ライフサイエンスコーパス: Aurora-A

1 latter defect was also rescued by inhibiting Aurora A.

2 is significantly reduced upon inhibition of Aurora A.

3 inhibition of another 49 kinases, including Aurora A.

4 a DFG conformation change at the ATP site of Aurora A.

5 rough its interaction with and activation of Aurora A.

6 espectively, and is >250-fold selective over Aurora A.

7 activation towards its centrosomal substrate Aurora A.

8 rylation on its activator T loop in vitro by Aurora A.

9 otein ALADIN is a novel spatial regulator of Aurora A.

10 in part by a kinase-independent function of Aurora A.

11 D pathogenesis involving failure to activate Aurora-A.

12 ance and ERalpha is a bona fide substrate of Aurora-A.

13 kdown of USP2a reduced the protein levels of Aurora-A.

14 c progression by regulating the stability of Aurora-A.

15 role of USP2a in mediating the stability of Aurora-A.

16 on impairs activating autophosphorylation of Aurora A, a cell-cycle kinase critical for meiotic trans

17 scale compartments that recruit and activate Aurora A, a critical kinase for spindle assembly.

18 rt the discovery of a selective inhibitor of Aurora A, a key regulator of cell division and potential

19 Here we report the effects of Aurora A ablation on embryo patterning at early post-imp

20 Addition of the Aurora A activating protein TPX2 shifts the equilibrium

21 and demonstrate that its depletion inhibits Aurora A activation at the centrosome and impairs the ab

22 arrests cells in early mitosis by decreasing aurora A activation.

23 in, indicating an MT-dependent regulation of Aurora A activation.

24 alysis, we propose a revised, fluid model of Aurora-A activation in which the first step is a reducti

25 Ciliary phenotypes imply a failure of Aurora-A activation: Compatible with this idea, Pkd1(-/-

26 s both INCENP and Aurora B activity (but not Aurora A activity) and is critical for Polo function at

27 nd chromosome alignment because of increased Aurora A activity.

28 gamma-tubulin at centrosomes and stimulates Aurora A activity.

29 quently, loss of CHK2 or PP6C-SAPS3 promotes Aurora-A activity associated with BRCA1 in mitosis.

30 hich the CHK2-BRCA1 axis restrains oncogenic Aurora-A activity during mitosis and identify BRCA1 itse

31 lation of BRCA1 leads to increased oncogenic Aurora-A activity, which acts as a mediator for abnormal

32 n be significantly rescued by drug-resistant Aurora A alone.

33 o-distribution of HEF1 and cell cycle kinase Aurora A along spindle asters during cell division.

34 stabilization mechanism in which binding to Aurora-A alters how N-Myc interacts with SCF(FbxW7) to d

35 loenzyme is the major T-loop phosphatase for Aurora A, an essential mitotic kinase.

36 d from cytokinesis upon inactivation of both Aurora A and Aurora B kinases and continues to oscillate

37 These findings reveal that both Aurora A and B contribute to kinetochore-microtubule att

38 In addition, AR-42 decreased Aurora A and B expression.

39 The Aurora A and B kinases directly phosphorylate Lgl to pro

40 y as a consequence of cellular inhibition of aurora A and B kinases.

41 amine (18; K(i) values of 8.0 and 9.2 nM for aurora A and B, respectively) were shown to emanate from

42 ors that disrupts the native conformation of Aurora A and drives the degradation of MYCN protein acro

43 cilia in proliferating cells, independent of Aurora A and HDAC6.

44 ALADIN interacts with inactive Aurora A and is recruited to the spindle pole after Auro

45 protein was overexpressed concurrently with Aurora A and NF-kappaB signaling factors in patients wit

46 Aurora A and Plk1 are likely regulated downstream of sta

47 tion and entry into mitosis, suggesting that Aurora A and Plk1 have redundant functions in the feedba

48 However, simultaneous inactivation of both Aurora A and Plk1 markedly delays Cdk1 activation and en

49 propose that Gravin-mediated recruitment of Aurora A and Plk1 to the mother (oldest) spindle pole co

50 tion of stathmin knockdown and inhibition of Aurora A and Plk1 was not additive and again delayed mit

51 Chemical inhibition of both Aurora A and Plk1 was sufficient to delay mitotic entry

52 y a variety of cell cycle kinases, including Aurora A and Plk1, albeit at distinctive sites.

53 e, we monitor the phosphorylation of Bora by Aurora A and Plk1, analyzing the generated distinctive p

54 Here, we show that Cep192 binds Aurora A and Plk1, targets them to centrosomes in a peri

55 otein Gravin/AKAP12 and the mitotic kinases, Aurora A and Plk1, that is down regulated in human semin

56 control localization and activation of both Aurora A and Plk1.

57 tivity of CDC25 and its upstream activators, Aurora A and Plk1.

58 We conclude that Aurora A and Plk4 are rate-limiting factors contributing

59 ially overlapping, nonredundant functions of Aurora A and Plk4 kinases contribute to initiate acentri

60 protein that activates the cell-cycle kinase Aurora A and regulates the mitotic spindle.

61 f a domain-swapped dimer of dephosphorylated Aurora A and TPX2(1-25).

62 further demonstrate that the mitotic kinases Aurora-A and -B phosphorylate KIBRA both in vitro and in

63 BRA is phosphorylated by the mitotic kinases Aurora-A and -B.

64 interaction between the catalytic domain of Aurora-A and a site flanking Myc Box I that also binds S

65 A depletion impaired the interaction between Aurora-A and PP1.

66 SMAD5, indicating a novel interplay between Aurora-A and SMAD5 signaling pathways in the development

67 hese data indicate that AR is a substrate of Aurora-A and that elevated Aurora-A could contribute to

68 the crystal structure of the complex between Aurora-A and this region of N-Myc to 1.72-A resolution.

69 t not BRAF, associates with Aurora kinase A (Aurora-A) and Polo-like kinase 1 (Plk1) at the centrosom

70 it acts independently of Galphai, the kinase Aurora A, and the phosphatase PP2A.

71 ch can individually increase the activity of Aurora-A, and the effect of both bound together is the e

72 Elevated levels of Aurora-A are significantly associated with disease-free

73 ons because it highlights the mitotic kinase Aurora-A as a novel promising therapeutic target to sele

74 ogues p37/p47 resulted in an accumulation of Aurora A at centrosomes and a delay in centrosome separa

75 ation of active key mitotic kinases Plk1 and Aurora A at centrosomes and spindle poles.

76 ivity of cognate kinases (Erk1/2, Msk1/2 and Aurora A) at the Tnf-alpha locus.

77 Most studies of Aurora A (AurA) describe it as a mitotic centrosomal kin

78 Aurora A (AurA) is a major mitotic protein kinase involv

79 The mitotic kinase Aurora A (AurA) is regulated by a complex network of fac

80 events require the serine/threonine kinase, Aurora A (AurA), and the centrosomal protein of 192 kDa

81 HEF1 scaffold and activating its associated Aurora-A (AurA), a kinase crucially required for primary

82 The essential mitotic kinase Aurora A (AURKA) is controlled during cell cycle progres

83 nce-inducing inhibitor of the mitotic kinase Aurora A (AURKA) with an MDM2 antagonist activates p53 i

84 The Aurora kinases, which include Aurora A (AURKA), Aurora B (AURKB) and Aurora C (AURKC),

85 ed during cancer progression, interacts with Aurora-A (AURKA) kinase to control ciliary resorption, a

86 pment and homeostasis, we interbred a floxed Aurora-A (Aurora-A(fl)) mouse with the Cre-deleter strai

87 c M-phase, and identify a crucial APC/C-PP6c-Aurora A axis in the resumption of female meiosis.

88 s led to SAR156497, an exquisitely selective Aurora A, B, and C inhibitor with in vitro and in vivo e

89 Serine/threonine protein kinases Aurora A, B, and C play essential roles in cell mitosis

90 In mammalian cells, the aurora kinases (aurora-A, -B, and -C) play essential roles in regulating

91 regulators LIM domain kinase 1, cofilin, and Aurora A/B/C.

92 Unlike wild-type cells, Aurora-A(-/-) basal progenitors were delayed in forming

93 Moreover, Aurora A binding and phosphorylation of BRCA1 enhanced i

94 We show that Aurora A binds TPX2 and MLN8054 simultaneously and provi

95 It was known that Aurora A/Bora activates Polo at centrosomes during late

96 hich acts as a T-loop phosphatase inhibiting Aurora-A bound to BRCA1.

97 e, our results suggest that unphosphorylated Aurora-A bound to the mitotic spindle by TPX2 is catalyt

98 ation process of the serine/threonine kinase Aurora-A by phosphorylation and by its protein partner,

99 Activation of Aurora A can impinge on YAP activity through direct phos

100 tudies and biochemical assays, delineates an Aurora A conformation-specific effect on proteolytic deg

101 teric activation by TPX2 of dephosphorylated Aurora A could be at play in the spindle microtubules.

102 is a substrate of Aurora-A and that elevated Aurora-A could contribute to androgen-independent cell g

103 Furthermore, our data also illustrated that Aurora-A could not only induce mRNA and protein expressi

104 Ectopic expression of Aurora-A decreases and depletion of Aurora-A enhances ta

105 vels of apoptosis or senescence, but because Aurora-A-deficient tumors accumulate polyploid cells wit

106 bitor, suggesting a centrosomal role for the Aurora A-dependent complex of clathrin, ch-TOG, and TACC

107 Aurora A-dependent NF-kappaB signaling portends poor pro

108 Here we show that Aurora-A determines tamoxifen sensitivity by regulation

109 Aurora-A differs from Aurora-B/C at three positions in t

110 Using in vitro kinase assays, we show that Aurora A directly phosphorylates YY1 at serine 365 in th

111 USP2a interacts with Aurora-A directly in vitro and in vivo.

112 A1 tumor suppressor axis restrains oncogenic Aurora-A during mitosis to ensure karyotype stability re

113 ssion of Aurora-A decreases and depletion of Aurora-A enhances tamoxifen sensitivity in ERalpha-posit

114 Injection of ES cells into Aurora A epiblast knockout blastocysts reconstitutes emb

115 and polyploid keratinocytes were evident in Aurora-A(-/-) epidermis, indicating that a deficiency in

116 ferentiation marker keratin 1 was evident in Aurora-A(-/-) epidermis, there was a marked reduction in

117 We propose that a high degree of Aurora A expression may play a role in aggressive behavi

118 ntly positive correlation between Rap-1A and Aurora-A expression.

119 We find that activation of Aurora A first occurs at centrosomes at late G(2) and is

120 homeostasis, we interbred a floxed Aurora-A (Aurora-A(fl)) mouse with the Cre-deleter strain, K14.Cre

121 Aurora-A(fl/fl);Krt14.Cre (Aurora-A(-/-)) mice died shor

122 This paper thus describes a new Aurora A function that takes place after the metaphase-t

123 ew powerful tool to search for and study new Aurora A functions.

124 These data suggest that Aurora-A has a pivotal role in tamoxifen resistance and

125 pyrimidine 1 was identified as a potent hit (Aurora A IC(50) = 6.1 +/- 1.0 nM) from in-house screenin

126 ich is a potent inhibitor of Aurora kinases (Aurora-A IC(50) = 0.015 +/- 0.003 muM, Aurora-B IC(50) =

127 Knockdown of Aurora A impaired cell growth, induced mitotic arrest an

128 This inhibitor locks Aurora A in an inactive conformation and disrupts bindin

129 The involvement of Aurora A in events after metaphase has only been suggest

130 and suggest therapeutic use from inhibiting Aurora A in head and neck cancers, which overexpress BMI

131 ics, and they uncover an unexpected role for Aurora A in late mitosis.

132 B-ring inhibited the autophosphorylation of Aurora A in MDA-MB-468 breast cancer cells.

133 Inactivation of Aurora A in the epiblast or visceral endoderm layers of

134 ts uncover a novel mechanism that implicates Aurora A in the mitotic inactivation of transcription fa

135 In contrast, mutation of Aurora A in the visceral endoderm, leads to posterioriza

136 I1/hSNF5 leads to aberrant overexpression of Aurora A in these tumors, which is required for their su

137 phosphorylate and potentiate the activity of Aurora A in vitro.

138 cells, confirming that INI1/hSNF5 represses Aurora A in vivo.

139 lized in neuroblastoma by the protein kinase Aurora-A in a manner that is sensitive to certain Aurora

140 Conditional genetic ablation of Aurora-A in adult tissues results in polyploid cells tha

141 his study, we demonstrate elevated levels of Aurora-A in androgen-refractory LNCaP-RF but not androge

142 cal tools to further explore the function of Aurora-A in cells.

143 To address the role of Aurora-A in skin development and homeostasis, we interbr

144 Thus, the deletion of Aurora-A in the developing epidermis alters centrosome f

145 sters on Hice1 that can be phosphorylated by Aurora-A in vitro.

146 Aurora-A, in turn, then phosphorylates BRCA1 itself, the

147 structure indicates that the conformation of Aurora-A induced by compounds such as alisertib and CD53

148 We show that ectopic expression of Aurora-A induces AR transactivation activity in the pres

149 pharmacodynamic assays provide evidence for Aurora A inhibition by MLN8054 in patient skin and tumor

150 Critically, these effects are reproduced by Aurora A inhibition.

151 A and is recruited to the spindle pole after Aurora A inhibition.

152 verning the observed isoform selectivity for Aurora-A inhibition.

153 imized by structure-based design to a potent Aurora A inhibitor (IC50 = 2 nM) with very high kinome s

154 IBPR compounds as well as MLN8237, a proven Aurora A inhibitor, as chemical probes to investigate th

155 et in tamoxifen-resistant breast cancer, and Aurora-A inhibitor could be used as either an independen

156 Notably, Aurora-A inhibitor MLN8237, which is currently in clinic

157 so observed in glioma cells treated with the Aurora-A inhibitor TC-A2317 or anti-Aurora-A siRNA.

158 activity of Aurora-A, we show here that two Aurora-A inhibitors, MLN8054 and MLN8237, disrupt the Au

159 Furthermore, Aurora-A interacts with and phosphorylates ERalpha on se

160 Aurora-A interacts with AR and phosphorylates AR at Thr(

161 These results indicated that Aurora A is a direct downstream target of INI1/hSNF5-med

162 Aurora A is a mitotic kinase essential for cell prolifer

163 The mitotic kinase Aurora A is an important therapeutic target for cancer t

164 Here, we report that Aurora A is essential for Thr9 phosphorylation of the TR

165 he as-AurA with 1-Na-PP1, we discovered that Aurora A is required for central spindle assembly in ana

166 Aurora-A is a kinase involved in the formation and matur

167 In addition, Aurora-A is a substrate for USP2a in vitro and in vivo.

168 We conclude that Aurora-A is an accessible target that makes destabilizat

169 active and that the phosphorylation state of Aurora-A is an inaccurate surrogate for its activity.

170 androgen receptor (AR) and whether elevated Aurora-A is involved in androgen-independent cell growth

171 However, Aurora-A is not required for KIBRA to associate with Lat

172 Thus, Aurora-A is required for tumor formation in vivo, and th

173 (27e), a potent inhibitor of Aurora kinases (Aurora-A K(d) = 7.5 nM, Aurora-B K(d) = 48 nM), FLT3 kin

174 Finally, Aurora-A(-/-) keratinocytes displayed centrosomal abnorm

175 Aurora A kinase (AAK) is overexpressed in aggressive lym

176 Aurora A kinase (AAK) is upregulated in highly prolifera

177 Here, we report that Aurora A kinase (AAK) opposes the stabilizing effect of

178 We report here the design of the first human Aurora A kinase (as-AurA) engineered by chemical genetic

179 We established a conditional deletion of Aurora A kinase (AurA) in Cdk1 analogue-sensitive DT40 c

180 Aurora A kinase (AURKA) is overexpressed in 96% of human

181 y activates the mitotic programme, including Aurora A kinase (Aurka), in stratified epithelia, and en

182 le Arpc1b mutant in mammalian cells leads to Aurora A kinase activation and abnormal centrosome ampli

183 Inhibiting Aurora A kinase activity attenuated BMI1-induced tumor g

184 Inhibition of Cdk1 activity, but not Aurora A kinase activity, prevents the translation of Mo

185 er than simple nanomolar-level inhibition of Aurora A kinase activity.

186 In this study, we determined that Aurora A kinase acts as a positive regulator for YAP-med

187 eased expression of p53, reduced activity of aurora A kinase and a subsequent delay in the activation

188 totic entry predominantly occurs upstream of Aurora A kinase and Polo-like kinase 1, resulting in a f

189 h a physiological activator and substrate of Aurora A kinase and these interactions help to maintain

190 Additionally, we demonstrate that Aurora A kinase associates with inner centromere protein

191 cells showed reduced activation of Plk1 and Aurora A kinase at spindle poles and an impaired localiz

192 le attachments are restored by inhibition of Aurora A kinase at spindle poles.

193 Knowledge of Aurora A kinase functions is limited to premetaphase eve

194 n but also shed new light on the function of Aurora A kinase in the reprogramming process.

195 enance, and destabilization of N-Myc through Aurora A kinase inhibition reduces tumor burden.

196 Alisertib is an oral Aurora A kinase inhibitor with preclinical activity in n

197 This was phenocopied by treatment with Aurora A kinase inhibitor, suggesting a centrosomal role

198 agement of neuroendocrine prostate cancer as Aurora A kinase inhibitors promoting N-Myc destabilizati

199 date the efficacy of novel therapies such as Aurora A kinase inhibitors.

200 copy, we have determined that phosphorylated Aurora A kinase is in dynamic equilibrium between a DFG-

201 Here we investigate the role of Aurora A kinase on AR-Vs in models of CRPC and show depl

202 oduce (18)O label into bacterially expressed Aurora A kinase phosphorylation sites and resulted in th

203 of p38, inositol trisphosphate 3-kinase, and Aurora A kinase potently enhance iPSC generation, and iP

204 ypertension drug felodipine to the oncogenic Aurora A kinase protein via hydrogen bonding interaction

205 In this study, we demonstrate that Aurora A kinase regulates kinetochore-microtubule dynami

206 tor YY1 as a novel mitotic substrate for the Aurora A kinase, a key regulator of critical mitotic eve

207 ic spindle formation and known substrates of Aurora A kinase, resulting in spindle assembly and cytok

208 We show that Aurora A kinase, which functions in centrosome activity

209 One of these mitotic controllers is Aurora A kinase, which is itself highly regulated.

210 Regulation of MCAK function is dependent on Aurora A kinase, which is regionally enhanced by signali

211 dipine as a specific inhibitor for oncogenic Aurora A kinase.

212 ation and TPX2-mediated activation) in human Aurora A kinase.

213 le in two similar hydrophobic pockets in the Aurora A kinase.

214 The centrosomal Aurora-A kinase (AURKA) regulates mitotic progression, a

215 Moreover, aberrant Aurora-A kinase activity induced phosphorylation and nuc

216 pharmacological and molecular inhibition of Aurora-A kinase activity restored a CD24(+) epithelial p

217 oss, which also requires the activity of the Aurora-A kinase AIR-1.

218 pindle assembly factor TPX2, which activates Aurora-A kinase and stimulates local microtubule nucleat

219 findings, our data clearly demonstrate that Aurora-A kinase does not regulate TACC3-chTOG complex fo

220 s show for the first time the causal role of Aurora-A kinase in the activation of EMT pathway respons

221 Here, we report that the Aurora-A kinase inhibitor alisertib exhibits potent effi

222 treatment of Pkd1(-/-) mice with a clinical Aurora-A kinase inhibitor exacerbated cystogenesis.

223 Aurora-A kinase is frequently overexpressed/activated in

224 amics is spatially controlled through a Rac1-Aurora-A kinase pathway that locally inhibits the MT dep

225 Here, we found that Aurora-A kinase, a major mitotic kinase, specifically bi

226 N-Myc forms a complex with the Aurora-A kinase, which protects N-Myc from proteasomal d

227 n carcinoma cells, 28c and 40f inhibited the Aurora-A L215R and R220K mutants with IC50 values simila

228 In agreement, overexpression of Aurora-A leads to increased H3 T118ph levels, causing co

229 We show that Aurora A levels increase in advanced disease and AURKA i

230 to its activator protein TPX2, which impairs Aurora A localization at the mitotic spindle and induces

231 Aurora A localization to the centrosome required MTs, wh

232 s embryos, centrosomes recruited more AIR-1 (Aurora A), matured precociously, and alignment of the mi

233 Thus, a Rac1-Aurora A-MCAK signaling pathway mediates EC polarization

234 We show that Aurora-A mediated H3 T118ph occurs at pericentromeres an

235 Two new studies describe an Aurora A-mediated error correction mechanism based on th

236 Drug-resistant Plk4 can enhance Aurora A-mediated rescue, and, accordingly, Plk4 can pho

237 Aurora-A(fl/fl);Krt14.Cre (Aurora-A(-/-)) mice died shortly after birth.

238 ng induces stabilization and accumulation of Aurora-A mitotic kinase that ultimately drives the trans

239 Taken together, these results suggest that Aurora-A modulates the microtubule binding activity of H

240 notype can be rescued by inhibitor-resistant Aurora A mutants.

241 inhibitors, MLN8054 and MLN8237, disrupt the Aurora-A/N-Myc complex and promote degradation of N-Myc

242 Disruption of the Aurora-A/N-Myc complex inhibits N-Myc-dependent transcri

243 Inactivation of Aurora A or Plk1 individually during a synchronized cell

244 lective inhibitors, such as compound 28c, of Aurora-A over Aurora-B.

245 Elevated cytoplasmic p73 in Aurora-A overexpressing primary human tumors corroborate

246 These effects were phenocopied by the Aurora A phosphomimetic mutation, S719E.

247 Aurora-A phosphorylated p73 also facilitates inactivatio

248 A dileucine motif and Aurora A-phosphorylated serine 558 on TACC3 bound to the

249 Aurora A phosphorylates Arpc1b on threonine 21, and expr

250 We report that Aurora-A phosphorylation of p73 at serine235 abrogates i

251 In all, our data suggests that Aurora A plays a pivotal role in regulation of AR-V7 exp

252 We further found that the Cep192-dependent Aurora A-Plk1 activity is essential for kinesin-5-mediat

253 Manipulating elements of the Gravin-Aurora A-Plk1 axis prompts mitotic delay and prevents ap

254 late the activation/deactivation of Plk1 and Aurora A, possibly by linking them to mTOR signaling in

255 Specifically, YAP associates with Aurora A predominantly in the nucleus.

256 Therapeutic elimination of Aurora-A prevents the progression of skin and mammary gl

257 Thus, CRM1, BARD1 and Aurora A promote the targeting and function of BRCA1 at

258 ay indicated that INI1/hSNF5 associates with Aurora A promoter in RT and normal cells but not in non-

259 ) epidermis, indicating that a deficiency in Aurora-A promotes aberrant mitosis, mitotic slippage, an

260 Aurora kinase-A (Aurora-A) promotes timely entry into mitosis, centrosome

261 Embryos with an epiblast ablation of Aurora A properly establish the anteroposterior axis but

262 Taken together, our results suggest that the Aurora-A/Rap-1A pathway is associated with survival, tum

263 Importantly, knockdown of Aurora A reconfigures splicing of AR pre-mRNA to discrim

264 R-Vs in models of CRPC and show depletion of Aurora A reduces AR-V target gene expression.

265 itosis, ATR localizes to centromeres through Aurora A-regulated association with centromere protein F

266 cells, which prompted us to examine whether Aurora-A regulates the androgen receptor (AR) and whethe

267 is and identify BRCA1 itself as a target for Aurora-A relevant for CIN.

268 Thus, Aurora-A represents a prognostic marker in ERalpha-posit

269 In mice, ablation of Aurora A results in mitotic arrest and pre-implantation

270 Inhibition of Aurora-A results in mitotic defects, and this kinase is

271 principle for imidazo[4,5-b]pyridine-derived Aurora-A-selective inhibitors.

272 a-A in a manner that is sensitive to certain Aurora-A-selective inhibitors.

273 Moreover, aberrant expression of YAP and Aurora A signaling is highly correlated with triple-nega

274 with the Aurora-A inhibitor TC-A2317 or anti-Aurora-A siRNA.

275 CC3-chTOG complex formation, indicating that Aurora-A solely functions as a recruitment factor for th

276 Pulsating aurora, a spectacular emission that appears as blinking

277 Without ALADIN, Aurora A spreads from centrosomes onto spindle microtubu

278 of mitotic genes including Aurora Kinase A (Aurora A, STK6).

279 target site in the Hec1 tail, as a critical Aurora A substrate for this regulation.

280 k1 promotes phosphorylation of human Plk1 by Aurora A, suggesting that this mechanism is conserved in

281 Aurora A T-loop phosphorylation and the stability of the

282 However, the Aurora-A T217E mutant was significantly less sensitive t

283 s upstream activators polo-like kinase 1 and Aurora-A, targeted Hsp72 to the poles of cells with ampl

284 r 31, 2015, at Children's Hospital Colorado, Aurora, a tertiary care children's hospital.

285 -position led to highly potent inhibitors of Aurora A that bind in a DFG-out conformation.

286 t an indirect regulatory mechanism involving Aurora A that may account for Gwl-dependent regulation o

287 Upon entry into mitosis, Aurora A then becomes fully activated downstream of Cdk1

288 ur results suggest that Wdr62 interacts with Aurora A to control mitotic progression, and loss of the

289 62 associates and genetically interacts with Aurora A to regulate spindle formation, mitotic progress

290 oop phosphorylation and the stability of the Aurora A-TPX2 complex are increased in cells depleted of

291 Here, we found that INI1/SNF5 represses Aurora A transcription in a cell-type-specific manner.

292 patches that may aid in distinguishing human Aurora A versus human Aurora B kinase in vivo.

293 mutations in INI1/hSNF5 gene indicated that Aurora A was overexpressed/derepressed in these tumor ce

294 We found that Aurora A was required to mediate mitosis-driven GR phosp

295 Elevated Aurora-A was significantly associated with the recurrenc

296 c does not require the catalytic activity of Aurora-A, we show here that two Aurora-A inhibitors, MLN

297 1-activated kinase and its downstream kinase Aurora A, which are critical regulators of centrosome ma

298 s through upregulation of the mitotic kinase Aurora A, which is encoded by the AURKA gene.

299 uppressor 2 (Lats2) on Ser(83) by activating Aurora-A, which controls Lats2 centrosome localization.

300 to inhibition by 28c and 40f compared to the Aurora-A wild type, suggesting that the T217 residue pla

301 th IC50 values similar to those seen for the Aurora-A wild type.