ライフサイエンスコーパス: PLK1

1 PLK1 activity continually accumulates from initial level

2 PLK1 binds to the N-terminal residue serine 31 (S31) of

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 inhibition results in tumour shrinkage in highly pr

7 PLK1 is a proviral host factor that could be envisaged a

8 PLK1 is proposed to pattern RhoA activation by creating

9 PLK1 knockdown or use of PLK1 inhibitor can mitigate onc

10 PLK1 phosphorylates NDR1 at three putative threonine res

11 PLK1-mediated phosphorylation of FoxM1b abrogates the in

12 During cytokinesis, polo-like kinase 1 (PLK1) activates the small GTPase RhoA to assemble a cont

13 higher cyclin B/CDK1 and Polo-like kinase 1 (PLK1) activities in an S-phase-enriched population that

14 Cells lacking Polo-like kinase 1 (PLK1) activity suffer severe chromosome alignment defect

15 tified a central role of Polo-like kinase 1 (PLK1) and known PLK1 targets.

16 serine/threonine kinase Polo-like kinase 1 (PLK1) as a host kinase that phosphorylates P and have fo

17 vious studies identified polo-like kinase 1 (PLK1) as a major regulator of FoxM1b.

18 ellular serine/threonine Polo-like-kinase 1 (PLK1) as a positive effector of HBV replication.

19 g kinases and identified Polo-like kinase 1 (PLK1) as one of the kinases involved in arsenite-induced

20 g 720 kinases identified Polo-like kinase 1 (PLK1) as one of the top genes whose downregulation resul

21 arily required to remove Polo-like kinase 1 (PLK1) from the BUB complex, which can otherwise maintain

22 int and up-regulation of Polo-like kinase 1 (PLK1) in PDX.

23 a site phosphorylated by Polo-like kinase 1 (PLK1) in the GRASP65 N-terminal domain for which mutatio

24 Polo-like kinase 1 (PLK1) is a key cell cycle regulator implicated in the de

25 Polo-like kinase 1 (PLK1) is an essential cell-cycle regulator that is frequ

26 Polo-like kinase 1 (PLK1) is an oncogenic kinase that controls cell cycle an

27 We found that Polo-like kinase 1 (PLK1) is recruited into mitotic ripoptosomes, where PLK1

28 288, phosphorylation of Polo-like kinase 1 (PLK1) on threonine 210, and phosphorylation of targeting

29 phosphorylation requires polo-like kinase 1 (PLK1) rather than DNA-PKcs, that SAF-A interacts with PL

30 Here, we report that the polo-like kinase 1 (PLK1) regulates BMI1 expression, and that its inhibition

31 C-protein kinase A (PKA)-polo-like kinase 1 (PLK1) signaling loop in cells.

32 arrest via inhibition of polo-like kinase 1 (PLK1) signalling pathway and down-modulation of Aurora k

33 Polo-like kinase 1 (PLK1) was found to be significantly overexpressed in TNB

34 ious study revealed that Polo-like kinase 1 (PLK1), a serine/threonine kinase that is essential for c

35 riggering proteolysis of polo-like kinase 1 (PLK1), a tumor suppressor and multitasking mitotic kinas

36 Polo-like kinase 1 (PLK1), an essential regulator of cell division, is curre

37 The mitotic kinase, polo-like kinase 1 (PLK1), facilitates the assembly of the two mitotic spind

38 dent kinase 1 (CDK1) and Polo-like kinase 1 (PLK1), transitions through Anaphase-promoting complex (A

39 ed genes, in particular, Polo-like kinase 1 (PLK1), were associated with disease aggressiveness.

40 of G2/M kinases such as polo-like kinase 1 (PLK1).

41 er-4, a site shared with polo-like kinase 1 (PLK1).

42 of potent inhibitors of Polo-like kinase 1 (PLK1).

43 parently by antagonizing polo-like kinase 1 (PLK1).

44 ytokinesis 1 (PRC1), and polo-like kinase 1 (PLK1).

45 ivation by overexpressed Polo-like kinase 1 (PLK1).

46 lation is carried out by Polo-like kinase 1 (PLK1).

47 rora A kinase (Aurora A)/Polo-like kinase 1 (PLK1)/cyclin-dependent kinase 1 (CDK1) signaling pathway

48 g mechanism dependent on polo-like kinase-1 (PLK1) activity underlies this heterogeneity.

49 Polo-like kinase-1 (PLK1) plays a major role in driving mitotic events, incl

50 hibitors for one target, Polo-like kinase-1 (PLK1), are already in clinical trials for other malignan

51 beta-TrCP, Aurora A, and Polo-like kinase-1 (PLK1).

52 iferation genes CCNA1, CCND2, IGFII, MCM4-6, PLK1, RPA2, and TYMS.

53 nd activity, we utilized photokinetics and a PLK1 activity biosensor.

54 his respect, our studies identified HBc as a PLK1 substrate in vitro, and mapped PLK1 phosphorylation

55 1 depletion requires PLK1 activity because a PLK1 inhibitor, BI-2536, blocked precocious segregation.

56 t arsenite-induced genotoxic stress causes a PLK1-dependent signaling response that antagonizes the i

57 n errors, with a specific focus on Gravin, a PLK1 scaffold.

58 discover that HMMR acts at centrosomes in a PLK1-dependent pathway that locates active Ran and modul

59 demonstrate that HBV core protein (HBc) is a PLK1 substrate.

60 o maximally effective doses of paclitaxel, a PLK1 inhibitor, or cisplatin.

61 In support of this idea, treatment with a PLK1 inhibitor potently induced G(2)-M growth arrest and

62 Knockdown of MLL5 caused aberrant PLK1 aggregation that led to acentrosomal microtubule-or

63 pment of effective treatment regimens across PLK1-overexpressing and CIN-positive cancers.

64 Active PLK1, in turn, phosphorylates MCAK at Ser715 which promo

65 and overexpression of constitutively active PLK1 (PLK1(CA) ).

66 action, causing the redistribution of active PLK1, which leads to increased defocusing and phosphoryl

67 examine whether the loss of Gravin affected PLK1 distribution and activity, we utilized photokinetic

68 ents) using NanoString nCounter analysis and PLK1 mRNA was assessed.

69 cells this process is controlled by ATR and PLK1, and that in the absence of FANCM, stalled replicat

70 c-myc bitransgenic livers, whereas BAMBI and PLK1 were overexpressed in hepatic tumors from X/c-myc b

71 Combined inhibition of BRAF and PLK1 resulted in significantly greater antiproliferative

72 causes premature inactivation of Cdc25C and PLK1, leading to faster mitotic exit.

73 yperactivation of Cdc25C, cyclin B/CDK1, and PLK1 in a G(2)-M-enriched population, LMW-E overexpressi

74 rd the oldest spindle pole in a cenexin- and PLK1-dependent manner.

75 ients with PAH, where it regulates FoxM1 and PLK1, proteins implicated in the DNA damage response.

76 entially through interactions with FoxM1 and PLK1.

77 NPM1 phosphorylation by GRK5 and PLK1 correlates with the sensitivity of cells to undergo

78 ty are regulated by associating with JLP and PLK1.

79 ends on a well-organized spindle midzone and PLK1, while the other depends on Aurora B activity and c

80 dentify a novel interaction between MLL5 and PLK1 in the cytosol that is crucial for sustaining spind

81 ound that the interaction between NOTCH1 and PLK1 is functionally important during the DNA damage res

82 at sequential MYC phosphorylation by PKA and PLK1 protects MYC from proteasome-mediated degradation.

83 , the mother centriole appendage protein and PLK1 binding partner, resides.

84 ffold protein SLX4, suggesting that RNF4 and PLK1 either help activate the SLX4 complex or make DNA r

85 ynthetic lethal interaction between TP53 and PLK1, other potential synthetic lethal interactions with

86 As PLK1 activity drives mitotic entry but also is inhibited

87 romoter regions of several oncogenes such as PLK1 (Polo-like kinase 1), C-MYC, serine-threonine kinas

88 gical inhibition of APC-CDH1 targets such as PLK1 and Aurora kinases.

89 implications for current approaches aimed at PLK1 inhibition for cancer therapy.

90 itin ligase RNF4 and activation of the AURKA-PLK1 pathway.

91 marily to restrain and extinguish autonomous PLK1 activity.

92 scribe a novel pathway involving an Aurora B-PLK1 axis for regulation of MCAK activity in mitosis.

93 We reason that the Aurora B-PLK1 signaling at the kinetochore orchestrates MCAK acti

94 mation, but a mutant Gravin that cannot bind PLK1 did not.

95 Mechanistically, TOPBP1 physically binds PLK1 and promotes PLK1 kinase-mediated phosphorylation o

96 y serine 59 of SAF-A as a new target of both PLK1 and PP2A in mitosis and reveal that both phosphoryl

97 ) cells, prompting our investigation of BRAF/PLK1 combination treatment effects in an orthotopic GBM

98 become redundant if PLK1 is inhibited or BUB-PLK1 interaction is prevented.

99 and dephosphorylation of SAF-A serine 59 by PLK1 and PP2A, respectively, are required for accurate a

100 al modification of FoxM1b was antagonized by PLK1-mediated phosphorylation.

101 bition and overcomes senescence induction by PLK1 inhibitors.

102 of phosphoinhibition as direct inhibition by PLK1 of the PDZ ligand underlying the GRASP65 self-inter

103 and have found that phosphorylation of P by PLK1 is enhanced by NP.

104 er-189) that in GRASP65 is phosphorylated by PLK1, causing a block in membrane tethering and Golgi ri

105 2 along chromosome arms is phosphorylated by PLK1, leading to SA2 dissociation at chromosome arms.

106 sults indicate that JLP is phospho-primed by PLK1 on Thr-351, which is recognized by the Polo box dom

107 n which NDR1 kinase activity is regulated by PLK1 in mitosis.

108 These effects were replicated by PLK1 insufficiency, indicating that PLK1 is responsible

109 , DLGAP5, CENPF, CENPE, MKI67, PTTG1, CDC20, PLK1, HMMR, and CCNB1) and decreased dependence upon and

110 trated that HBV infection activated cellular PLK1 in PHHs and differentiated HepaRG cells.

111 Combining PLK1 inhibition with nocodazole (to induce mitotic arres

112 volasertib, a small-molecule ATP-competitive PLK1 inhibitor, decreased LTED cell growth, ER transcrip

113 +) cells, suggesting the need for concurrent PLK1 inhibition to improve antitumor activity against a

114 Consistently, PLK1 downregulation in metastatic prostate cancer cells

115 he other is myosin phosphatase counteracting PLK1.

116 uggested that the only functionally critical PLK1 target sites are in a single cluster in the CYK4 N

117 dle bipolarity through maintaining cytosolic PLK1 in a nonaggregated form.

118 n G(2) phase are challenged with DNA damage, PLK1 is inhibited to prevent entry into mitosis.

119 kinome siRNA and small molecules, we defined PLK1 as an upstream-acting regulator.

120 rved cellular effects of PLK1 involve direct PLK1-dependent phosphorylation of CRAF with subsequent s

121 distinguish the C1 subtype with key drivers PLK1 and ECT2, whereas the C2 subtype is linked to obesi

122 icient cells is caused, in part, by elevated PLK1 kinase-mediated phosphorylation of FANCM, constitut

123 83 and T407) at mitotic entry, which elicits PLK1-dependent suppression of NDR1 activity and ensures

124 First, PLK1 triggers a decondensation of the MTOC structure.

125 emical biology to identify a determinant for PLK1 substrate recognition that is essential for proper

126 These findings establish roles for PLK1 as a potent proto-oncogene and a CIN gene and provi

127 lung maturation and was regulated by FOXM1, PLK1, chromobox, and high mobility group families of tra

128 ion of specific intracellular kinases (e.g., PLK1) can significantly enhance non-viral transgene expr

129 findings suggest that disruption of a Gravin-PLK1 interface leads to inappropriate PLK1 activity cont

130 High PLK1 expression was confirmed by reverse phase protein a

131 High PLK1 mRNA and protein correlated with a high Ki-67 score

132 of human aRMS tumor biopsies documented high PLK1 expression to offer prognostic significance for bot

133 ppressed the self-renewal of cells with high PLK1 but not low PLK1 expression.

134 Taken together, these findings highlight PLK1 as a rational therapeutic target for ccRCC.

135 How PLK1 activity is directed to specific substrates via pho

136 ensable for cytokinesis, indicating that how PLK1 controls RhoA activation remains unresolved.

137 onarily conserved, Tyr-lined pocket in human PLK1 PBD trigger cellular anomalies in mitotic progressi

138 scrimination via the Tyr pocket in the human PLK1 PBD regulates mitotic chromosome segregation to pre

139 Here we identified PLK1 (Polo-like kinase 1) as a novel interaction partner

140 LC-MS/MS analysis was performed to identify PLK1-dependent JLP-interacting proteins.

141 ecause both phosphatases become redundant if PLK1 is inhibited or BUB-PLK1 interaction is prevented.

142 Tyr pocket mutations selectively impair PLK1 binding to the kinetochore phosphoprotein substrate

143 tion' that drives chromosome misalignment in PLK1-inactivated cells.

144 Gravin-PLK1 interface leads to inappropriate PLK1 activity contributing to chromosome segregation err

145 Gravin depletion resulted in an increased PLK1 mobile fraction, causing the redistribution of acti

146 lines at concentrations required to inhibit PLK1 kinase activity, and sustained inhibition of PLK1 b

147 Dacominitib inhibited PLK1-FOXM1 signalling pathway and its down-stream target

148 Interestingly, PLK1 was phosphorylated and PLK 2 and 3 mRNA induced upo

149 The human polo-like kinase PLK1 coordinates mitotic chromosome segregation by phosp

150 lly potent inhibitor of the polo-like kinase PLK1.

151 propose to understand how the mitotic kinase PLK1 drives chromosome segregation errors, with a specif

152 cribe a pathway involving the mitotic kinase PLK1, the anaphase-promoting complex/cyclosome, and the

153 ERF2(TRF2)-TERF2IP(RAP1), the protein kinase PLK1 and the uncharacterized protein C20orf94.

154 , specifically the cell cycle related kinase PLK1, has been shown have an effect in cells that harbor

155 e serine/threonine kinase, polo-like kinase (PLK1) regulates multiple steps in the mitotic and cell c

156 he optimal activation of the mitotic kinases PLK1 and Aurora B and thereby the proper kinetochore loc

157 Whereas several kinases (PLK1, HK1) were equally vulnerable in epithelial cells,

158 role of Polo-like kinase 1 (PLK1) and known PLK1 targets.

159 -renewal of cells with high PLK1 but not low PLK1 expression.

160 HBc as a PLK1 substrate in vitro, and mapped PLK1 phosphorylation sites on this protein.

161 Mechanistically, PLK1 interacted with and phosphorylated PAX3-FOXO1 at th

162 Mechanistically, PLK1-mediated phosphorylation protects the binding of Mo

163 In triple-negative cell lines, RNAi-mediated PLK1 depletion or inhibition of PLK1 activity with a sma

164 at during mitosis SETD6 binds and methylates PLK1 on two lysine residues: K209 and K413.

165 we identified that the PKMT SETD6 methylates PLK1-a key regulator of mitosis and highly expressed in

166 During chromosome misalignment, PLK1 activity is increased specifically at the oldest sp

167 s deregulated ripoptosome activity modulates PLK1-dependent phosphorylation of downstream effectors,

168 Moreover, PLK1 activity is important for FOXC2 protein stability,

169 reporter and quantitative analysis of native PLK1 substrate phosphorylation.

170 gnaling by cyclopamine reduced PLK2, but not PLK1 or PLK3, messenger RNA and protein expression in ve

171 Notably, PLK1 inhibition led to elevated ubiquitination and rapid

172 2 as a kinase that phosphorylates Ser-137 of PLK1, which is sufficient to mediate this survival signa

173 The proviral action of PLK1 is associated with the biogenesis of the nucleocaps

174 as a mitosis regulator through activation of PLK1 and also suggested metadherin as a putative TBK1 do

175 dues results in increased kinase activity of PLK1, leading to accelerated mitosis and faster cellular

176 The association of PLK1 in both disease aggression and in vitro growth prom

177 tion, pairwise and three-way combinations of PLK1 inhibitors with the histone deacetylase-1 (HDAC-1)

178 Here, we delineated the contributions of PLK1 and Aurora B to RhoA activation and cytokinesis ini

179 Thus, homeostatic control of PLK1 by the dynamic opposition between checkpoint signal

180 Premitotic destruction of PLK1 disrupts centrosome separation, causing mitotic spi

181 our findings support clinical development of PLK1 inhibitors in patients with advanced CCND1-driven B

182 hich is recognized by the Polo box domain of PLK1 leading to phosphorylation of JLP at additional sit

183 as used to determine the antiviral effect of PLK1 inhibitor BI-2536 on HBV infection in vivo.

184 pression mitigates anti-oncogenic effects of PLK1 inhibition and overcomes senescence induction by PL

185 underlying the observed cellular effects of PLK1 involve direct PLK1-dependent phosphorylation of CR

186 trong association between high expression of PLK1 and a shorter metastases-free survival and poor res

187 Clinically, higher expression of PLK1 positively associated with an increase in genome-wi

188 in vivo evidence that aberrant expression of PLK1 triggers CIN and tumorigenesis and highlights poten

189 concurrent with a delay in the expression of PLK1, Cyclin A and pH3.

190 lines, suggest an ER-independent function of PLK1 in regulating cell proliferation.

191 s highlight novel non-canonical functions of PLK1 as a key regulator of EMT and cell motility in norm

192 However, the functions of PLK1 beyond cell cycle regulation remain poorly characte

193 our results suggest that hyperactivation of PLK1 caused by MYPT1 reduction could override the counte

194 rial cortex and can operate independently of PLK1.

195 NAi-mediated PLK1 depletion or inhibition of PLK1 activity with a small molecule (BI-2536) induced an

196 YK4 cluster phosphorylation or inhibition of PLK1 activity.

197 kinase activity, and sustained inhibition of PLK1 by BI 2536 led to dramatic regression of ccRCC xeno

198 Importantly, inhibition of PLK1 kinase activity or expression of a non-phosphorylat

199 Pharmacologic inhibition of PLK1 with volasertib, a small-molecule ATP-competitive P

200 rug perturbations, such as the inhibition of PLK1, which is verified experimentally.

201 ks was enhanced by concomitant inhibition of PLK1.

202 produced an orally bioavailable inhibitor of PLK1 (12c, MLN0905).

203 the effects of a small-molecule inhibitor of PLK1, BI 2536, in ccRCC cell lines.

204 significant protection against inhibitors of PLK1, but the events underpinning this effect are not kn

205 Moreover, knockdown of PLK1 affected the interaction between JLP and FOXK1.

206 As expected, RNAi-mediated knockdown of PLK1 and other cell-cycle kinases was sufficient to supp

207 RNAi-mediated knockdown of PLK1 inhibited ER expression, estrogen-independent growt

208 We show that knockdown of PLK1, PLK3, and PLK4, as well as inhibition of PLK kinas

209 th medulloblastoma expressing high levels of PLK1 are at elevated risk.

210 DNA biosynthesis, whereas overexpression of PLK1(CA) increased it, suggesting that the PLK1 effects

211 s revealed that the polo-box domain (PBD) of PLK1 interacted with a binding motif on MLL5 (Thr887-Ser

212 of TBK1 impaired mitotic phosphorylation of PLK1 in TBK1-sensitive lung cancer cells.

213 ecurin, and cyclin B1 and phosphorylation of PLK1, Aurora A, and TPX2 were rescued by inhibition of t

214 kinase-1 (PDK1) to induce phosphorylation of PLK1, which in turn induces c-MYC transcription.

215 a novel role for SKAP1 in the regulation of PLK1 and optimal cell cycling needed for T-cell clonal e

216 gest that ripoptosome-mediated regulation of PLK1 contributes to faithful chromosome segregation duri

217 Our study unveils an unexpected role of PLK1 as a chromosome guardian to maintain centromere int

218 uncovers a previously unanticipated role of PLK1 as a potent activator of MAPK signaling.

219 Previous studies assessing the role of PLK1 have relied on RNA knockdown and kinase inhibition

220 These data support a critical role of PLK1 in acquired hormone-independent growth of ER(+) hum

221 tudy was to demonstrate the proviral role of PLK1 in HBV biosynthesis and validate PLK1 inhibition a

222 hough recent work has identified the role of PLK1 in spindle orientation, the mechanisms underlying P

223 To further assess the roles of PLK1 during meiotic resumption, we developed a Plk1 cond

224 PLK1 knockdown or use of PLK1 inhibitor can mitigate oncogenic function of SUB1 i

225 has therapeutic implications for the use of PLK1 inhibitors in the clinic.

226 , we embarked on a preclinical validation of PLK1 as a target in a xenograft mouse model of aRMS, whe

227 f stressed cells without WT TP53 depended on PLK1.

228 P1 and the interaction is needed for optimal PLK1 kinase activity.

229 However, suppression of RNF4, AURKA, or PLK1 returned the reinitiation of replication in Atr-del

230 Aurora B-orchestrated PLK1 kinase activity was examined in real-time mitosis u

231 a previously unrecognised link between p53, PLK1 and centrosome separation that has therapeutic impl

232 wnregulation of PRC1 and its docking partner PLK1 suggests that miR-143 inhibits cytokinesis in these

233 78 acts as an upstream regulator of the PDK1/PLK1 signaling axis to modulate c-MYC transcription and

234 paRG cells in conjunction with pharmacologic PLK1 inhibitors, small interfering RNA (siRNA)-mediated

235 We found that TBK1 directly phosphorylated PLK1 in vitro.

236 Aurora B phosphorylates PLK1 on Thr210 to activate its kinase activity at the ki

237 L1, CDK5R2, FES, FLT4, GAK, GRK6, HK1, PKN1, PLK1, SMG1, and TNK2.

238 verexpression of constitutively active PLK1 (PLK1(CA) ).

239 Mammals express four kinase-proficient PLKs (PLK1-4).

240 n unbiased approach targeting ~100 predicted PLK1 sites in two RhoA regulators: ECT2 and the centrals

241 y, TOPBP1 physically binds PLK1 and promotes PLK1 kinase-mediated phosphorylation of RAD51 at serine

242 ture of the metazoan SAC, since the relevant PLK1 and PP2A-B56 binding motifs have coevolved in the s

243 regation induced by MYPT1 depletion requires PLK1 activity because a PLK1 inhibitor, BI-2536, blocked

244 ression of wild-type MLL5 was able to rescue PLK1 mislocalization and aMTOC formation in MLL5-KD cell

245 nd exemplifying a new approach for selective PLK1 inhibition.

246 -like kinase 1 (siPLK1) efficiently silenced PLK1 expression in cancer cells with concomitant cytotox

247 important for FOXC2 protein stability, since PLK1 inhibition reduces FOXC2 protein levels.

248 SKAP1-PLK1 binding is dynamically regulated during the cell cy

249 Altogether, our observations suggest PLK1 inhibition as an attractive therapeutic approach, i

250 thways in advanced PCa and support targeting PLK1-FOXO1 pathways as a novel approach for treating adv

251 on viral biosynthesis are specific and that PLK1 is a proviral cellular factor.

252 We demonstrate that PLK1 binds directly to c-MYC and promotes its transcript

253 ediatric medulloblastoma and determined that PLK1 inhibitors were the most promising class of agents

254 Here, we provided evidence that PLK1-dependent phosphorylation of FOXO1 induces its nucl

255 We find that PLK1 inhibition does not necessarily compromise metaphas

256 Our studies found that PLK1 asymmetrically localizes between spindle poles unde

257 Here, we found that PLK1 regulates NOTCH1 expression at G(2)/M transition.

258 We hypothesized that PLK1 activity is greater at the cenexin-positive older s

259 cated by PLK1 insufficiency, indicating that PLK1 is responsible for the mitotic defects associated w

260 We propose that PLK1 activity controls a polarity checkpoint and compens

261 We propose that PLK1 activity promotes the release of centralspindlin fr

262 Here, we report that PLK1 overexpression in prostate epithelial cells trigger

263 We further show that PLK1 inhibition down-regulates BMI1 by upregulating the

264 We further show that PLK1 inhibition sequesters centralspindlin onto the spin

265 A soft-agar colony assay showed that PLK1 silencing impaired clonogenic potential of TNBC cel

266 Thus, our data suggest that PLK1 inhibitors can be successfully used to inhibit grow

267 activity in MCF7/LTED cells, suggesting that PLK1 drives ER expression and estrogen-independent growt

268 The PLK1 binding site in MuV P was mapped to residues 146 to

269 When administrated as a single agent, the PLK1 inhibitor significantly impaired tumor growth in vi

270 Blocking the PLK1-dependant phosphorylation of FOXO1 restored the pro

271 a identify an essential role for HMMR in the PLK1-dependent regulatory pathway that orients progenito

272 ibited after DNA damage, we investigated the PLK1-NOTCH1 interplay in the G(2) phase of the cell cycl

273 erived primary medulloblastoma isolates, the PLK1 small-molecule inhibitor BI2536 suppressed the self

274 ic interventions that focus on targeting the PLK1-mediated and/or FoxM1-mediated signaling network.

275 f PLK1(CA) increased it, suggesting that the PLK1 effects on viral biosynthesis are specific and that

276 ther, these preclinical studies validate the PLK1-PAX3-FOXO1 axis as a rational target to treat aRMS.

277 n a xenograft mouse model of aRMS, where the PLK1 inhibitor BI 2536 reduced PAX3-FOXO1-mediated gene

278 Treatment of cells with the PLK1 kinase inhibitor BI2536 suppressed binding of the F

279 ing the treatment of medulloblastoma through PLK1 inhibition.

280 that SKAP1 is phosphorylated by and binds to PLK1 for the optimal cycling of T-cells.

281 in and regulates the sensitivity of cells to PLK1 inhibition.

282 ivity of CSC-enriched breast cancer cells to PLK1 inhibitor.

283 ing CSC-enriched TNBC cells are sensitive to PLK1 inhibition.

284 ells with lower GRK5 being more sensitive to PLK1 inhibitor-induced apoptosis.

285 out WT TP53 alleles were highly sensitive to PLK1 inhibitors, both in vivo and in vitro.

286 at functional p53 reduces the sensitivity to PLK1 inhibitors by permitting centrosome separation to o

287 Stable shRNA transfectants (PLK1-PLK5) that express significantly reduced CXCR1 mRNA

288 During G2/M transition, PLK1 directly interacts with and phosphorylates FoxM1b,

289 indle orientation, the mechanisms underlying PLK1 signaling in spindle positioning and orientation ha

290 ole of PLK1 in HBV biosynthesis and validate PLK1 inhibition a potential antiviral strategy.

291 strongly inhibited HBV infection, validating PLK1 as an antiviral target in vivo.

292 Finally, in vitro PLK1 kinase assays and site-directed mutagenesis were em

293 ciated with poor outcomes in children as was PLK1 using Cox regression analyses.

294 We propose a model where PLK1 activity elevates in response to misaligned chromos

295 s recruited into mitotic ripoptosomes, where PLK1's activity is controlled via RIPK1-dependent recrui

296 NA damage response, as we found that whereas PLK1 activity is inhibited, NOTCH1 expression is maintai

297 s have revealed a working mechanism by which PLK1 positively regulates the activity and level of FoxM

298 However, the molecular mechanism by which PLK1-mediated phosphorylation enhances the transcription

299 JLP was found to interact with PLK1 and FOXK1 during mitosis.

300 her than DNA-PKcs, that SAF-A interacts with PLK1 in nocodazole-treated cells, and that serine 59 is