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 nd biomarkers to use with drugs that inhibit aurora kinases.

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

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

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

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

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

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

11 exit but strongly and specifically stabilize Aurora kinases.

12 antimyeloma effects of 2 agents that inhibit aurora kinases.

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

14 lar proteins, particularly substrates of the aurora kinases.

15 2 nM) with very high kinome selectivity for Aurora kinases.

16 mitosis in a distribution that overlaps with Aurora kinases.

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

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

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

20 ance in response to EGFR inhibitors requires Aurora kinase A (AURKA) activity.

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

22 of KRAS signaling and overexpression of the aurora kinase A (AURKA) are often detected in luminal ga

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

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

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

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

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

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

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

30 Aurora kinase A (AURKA) is frequently overexpressed in s

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

32 Aurora kinase A (AURKA) is necessary for proper primary

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 n with Aurora kinase B (AURKB), but not with Aurora kinase A (AURKA).

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

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

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

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

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

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

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

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

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

49 These findings show that Aurora kinase A and Bcl-2 family proteins are potential

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

51 ugh the proteasomal-dependent degradation of aurora kinase A and induces premature senescence in huma

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

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

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

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

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

57 Aurora kinase A inhibition also destabilized MYCN, which

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

59 ting mutations in TP53 were sensitive to the Aurora kinase A inhibitor alisertib.

60 Combined treatment with an Aurora kinase A inhibitor and navitoclax in FP-RMS cell

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

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

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

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

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

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

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

68 This revealed that inhibition of Aurora kinase A most efficiently negatively affected PAX

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

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

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

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

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

74 s identify a novel functional interaction of Aurora kinase A with both PAX3-FOXO1 and its effector MY

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

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

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

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

79 teins instrumental in driving NEPC including Aurora Kinase A, N-Myc, E2F1 and STAT3.

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

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

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

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

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

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

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

87 educed Ser315 phosphorylation in response to aurora kinase A.

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

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

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

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

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

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

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

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

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

97 6a as a moderately potent dual inhibitor of aurora kinases -A and -B.

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

99 Elevated Aurora kinase-A expression is correlated with abrogation

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

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

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

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

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

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

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

107 Aurora kinase activity organizes the targeted microtubul

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

109 In the absence of Aurora kinase activity, SPICE1 remains at centrioles but

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

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

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

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

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

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

116 7, and 5azadC, which are known to target the Aurora kinase and DNA methylation pathways.

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

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

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

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

121 ectively inhibit the gene expression of both aurora kinases and induce apoptosis in K-562 cells, howe

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

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

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

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

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

127 Aurora kinases are a family of serine/threonine kinases

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

129 The Aurora kinases are essential for the regulation of chrom

130 Aurora kinases are highly conserved, essential regulator

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

132 Aurora kinases are key effectors of mitosis.

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

134 In particular, aurora kinases are significantly overexpressed in patien

135 In this study, we discover that Aurora kinases are synergistic determinants of a switch

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

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

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

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

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

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

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

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

144 Aurora kinases (AURKA and AURKB) are mitotic kinases wit

145 The aurora kinases (AURKs) comprise an evolutionarily conser

146 1, CCT137690) which is a potent inhibitor of Aurora kinases (Aurora-A IC(50) = 0.015 +/- 0.003 muM, A

147 [4,5-b]pyridine (27e), a potent inhibitor of Aurora kinases (Aurora-A K(d) = 7.5 nM, Aurora-B K(d) =

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

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

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

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

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

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

154 as mediated by the inhibition of Haspin with Aurora kinase B (AURKB), but not with Aurora kinase A (A

155 a from B-ALL patient specimens revealed that Aurora kinase B (AURKB), which restrains GC signaling by

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

157 cant upregulation of the cell cycle promoter Aurora kinase B (AURKB).

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

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

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

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

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

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

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

165 Aurora kinase B inhibitors induce apoptosis secondary to

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

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

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

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

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

171 Aurora kinases B and C (AURKB/AURKC) are activated by bi

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

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

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

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

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

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

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

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

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

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

182 The Aurora kinase complex, also called the chromosomal passe

183 The Aurora kinases comprise an evolutionarily conserved prot

184 The Aurora kinases control multiple aspects of mitosis, amon

185 Aurora kinases create phosphorylation gradients within t

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

187 ate that SPICE1 localization is regulated by Aurora kinases during mitosis.

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

189 Elevated aurora kinase expression was accompanied by increased ph

190 The aurora kinases facilitate transit from G2 through cytoki

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

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

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

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

195 stream targets is important in understanding Aurora kinase function.

196 Aurora kinase genes were enriched in STAT5BN642H-express

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

198 rtant roles in mitosis, inhibitors targeting Aurora kinases have attracted attention in cancer therap

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

200 The Aurora kinases have been implicated in tumorigenesis and

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

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

203 Because of the overexpression of Aurora kinases in a broad range of cancers and their imp

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

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

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

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

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

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

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

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

212 Partial Aurora kinase inhibition increased the frequency of mero

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

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

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

216 stmitotic checkpoint governs the response to Aurora kinase inhibition.

217 phase is substantially suppressed by partial Aurora kinase inhibition.

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

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

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

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

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

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

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

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

226 RD-7880, and demonstrate that the well-known Aurora kinase inhibitor VX-680 disrupts binding of the p

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

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

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

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

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

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

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

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

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

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

237 VX-680 is an effective pan-Aurora kinase inhibitor; however, its clinical efficacy

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

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

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

241 represent a fundamental cellular response to Aurora kinase inhibitors and contributes to therapy resi

242 el insight about how cancer cells respond to Aurora kinase inhibitors and identify a new mechanism re

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

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

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

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

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

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

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

250 Aurora kinase inhibitors have attracted a great deal of

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

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

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

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

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

256 Aurora kinase inhibitors suppress this adaptive survival

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

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

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

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

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

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

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

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

265 Aurora kinase may represent novel therapeutic targets in

266 our work indicates that temporal and spatial Aurora kinase-mediated regulation of SPICE1 is important

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

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

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

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

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

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

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

274 Aurora kinases play a critical role in regulating mitosi

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

276 Aurora kinases play a major role in mitosis by regulatin

277 Aurora kinases play an important role in chromosome alig

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

279 The Aurora kinases play critical roles in the regulation of

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

281 Specificity is enforced by Polo-like and Aurora kinases (PLK-1 and AIR-1 in C. elegans), which im

282 These kinases comprise the Aurora kinases, Polo kinases, and calcium/calmodulin-dep

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

284 her condensin I or PRC1 or are deficient for Aurora kinase regulation.

285 d KIF4A bound to condensin I is regulated by Aurora kinases remain unclear.

286 Failure to degrade Aurora kinases results in abnormal anaphase microtubule

287 tate by epidermal growth factor receptor and aurora kinase signalling.

288 iased computational approach to identify new Aurora kinase substrates based on phosphorylation site c

289 ch tool that enables rapid identification of Aurora kinase substrates.

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

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

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

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

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

295 equence substitutions that putatively caused Aurora kinases to evolve allosteric regulation.

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

297 Aurora kinase was upregulated and pCDK1 was downregulate

298 When Aurora kinases were inhibited together, lung cancer cell

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

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