ライフサイエンスコーパス: Aurora kinase

1 ing interaction impair catalytic activity in Aurora kinase.

2 efficient checkpoint silencing downstream of Aurora kinase.

3 its effect can be mimicked by nondegradable Aurora kinase.

4 re segregation-a process that requires Ipl1p Aurora kinase.

5 tify a consensus phosphorylation site for an Aurora kinase.

6 s a signal that results in the activation of Aurora kinase.

7 the activity of small-molecule inhibitors of aurora kinases.

8 , and plants-is a genuine substrate of alpha Aurora kinases.

9 ibition of APC-CDH1 targets such as PLK1 and Aurora kinases.

10 539) as the primary phosphorylation site for Aurora kinases.

11 s of this novel class of inhibitors with the Aurora kinases.

12 of the compounds, OM137, as an inhibitor of Aurora kinases.

13 ny Cdh1 substrates with the exception of the Aurora kinases.

14 exit but strongly and specifically stabilize Aurora kinases.

15 antimyeloma effects of 2 agents that inhibit aurora kinases.

16 lar proteins, particularly substrates of the aurora kinases.

17 2 nM) with very high kinome selectivity for Aurora kinases.

18 mitosis in a distribution that overlaps with Aurora kinases.

19 nd biomarkers to use with drugs that inhibit aurora kinases.

20 ction during interphase, and is dependent on aurora kinase 1 (AIR-1), a protein involved in centrosom

21 Here, we evaluate whether Aurora kinase-1 (TbAUK1) from pathogenic Trypanosoma bru

22 Aurora kinase A (also called STK15 and BTAK) is overexpr

23 ion and the phosphorylation of its substrate Aurora kinase A (AurA).

24 by loss of VHL and associated with increased Aurora kinase A (AURKA) and histone deacetylase 6 (HDAC6

25 and overexpression of the mitotic regulator Aurora kinase A (AURKA) drives tumor aneuploidy and chro

26 Centrosome-localized mitotic Aurora kinase A (AURKA) facilitates G2/M events.

27 The aurora kinase A (AURKA) gene is frequently amplified and

28 Recently, we reported a novel role of Aurora kinase A (AURKA) in BCSCs, as a transactivating c

29 We investigated the role of Aurora kinase A (AURKA) in regulating p73-dependent apop

30 We find that Aurora kinase A (AURKA) is a novel, hypoxia-independent

31 Aurora kinase A (AURKA) is a therapeutic target in acute

32 Aurora kinase A (AURKA) is located at 20q13, a region th

33 Our previous analyses suggested that Aurora kinase A (AURKA) is regulated by androgens in pro

34 Aurora kinase A (AURKA) localizes to centrosomes and mit

35 rough pharmacologic and genetic studies that aurora kinase A (AURKA) represents a new therapeutic tar

36 Depletion of one such molecule, aurora kinase A (Aurka), resulted in compromised self-re

37 Here, we report that LKB1 undergoes Aurora kinase A (AURKA)-mediated phosphorylation, which

38 ning revealed that a major target of diMF is Aurora kinase A (AURKA).

39 of a high degree of mitotic genes including Aurora Kinase A (Aurora A, STK6).

40 tically, CRAF, but not BRAF, associates with Aurora kinase A (Aurora-A) and Polo-like kinase 1 (Plk1)

41 Aurora kinase A (Aurora-A) belongs to a highly conserved

42 screening, we showed PTTG1 interacting with Aurora kinase A (Aurora-A), and confirmed the interactio

43 nduced apoptosis, and elevated expression of aurora kinase A abolishes this response.

44 a convergence of LIN28B and RAN signaling on Aurora kinase A activity.

45 with decreased survival, and a reduction in aurora kinase A and aurora kinase B expression inhibits

46 finitively test the clinical benefit of dual Aurora kinase A and B inhibition.

47 lso interacted with a selective inhibitor of aurora kinase A and B to potentiate apoptosis without mo

48 multiple microtubule organizing centers with Aurora kinase A and gamma-tubulin.

49 al stabilization of the CDH1 targets such as Aurora kinase A and Polo-like kinase 1.

50 Cells depleted of aurora kinase A are more sensitive to cisplatin-induced

51 beta-catenin and Aurora kinase A are present in most MM but not in normal

52 Ectopic overexpression of aurora kinase A in mammalian cells induces centrosome am

53 oughput datasets that particularly implicate aurora kinase A in the pathogenesis of squamous-cell car

54 data provide a promising rationale for using Aurora kinase A inhibition as a therapeutic modality of

55 Moreover, treatment with a specific Aurora kinase A inhibitor blocks cell proliferation by i

56 fied neuroblastomas, we demonstrate that the Aurora Kinase A inhibitor MLN8237 combines with ABT-199

57 We conclude that aurora kinase A is a key regulatory component of the p53

58 Destabilization of p53 by aurora kinase A is abrogated in the presence of mutant M

59 omas of the head and neck, overexpression of aurora kinase A is associated with decreased survival, a

60 e demonstrate by gene expression arrays that Aurora kinase A is one of the highly overexpressed genes

61 f the p53 pathway and that overexpression of aurora kinase A leads to increased degradation of p53, c

62 is not degraded in the presence of inactive aurora kinase A or ubiquitination-defective Mdm2.

63 Here we show that aurora kinase A phosphorylates p53 at Ser315, leading to

64 ed of glandular atypia, P53 abnormality, and Aurora kinase A positivity, and the interaction of age,

65 Silencing of aurora kinase A results in less phosphorylation of p53 a

66 s with wild-type p53, elevated expression of aurora kinase A was correlated with low p53 concentratio

67 ng three protein biomarkers (P53, c-Myc, and Aurora kinase A), two methylation markers (MYOD1 and RUN

68 uced cyclin-dependent kinase 2 (Cdk2), Cdk4, Aurora kinase A, and Aurora kinase B expression.

69 ations were found to affect SRC, SMAD genes, aurora kinase A, epidermal growth factor receptor, heat

70 monstrate regulation of a novel target gene, Aurora kinase A, implicating beta-catenin in G2/M regula

71 nvolved in cell cycle progression, including Aurora Kinase A, that has previously been implicated in

72 vel functional link between beta-catenin and Aurora kinase A, underscoring a critical role of these p

73 f several known oncogenes, such as ErbB2 and Aurora Kinase A, was increased in tumor samples.

74 p-regulated protein (HURP) is a substrate of Aurora kinase A, which plays a crucial role in the stabi

75 crease in its expression and deregulation of Aurora Kinase A.

76 f Cyclin B1 and decreased phosphorylation of Aurora kinase A.

77 educed Ser315 phosphorylation in response to aurora kinase A.

78 sive network of cell-cycle factors linked to aurora kinase A.

79 nvestigational, oral, selective inhibitor of aurora kinase A.

80 polyploid cells caused by the suppression of Aurora kinases A and B (AURKA/B), which are critical med

81 Finally, we show that down-regulation of Aurora kinases A and B and chromatin licensing and DNA r

82 ive mesotheliomas expressed higher levels of Aurora kinases A and B and functionally related genes in

83 Overexpression and hyperactivation of aurora kinases A and B have major roles in tumorigenesis

84 Here, we demonstrate that Aurora kinases A and B phosphorylate a conserved residue

85 Aurora kinases A and B, both of which were highly expres

86 1) signalling pathway and down-modulation of Aurora kinases A and B, cyclin B1 and CDC25C.

87 cyclin-dependent kinases (CDK1 and CDK4) and Aurora kinases A, B, and C, were found to be hyperactiva

88 6a as a moderately potent dual inhibitor of aurora kinases -A and -B.

89 Aurora kinase-A (Aurora-A) promotes timely entry into mi

90 Elevated Aurora kinase-A expression is correlated with abrogation

91 entromeres and microtubules and includes the Aurora kinase-activating domain of INCENP family protein

92 pound 1 is a type I inhibitor that binds the Aurora kinase active site in a DFG-in conformation.

93 r physical interactions, and the blockade of Aurora kinase activity by pan-Aurora kinase inhibitors (

94 e is very sensitive to partial inhibition of Aurora kinase activity by ZM447439 at a dose, 3 microM,

95 uired to activate the APC upon inhibition of Aurora kinase activity in checkpoint-arrested cells, sug

96 B in MM, and the pharmacological blockade of Aurora kinase activity induces TRAIL sensitization in MM

97 These results show that Aurora kinase activity is required to ensure the mainten

98 Aurora kinase activity organizes the targeted microtubul

99 otein, provides a means to ensure sufficient Aurora kinase activity, despite loss of AURKB, to suppor

100 d, a subset of Aurora substrates can enhance Aurora kinase activity.

101 rates that, once phosphorylated, can enhance Aurora kinase activity.

102 MK-0457 (VX-680) is a small-molecule aurora kinase (AK) inhibitor with preclinical antileukem

103 Drug-induced down-regulation of the aurora kinases, among other targets, seems to be suffici

104 new therapy for the treatment of tumors with Aurora kinase amplification.

105 act SAC as well as increase in ploidy (Ipl1)/Aurora kinase and a centromere-associated protein ShuGOs

106 7, and 5azadC, which are known to target the Aurora kinase and DNA methylation pathways.

107 at the response is dependent on Mps1 kinase, aurora kinase and Haspin.

108 Here we report that Ipl1/aurora kinase and its genetically interacting phosphatas

109 Combined inhibition of Aurora kinase and SRC potentiated dasatinib-dependent lo

110 A balance in the activities of the Ipl Aurora kinase and the Glc7 phosphatase is essential for

111 idine core, IBPR001 and IBPR002, that target Aurora kinases and induce a DFG conformation change at t

112 Here, we show that KIBRA activates the Aurora kinases and is required for full activation of Au

113 Opposing roles of Aurora kinases and protein phosphatase 1 (PP1) during mi

114 t that KIBRA is a physiological substrate of Aurora kinases and reveal a new avenue between KIBRA/Hip

115 f several cyclin-dependent kinases (CDK) and Aurora kinases and selectively blocked proliferation of

116 The Aurora kinases are a family of serine/threonine kinases

117 Several early studies found that Aurora kinases are amplified and overexpressed at the tr

118 The Aurora kinases are essential for the regulation of chrom

119 Aurora kinases are highly conserved, essential regulator

120 usceptible to apoptosis in mitosis and since aurora kinases are intermediaries in checkpoint pathways

121 Aurora kinases are key effectors of mitosis.

122 rgets for cancer, and inhibitors for SRC and Aurora kinases are now being used in the clinic.

123 In particular, aurora kinases are significantly overexpressed in patien

124 s in the field and analyses the potential of Aurora kinases as anticancer targets.

125 The discovery of aurora kinases as essential regulators of cell division

126 development of small-molecule inhibitors of Aurora kinases as leukemia therapies.

127 ML cells through inactivation of Bcr/Abl and aurora kinases, as well as by induction of Bim.

128 est that Clp1p/Flp1p functions together with Aurora kinase at kinetochores.

129 Targeting of Aurora kinases at anaphase by APC/C(Cdh1) participates i

130 (palbociclib, ribociclib, and abemaciclib), aurora kinases (AT9283 and MLN8237), Wee1 kinase (MK-177

131 ed, exposure of tumor cells to inhibitors of Aurora kinase (Aurk) and Polo-like kinases (Plk), key re

132 The aurora kinases (AURKs) comprise an evolutionarily conser

133 1, CCT137690) which is a potent inhibitor of Aurora kinases (Aurora-A IC(50) = 0.015 +/- 0.003 muM, A

134 [4,5-b]pyridine (27e), a potent inhibitor of Aurora kinases (Aurora-A K(d) = 7.5 nM, Aurora-B K(d) =

135 In mammalian cells, the aurora kinases (aurora-A, -B, and -C) play essential rol

136 Here we show that LANA interacts with Aurora kinase B (AK-B) and induces phosphorylation of su

137 Aurora kinase B (AK-B) is important for cell division, a

138 Involvement of aurora kinase B (AURKB) and Wee1-like protein kinase (WE

139 proteins epithelial cell transforming 2 and Aurora kinase B (AurkB) are localized to stress granules

140 mal passenger complex (CPC) population, with Aurora kinase B (AURKB) bound to INCENP.

141 ds that induce tetraploid senescence inhibit Aurora kinase B (AURKB).

142 serine 421 on MeCP2 is directly regulated by aurora kinase B and modulates the balance between prolif

143 nt forms, interacts with the CPC core enzyme Aurora kinase B and staining of CPC components at centro

144 gnalling pathway and its down-stream targets Aurora kinase B and survivin.

145 a proteomic approach, we have identified the Aurora kinase B as a novel binding partner of NIR.

146 ival, and a reduction in aurora kinase A and aurora kinase B expression inhibits cell growth and incr

147 kinase 2 (Cdk2), Cdk4, Aurora kinase A, and Aurora kinase B expression.

148 e checkpoint being dependent on Mad1 and the Aurora kinase B homolog Ipl1.

149 Aurora kinase B inhibitors induce apoptosis secondary to

150 ndent confirmation of the negative effect of Aurora kinase B was obtained by immunohistochemistry in

151 totic defects, along with mislocalization of Aurora kinase B, a key regulator of mitotic progression.

152 Aurora kinase B, one of the three members of the mammali

153 xhibit a twofold increase in transcripts for aurora kinase B, the centromeric cohesin ESCO2, DNMT1, t

154 a reduction in histone H3 phosphorylation by Aurora kinase B.

155 as a potent and highly specific inhibitor of aurora kinases B and C.

156 Aurora kinase C (AURKC) is essential for formation of eu

157 ), and loss of interchromatid axis-localized Aurora kinase C.

158 infections with T. brucei and that parasite Aurora kinases can be targeted with small-molecule inhib

159 Inappropriate expression of the Aurora kinases can induce aberrant mitosis, centrosome i

160 Development of new therapeutics that target aurora kinases can potentially improve RA management.

161 of Lgl that is a substrate for aPKC, but not Aurora kinases, can restore cell polarity in lgl mutants

162 The two major Aurora kinases carry out critical functions at distinct

163 nucleate cells, or by chemical inhibition of Aurora kinases, causing abnormal mitotic exit with forma

164 L-15 results in Myc-mediated upregulation of aurora kinases, centrosome aberrancies, and aneuploidy.

165 The Aurora kinase complex, also called the chromosomal passe

166 The Aurora kinases comprise an evolutionarily conserved prot

167 The Aurora kinases control multiple aspects of mitosis, amon

168 nases and is required for full activation of Aurora kinases during mitosis.

169 gs support a functional relationship between Aurora kinase expression and prostate cancer and the app

170 Elevated aurora kinase expression was accompanied by increased ph

171 The aurora kinases facilitate transit from G2 through cytoki

172 ers of the chromosomal passenger protein and aurora kinase families in MKs.

173 Aurora kinase family members co-ordinate a range of even

174 B, one of the three members of the mammalian Aurora kinase family, is the catalytic component of the

175 e found that danusertib, an inhibitor of the Aurora kinase family, preferentially inhibits bone micro

176 Aurora kinase genes were enriched in STAT5BN642H-express

177 Deregulation of human aurora kinases has been implicated in oncogenesis as a c

178 d selective small molecule inhibitors of the Aurora kinases has been long and resource intensive with

179 The chromosomal passenger protein aurora kinases have been implicated in regulating chromo

180 The Aurora kinases have been implicated in tumorigenesis and

181 Since their discovery nearly 20 years ago, Aurora kinases have been studied extensively in cell and

182 Three aurora kinase homologues were identified (TbAUK1, -2 and

183 e an overview of the biological functions of aurora kinases in healthy cells and in cancer cells, and

184 The overexpression of Aurora kinases in multiple tumors makes these kinases ap

185 The inhibition of Aurora kinases in order to arrest mitosis and subsequent

186 A role for Aurora kinases in the aggressive behavior of mesotheliom

187 tional cellular effects due to inhibition of Aurora kinases included endoreduplication and inhibition

188 In MYC-amplified SCLC cells Aurora kinase inhibition associates with G2/M-arrest, in

189 ministration of vorinostat markedly enhanced aurora kinase inhibition by MK-0457, and preferentially

190 It was shown that potency and selectivity of aurora kinase inhibition correlated with the presence of

191 Partial Aurora kinase inhibition increased the frequency of mero

192 Our data indicate that Aurora kinase inhibition provides a new approach for the

193 LC with high MYC expression is vulnerable to Aurora kinase inhibition, which, combined with chemother

194 drug exposures consistent with dual FLT3 and Aurora kinase inhibition.

195 stmitotic checkpoint governs the response to Aurora kinase inhibition.

196 phase is substantially suppressed by partial Aurora kinase inhibition.

197 ysical properties and metabolic stability of Aurora kinase inhibitor 14a revealed that potency agains

198 ptimization has led to the identification of Aurora kinase inhibitor 27 (IBPR001; LE = 0.26; LipE = 4

199 We recently reported a furano-pyrimidine Aurora kinase inhibitor 4 (LE = 0.25; LipE = 1.75), with

200 We further discovered that VX-680, an Aurora kinase inhibitor currently in phase II clinical t

201 more sensitive to Aurora-A knock down and to Aurora kinase Inhibitor III treatment.

202 Interactions between the dual Bcr/Abl and aurora kinase inhibitor MK-0457 and the histone deacetyl

203 oavailable, potent, and highly selective pan-aurora kinase inhibitor that is active in taxane-resista

204 We found that the Aurora kinase inhibitor VX-680 and the p38 inhibitor BIR

205 The Aurora kinase inhibitor VX-680, currently under clinical

206 urora-binding region of human INCENP and the Aurora kinase inhibitor VX-680.

207 mouse C1A cells were treated with the potent Aurora kinase inhibitor VX680, which attenuates phosphor

208 inase consensus phosphorylation site and the Aurora kinase inhibitor ZM447439 (ZM) blocks phosphoryla

209 by vincristine and paclitaxel but not by an aurora kinase inhibitor, colocalized with tubulin by con

210 Treatment with VX-680, a pan-aurora kinase inhibitor, promoted B cell apoptosis, prov

211 report that a circumscribed exposure to the aurora kinase inhibitor, VX-680, selectively kills cells

212 nd 27e, an orally bioavailable dual FLT3 and Aurora kinase inhibitor, was selected as a preclinical d

213 re more responsive to treatment with a novel aurora kinase inhibitor.

214 ere, we describe ZM447439, a novel selective Aurora kinase inhibitor.

215 was identified as a potential best-in-class Aurora kinase inhibitor.

216 MK-0457 and MK-5108 are novel aurora kinase inhibitors (AKi) leading to G(2)-M cell-cy

217 the antimitotic drug paclitaxel and to other aurora kinase inhibitors (AZD1152, MK-0457, and PHA-7393

218 he blockade of Aurora kinase activity by pan-Aurora kinase inhibitors (pan-AKIs) disrupts TRAIL-induc

219 an be exploited therapeutically by combining aurora kinase inhibitors and the orally bioavailable BH3

220 We show Aurora kinase inhibitors are effective in SCLC cell line

221 We report a novel class of Aurora kinase inhibitors based upon a phthalazinone pyra

222 The first generation of Aurora kinase inhibitors did not fare well in clinical t

223 trong support to the ongoing work to develop Aurora kinase inhibitors for clinically aggressive neuro

224 tense interest in identifying small molecule aurora kinase inhibitors for the potential treatment of

225 ation of second-generation, highly selective Aurora kinase inhibitors has increased the enthusiasm fo

226 Aurora kinase inhibitors have attracted a great deal of

227 These results suggest potential for aurora kinase inhibitors in MM especially in patients in

228 We summarise trials of aurora kinase inhibitors in squamous-cell carcinomas of

229 f the imidazo[4,5-b]pyridine-based series of Aurora kinase inhibitors led to the identification of 6-

230 Poly-ADP ribose polymerase and aurora kinase inhibitors may be synthetic lethal with th

231 Together, our data suggest that JAK and Aurora kinase inhibitors should be further explored as p

232 Currently a number of Aurora kinase inhibitors with different isoform selectiv

233 These findings suggest that combining Aurora kinase inhibitors with TRAIL may have therapeutic

234 which were exquisitely sensitive to JAK and Aurora kinase inhibitors.

235 al approach to improve the efficacy of tumor Aurora kinase inhibitors.

236 at arises in the EGFR signalling stream (eg, aurora-kinase inhibitors and STAT decoys).

237 In NoCut, Aurora kinase (Ipl1) at the spindle midzone negatively r

238 The Aurora kinase Ipl1p plays a crucial role in regulating k

239 Sli15p, the binding partner of yeast Aurora kinase Ipl1p, can be recognized as an INCENP fami

240 phospho-regulation of this attachment by the Aurora kinase Ipl1p.

241 hat Mif2 is a critical in vivo target of the Aurora kinase Ipl1p.

242 t requires survivin (Bir1p), a member of the aurora kinase (Ipl1p) complex, and Cdc14p phosphatase.

243 Two Aurora kinase isoforms, A and B (AURKA and AURKB), are e

244 Aurora kinase may represent novel therapeutic targets in

245 Whereas mCPEB-1 is regulated by the Aurora kinase, mCPEB-2, -3, and -4 do not contain Aurora

246 f proteins, including the CCT complex, USP7, Aurora kinase, Nedd4, and Trim24, that bind mutant p53 a

247 h cyclin dependent kinases, polo kinases and Aurora kinases, NIMA-related kinases are emerging as cri

248 The single aurora kinase of budding yeast, Ipl1, is required for th

249 Disruption of the function of the A-type Aurora kinase of Drosophila by mutation or RNAi leads to

250 In contrast, we find that the single aurora kinase of fission yeast, Ark1, is required for th

251 Typical mitotic regulators such as Aurora kinases or Cdk1 are dispensable for megakaryocyte

252 a synergism between the DNA methylation and Aurora kinase pathways as being one of interest for poss

253 etochore, the Ndc80 complex, is regulated by Aurora kinase phosphorylation of its N-terminal tail.

254 cts are not rescued by a Kif2a mutated in an Aurora kinase phosphorylation site, suggesting that the

255 a kinase, mCPEB-2, -3, and -4 do not contain Aurora kinase phosphorylation sites.

256 In this study, we demonstrate that Aurora kinases physically and functionally interact with

257 Aurora kinases play a critical role in regulating mitosi

258 Aurora kinases play a key role in the regulation of mito

259 Aurora kinases play an important role in chromosome alig

260 These results indicate that Aurora kinases play an important role in the growth supp

261 The Aurora kinases play critical roles in the regulation of

262 tion of histone H3 at serine 10 (H3S10ph) by Aurora kinases plays an important role in mitosis; howev

263 In healthy cells, controlled activation of aurora kinases regulates mitosis.

264 Failure to degrade Aurora kinases results in abnormal anaphase microtubule

265 s review will describe the functions of each Aurora kinase, summarize their involvement in leukemia a

266 ing yeast, the 10-protein Dam1 complex is an Aurora kinase target that plays essential roles maintain

267 VX-680 is a potent inhibitor of Aurora kinases that induces the accumulation of cells wi

268 f imidazo[4,5-b]pyridine-based inhibitors of Aurora kinases that possessed the 1-benzylpiperazinyl mo

269 lators such as p27(Kip1), p57(Kip2), and the aurora kinases through both an Akt-mediated nongenomic a

270 nt and selective small-molecule inhibitor of Aurora kinases, VX-680, that blocks cell-cycle progressi

271 This interaction between INCENP and Aurora kinase was found to be biologically relevant.

272 The Aurora kinases, which include Aurora A (AURKA), Aurora B

273 tination of individual substrates, including Aurora kinases, with their degradation kinetics tracked