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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
14 serine/threonine kinase Polo-like kinase 1 (PLK1) as a host kinase that phosphorylates P and have fo
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
20 a site phosphorylated by Polo-like kinase 1 (PLK1) in the GRASP65 N-terminal domain for which mutatio
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
27 arrest via inhibition of polo-like kinase 1 (PLK1) signalling pathway and down-modulation of Aurora k
29 riggering proteolysis of polo-like kinase 1 (PLK1), a tumor suppressor and multitasking mitotic kinas
31 when compared with AKT, polo-like kinase 1 (PLK1), CDK activating kinase (CAK), CAMKIIalpha, and thr
42 hibitors for one target, Polo-like kinase-1 (PLK1), are already in clinical trials for other malignan
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.
49 discover that HMMR acts at centrosomes in a PLK1-dependent pathway that locates active Ran and modul
52 In support of this idea, treatment with a PLK1 inhibitor potently induced G(2)-M growth arrest and
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
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
64 yperactivation of Cdc25C, cyclin B/CDK1, and PLK1 in a G(2)-M-enriched population, LMW-E overexpressi
67 dentify a novel interaction between MLL5 and PLK1 in the cytosol that is crucial for sustaining spind
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
74 romoter regions of several oncogenes such as PLK1 (Polo-like kinase 1), C-MYC, serine-threonine kinas
77 ey spindle assembly regulators (i.e., AURKA, PLK1, and gamma-tubulin) to the microtubule-organizing c
79 scribe a novel pathway involving an Aurora B-PLK1 axis for regulation of MCAK activity in mitosis.
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
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
90 of phosphoinhibition as direct inhibition by PLK1 of the PDZ ligand underlying the GRASP65 self-inter
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
97 , DLGAP5, CENPF, CENPE, MKI67, PTTG1, CDC20, PLK1, HMMR, and CCNB1) and decreased dependence upon and
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
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
110 nd -4 and an expanded consensus sequence for PLK1, which we use to design an optimal peptide substrat
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
117 of human aRMS tumor biopsies documented high PLK1 expression to offer prognostic significance for bot
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
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
132 , specifically the cell cycle related kinase PLK1, has been shown have an effect in cells that harbor
134 he optimal activation of the mitotic kinases PLK1 and Aurora B and thereby the proper kinetochore loc
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
145 gnaling by cyclopamine reduced PLK2, but not PLK1 or PLK3, messenger RNA and protein expression in ve
147 2 as a kinase that phosphorylates Ser-137 of PLK1, which is sufficient to mediate this survival signa
149 as a mitosis regulator through activation of PLK1 and also suggested metadherin as a putative TBK1 do
151 tion, pairwise and three-way combinations of PLK1 inhibitors with the histone deacetylase-1 (HDAC-1)
156 hich is recognized by the Polo box domain of PLK1 leading to phosphorylation of JLP at additional sit
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
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
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
176 As expected, RNAi-mediated knockdown of PLK1 and other cell-cycle kinases was sufficient to supp
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
185 ecificity and pharmacological relatedness of PLK1, -2, -3, and -4 that together comprise a conserved
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
193 , we embarked on a preclinical validation of PLK1 as a target in a xenograft mouse model of aRMS, whe
195 udies demonstrated that the effect of NO. on PLK1 expression was associated with decreased transcript
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
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
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
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
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
224 cated by PLK1 insufficiency, indicating that PLK1 is responsible for the mitotic defects associated w
231 activity in MCF7/LTED cells, suggesting that PLK1 drives ER expression and estrogen-independent growt
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
238 To do this, we disrupted both copies of the PLK1 locus in human cells through homologous recombinati
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
252 at functional p53 reduces the sensitivity to PLK1 inhibitors by permitting centrosome separation to o
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
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
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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