK1 in vitro.
206                      Aurora B phosphorylates PLK1 on Thr210 to activate its kinase activity at the ki
207 L1, CDK5R2, FES, FLT4, GAK, GRK6, HK1, PKN1, PLK1, SMG1, and TNK2.
208 verexpression of constitutively active PLK1 (PLK1(CA) ).
209 imilarity is observed between PLK2 and PLK3, PLK1 is next most similar, and PLK4 is least similar.
210 y, TOPBP1 physically binds PLK1 and promotes PLK1 kinase-mediated phosphorylation of RAD51 at serine
211  oxide (NO.) has been shown to down-regulate PLK1 and up-regulate p21/Waf1 independent of cGMP.
212 1/Waf1 signal transduction pathway represses PLK1 through a canonical CDE/CHR promoter element.
213 regation induced by MYPT1 depletion requires PLK1 activity because a PLK1 inhibitor, BI-2536, blocked
214 ression of wild-type MLL5 was able to rescue PLK1 mislocalization and aMTOC formation in MLL5-KD cell
215 -like kinase 1 (siPLK1) efficiently silenced PLK1 expression in cancer cells with concomitant cytotox
216 important for FOXC2 protein stability, since PLK1 inhibition reduces FOXC2 protein levels.
217                         The effects of STAT1/PLK1 binding motif mutations on the function the Nipah v
218         Altogether, our observations suggest PLK1 inhibition as an attractive therapeutic approach, i
219  on viral biosynthesis are specific and that PLK1 is a proviral cellular factor.
220                          We demonstrate that PLK1 binds directly to c-MYC and promotes its transcript
221 ediatric medulloblastoma and determined that PLK1 inhibitors were the most promising class of agents
222  breast carcinoma progression, we found that PLK1 expression is necessary but not sufficient to induc
223                        Results indicate that PLK1 is engaged by Nipah virus V protein amino acids 100
224 cated by PLK1 insufficiency, indicating that PLK1 is responsible for the mitotic defects associated w
225                             We observed that PLK1 phosphorylates vimentin on Ser82, which in turn reg
226                              We propose that PLK1 activity controls a polarity checkpoint and compens
227                         Here, we report that PLK1 overexpression in prostate epithelial cells trigger
228                         We further show that PLK1 inhibition down-regulates BMI1 by upregulating the
229         A soft-agar colony assay showed that PLK1 silencing impaired clonogenic potential of TNBC cel
230                  Thus, our data suggest that PLK1 inhibitors can be successfully used to inhibit grow
231 activity in MCF7/LTED cells, suggesting that PLK1 drives ER expression and estrogen-independent growt
232                                          The PLK1 binding site in MuV P was mapped to residues 146 to
233    When administrated as a single agent, the PLK1 inhibitor significantly impaired tumor growth in vi
234 virus, contact between the V protein and the PLK1 polo box domain is required for V protein phosphory
235 a identify an essential role for HMMR in the PLK1-dependent regulatory pathway that orients progenito
236 erived primary medulloblastoma isolates, the PLK1 small-molecule inhibitor BI2536 suppressed the self
237 o motif surrounding residue 199 mediates the PLK1 interaction with Hendra virus V protein.
238  To do this, we disrupted both copies of the PLK1 locus in human cells through homologous recombinati
239 activity and abolished NO. repression of the PLK1 promoter.
240 ts showed that NO. decreased activity of the PLK1 proximal promoter, an effect that was blocked by p3
241 ic interventions that focus on targeting the PLK1-mediated and/or FoxM1-mediated signaling network.
242 f PLK1(CA) increased it, suggesting that the PLK1 effects on viral biosynthesis are specific and that
243 ther, these preclinical studies validate the PLK1-PAX3-FOXO1 axis as a rational target to treat aRMS.
244 n a xenograft mouse model of aRMS, where the PLK1 inhibitor BI 2536 reduced PAX3-FOXO1-mediated gene
245                  Treatment of cells with the PLK1 kinase inhibitor BI2536 suppressed binding of the F
246 ing the treatment of medulloblastoma through PLK1 inhibition.
247 in and regulates the sensitivity of cells to PLK1 inhibition.
248 ivity of CSC-enriched breast cancer cells to PLK1 inhibitor.
249 ing CSC-enriched TNBC cells are sensitive to PLK1 inhibition.
250 ells with lower GRK5 being more sensitive to PLK1 inhibitor-induced apoptosis.
251 out WT TP53 alleles were highly sensitive to PLK1 inhibitors, both in vivo and in vitro.
252 at functional p53 reduces the sensitivity to PLK1 inhibitors by permitting centrosome separation to o
253                  Stable shRNA transfectants (PLK1-PLK5) that express significantly reduced CXCR1 mRNA
254                      During G2/M transition, PLK1 directly interacts with and phosphorylates FoxM1b,
255 indle orientation, the mechanisms underlying PLK1 signaling in spindle positioning and orientation ha
256 e interference, and data indicate that the V:PLK1 and V:STAT complexes are V mediated yet independent
257 ole of PLK1 in HBV biosynthesis and validate PLK1 inhibition a potential antiviral strategy.
258 strongly inhibited HBV infection, validating PLK1 as an antiviral target in vivo.
259                            Finally, in vitro PLK1 kinase assays and site-directed mutagenesis were em
260 ciated with poor outcomes in children as was PLK1 using Cox regression analyses.
261 s have revealed a working mechanism by which PLK1 positively regulates the activity and level of FoxM
262    However, the molecular mechanism by which PLK1-mediated phosphorylation enhances the transcription
263               JLP was found to interact with PLK1 and FOXK1 during mitosis.
264  PP1 regulatory subunit MYPT1 interacts with PLK1 and antagonizes essential mitotic functions of PLK1
265 her than DNA-PKcs, that SAF-A interacts with PLK1 in nocodazole-treated cells, and that serine 59 is

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