ライフサイエンスコーパス: AURKA

1 AURKA co-localized and interacted with RPS6KB1, mediatin

2 AURKA inhibitors may provide a therapeutic strategy for

3 AURKA inhibitors might be developed as therapeutic agent

4 AURKA knockdown or inhibition with alisertib reduced lev

5 AURKA stabilizes METTL14 by inhibiting its ubiquitylatio

6 AURKA upregulation by BMI1 exerts several effects, inclu

7 AURKA was found to regulate NF-kappaB activity by bindin

8 of FGFR4 (n = 6 [30%]), FLT1 (n = 4 [20%]), AURKA (n = 2 [10%]) and loss of ESR1 expression (n = 9 [

9 dels, proposing the TAp63-miR-30c-2*/miR-497-AURKA axis as a potential therapeutic target.See related

10 The essential mitotic kinase Aurora A (AURKA) is controlled during cell cycle progression via t

11 ng inhibitor of the mitotic kinase Aurora A (AURKA) with an MDM2 antagonist activates p53 in senescen

12 The Aurora kinases, which include Aurora A (AURKA), Aurora B (AURKB) and Aurora C (AURKC), are serin

13 cancer progression, interacts with Aurora-A (AURKA) kinase to control ciliary resorption, and with Sr

14 to EGFR inhibitors requires Aurora kinase A (AURKA) activity.

15 d associated with increased Aurora kinase A (AURKA) and histone deacetylase 6 (HDAC6) activities, whi

16 g and overexpression of the aurora kinase A (AURKA) are often detected in luminal gastrointestinal ca

17 on of the mitotic regulator Aurora kinase A (AURKA) drives tumor aneuploidy and chromosomal instabili

18 entrosome-localized mitotic Aurora kinase A (AURKA) facilitates G2/M events.

19 The aurora kinase A (AURKA) gene is frequently amplified and overexpressed in

20 Aurora kinase A (AURKA) has emerged as a drug target for glioblastoma (GB

21 we reported a novel role of Aurora kinase A (AURKA) in BCSCs, as a transactivating co-factor in the i

22 We investigated the role of Aurora kinase A (AURKA) in regulating p73-dependent apoptosis using the p

23 , increased the efficacy of aurora kinase A (AURKA) inhibitors, and limited the expression of neuroen

24 We find that Aurora kinase A (AURKA) is a novel, hypoxia-independent target for VHL ub

25 Aurora kinase A (AURKA) is a therapeutic target in acute megakaryocytic l

26 Aurora kinase A (AURKA) is an established oncogenic factor and therapeuti

27 Aurora Kinase A (AURKA) is an oncogenic kinase with major roles in mitosi

28 Aurora kinase A (AURKA) is frequently overexpressed in several cancers.

29 Aurora kinase A (AURKA) is located at 20q13, a region that is frequently

30 Aurora kinase A (AURKA) is necessary for proper primary cilium disassembl

31 ous analyses suggested that Aurora kinase A (AURKA) is regulated by androgens in prostate cancer cell

32 u (VHL) arise from elevated Aurora Kinase A (AURKA) levels.

33 Aurora kinase A (AURKA) localizes to centrosomes and mitotic spindles whe

34 ic and genetic studies that aurora kinase A (AURKA) represents a new therapeutic target in PMF.

35 his article, we report that Aurora kinase A (AURKA) responsive WNT signaling activates S. aureus infe

36 Aurora kinase A (AURKA), a critical cell cycle regulator, contributes to

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

38 t a major target of diMF is Aurora kinase A (AURKA).

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

40 response element, whereas FOXM1 can activate AURKA expression at the transcriptional level in a simil

41 Elevated HMMR activates AURKA and reduces ARPC2 localization in the mitotic cell

42 In addition, AURKA and N-myc proto-oncogene protein (MYCN) associate

43 In addition, AURKA/B inhibitors phenocopy the effects of BETi.

44 ble in myeloma cells, including AKT1, AK3L1, AURKA, AURKB, CDC2L1, CDK5R2, FES, FLT4, GAK, GRK6, HK1,

45 1) by AURKA and the effects of alisertib, an AURKA inhibitor, in mice xenograft tumors grown from hum

46 cells was also significantly inhibited by an AURKA specific inhibitor, alisertib (MLN8237).

47 ssemination and evaluated the efficacy of an AURKA-selective small molecule inhibitor, alisertib (MLN

48 r, we found that coamplification of BMI1 and AURKA correlated with poorer prognosis.

49 d incorporation of alternative cereblon- and AURKA-recruiting ligands, leading to two optimized PROTA

50 r the use of miR-30c-2*/miR-497 delivery and AURKA inhibition in the treatment of cuSCC, which curren

51 ra A levels increase in advanced disease and AURKA is an AR-V target gene demonstrating a positive fe

52 Moreover, both FOXM1 and AURKA were essential for maintaining the BCSC population

53 n between the expression levels of FOXM1 and AURKA.

54 d melanoma tumors to coadministered MDM2 and AURKA inhibitors offers a sound rationale for clinical e

55 ncogenic proteins in neuroblastoma (MYCN and AURKA) and components of the TGFbeta pathway.

56 A and decreased proliferation, and NANOG and AURKA expression are positively correlated in HNSCCs.

57 on therapy with NEDD9 short hairpin RNAs and AURKA inhibitors impairs tumor growth and distant metast

58 These functions nominate SRC and AURKA as valuable therapeutic targets for cancer, and in

59 ment and mitotic control, suggesting SRC and AURKA might interact directly.

60 SRC and AURKA share a common interaction partner, NEDD9, which s

61 mutual cross-phosphorylation between SRC and AURKA that enhanced SRC kinase activity.

62 transcriptionally upregulates both SRSF1 and AURKA.

63 al development of stem cells in AML, such as AURKA over-expression.

64 EZH2 and NE differentiation markers (ASCL1, AURKA and SYP) linked to NEPC progression.

65 Many aurora kinase A/B (AURKA/B) pathway genes are repressed in a p53-DREAM-depe

66 Two Aurora kinase isoforms, A and B (AURKA and AURKB), are expressed ubiquitously in mammals,

67 y the suppression of Aurora kinases A and B (AURKA/B), which are critical mediators of mitosis.

68 We identify a multiprotein complex between AURKA and the replisome components MCM7, WDHD1 and POLD1

69 of CaM activity reduces interaction between AURKA and its activator, NEDD9.

70 nduced cell death, suggesting a link between AURKA and ferroptosis.

71 results, suggesting a possible link between AURKA and GPX4.

72 ed positive feedback signalling loop between AURKA and FOXM1, crucial for BCSC self-renewal.

73 Blocking AURKA nuclear localization inhibits this newly discovere

74 lts link CSCs, EMT, and CIN through the BMI1-AURKA axis and suggest therapeutic use from inhibiting A

75 In ALL patients both AURKA and AURKB showed a significant overexpression, whe

76 e (m(6)A) modification which is activated by AURKA in BCSCs.

77 er, we propose that SDCBP phosphorylation by AURKA prevents SDCBP degradation and promotes ESCC tumor

78 as a downstream target that was repressed by AURKA.

79 ribosomal protein S6 kinase B1 (RPS6KB1) by AURKA and the effects of alisertib, an AURKA inhibitor,

80 significant increase of phosphor-AURKA/B/C, AURKA, AURKB, and PLK1, which fall into the mitotic kina

81 Indeed, allosteric but not catalytic AURKA inhibitors sensitize cancer cells to inhibition of

82 tly changed hub genes including KIF14, CDK1, AURKA, LCN2, TGM1, and DSG1.

83 in mitosis when it localizes to centrosomes, AURKA is allosterically activated on the mitotic spindle

84 Clinically, AURKA displays high levels in NSCLC patients, and correl

85 Combining AURKA inhibitors with inhibitors of FAO extends overall

86 point to the potential utility of combining AURKA inhibitors with taxanes as a therapeutic strategy

87 NEDD9 confers AURKA stability by limiting the binding of the cdh1-subs

88 creased AURKA expression in cells confirming AURKA as a new signaling node downstream of the PI3K cas

89 CHD1 plays a critical role in controlling AURKA activation and promoting Aurora kinase inhibitor s

90 acted synergistically to inhibit cytoplasmic AURKA activity and disrupt the nuclear AURKA/FOXM1-posit

91 Flash reporter activity, whereas kinase dead AURKA mutant (D274A) had no effect.

92 Indeed, kinase-dead AURKA can effectively transactivate the FOXM1 promoter t

93 dulation of AKT and mTOR signaling decreased AURKA expression in cells confirming AURKA as a new sign

94 ogenic property of the spatially deregulated AURKA in tumorigenesis and provide a potential therapeut

95 We detected AURKA-dependent phosphorylation of RPS6KB1 in cell lines

96 f the key spindle assembly regulators (i.e., AURKA, PLK1, and gamma-tubulin) to the microtubule-organ

97 6742X inhibitor decreased with more efficacy AURKA and AURKB expression in K-562 leukemia cells.

98 nockdown activated beta-catenin and elevated AURKA expression, decreased primary cilia formation, and

99 By contrast, we found that elevated AURKA expression is not increased by HIF-1alpha, suggest

100 The siRNA knockdown of endogenous AURKA reversed these effects and Western blot analysis s

101 AURKA 5' UTR alternative splicing, enhancing AURKA protein expression; AURKA positively regulates SRS

102 plicing, enhancing AURKA protein expression; AURKA positively regulates SRSF1 and MYC post-translatio

103 Binding of NEDD9 to AURKA is critical for AURKA stabilization, as mutation of S296E was sufficient

104 A short and a long 3'UTR isoform exist for AURKA mRNA, resulting from alternative polyadenylation (

105 unexpected, kinase-independent function for AURKA in DNA replication initiation whose inhibition thr

106 alpha, suggesting an alternate mechanism for AURKA dysregulation in VHL-null cells.

107 underscoring a novel oncogenic potential for AURKA in gastric tumorigenesis.

108 show that Ca(2+)/CaM binding is required for AURKA activation in mitosis and that inhibition of CaM a

109 ciated protein 5 (HURP/DLGAP5), required for AURKA-dependent, centrosome-independent mitotic spindle

110 together, these findings support a role for AURKA in EOC dissemination by regulating migration and a

111 urrent study, we identified a novel role for AURKA in regulating ovarian cancer cell dissemination an

112 noprecipitation with antibodies specific for AURKA and GSK-3beta indicated that the two proteins coex

113 n tissue samples, and mouse models, we found AURKA to be up-regulated during chronic inflammation to

114 cer cell lines with activated KRAS, we found AURKA to phosphorylate RPS6KB1, promoting cell prolifera

115 patients, including SRC, SMAD family genes, AURKA, EGFR, HSP90, and PDGFR.

116 e elevated levels of AURKA protein, few have AURKA gene amplification, implying that posttranscriptio

117 CLC initiation and progression, highlighting AURKA as a potential therapeutic target for combatting h

118 be a route of oncogenic activation of human AURKA.

119 The recombinant human AURKA protein phosphorylated the GSK-3beta protein at Se

120 herapeutic target for combatting hyperactive AURKA-driven NSCLCs.

121 Our findings identify AURKA alternative splicing as a critical regulatory node

122 We identify AURKA activity as essential in NSCLC cells lacking SMARC

123 Thus, we propose that impaired AURKA function induces premature senescence by preventin

124 These results implicate AURKA as an effective biomarker for bladder cancer detec

125 the Y- pocket induces structural changes in AURKA that inhibit catalytic activity in vitro and in ce

126 A decrease in AURKA, concomitant with increased ubiquitination and pro

127 No differences were found in AURKA and AURKB expression between gene fusions, immunop

128 activator of AURKA, is directly involved in AURKA stability.

129 o-fold increase in the proliferation rate in AURKA overexpressing cells.

130 miR-4715-3p mediated a reduction in AURKA levels leading to G2/M delay, chromosomal polyploi

131 A catalytically inactive AURKA mutant suffices to overcome this block.

132 FOSL1 targets include AURKA, whose inhibition impairs viability of mutant KRAS

133 a subset of novel cellular genes, including AURKA and CDCA3, controlled by sphingolipid metabolism,

134 l instability (CIN) related genes, including AURKA and TP53 alterations, were the most frequently acq

135 atic activity of multiple kinases, including AURKA, FLT3, GSK3A, MAP3K, MEK, RSK2, RSK4, PLK4, ULK1,

136 selectivity over related kinases, including AURKA/B and PLK1.

137 ata identified a 7-gene signature, including AURKA, KIF18B, PKMYT1, and ORC1, which were overexpresse

138 r accumulation of beta-catenin and increased AURKA signaling to HDAC6.

139 RBL2, or the DREAM component LIN37 increased AURKA/B pathway gene expression and reduced paclitaxel a

140 actor-1alpha (HIF-1alpha) mediates increased AURKA expression in VHL-null cells.

141 rlying mechanism by which VHL loss increases AURKA levels has not been clearly elucidated, although i

142 Indeed, AURKA overexpression led to a significant increase in th

143 ere found to be responsible for BMI1-induced AURKA expression.

144 Agents that inhibit AURKA might slow the growth of gastrointestinal tumors w

145 n unexpected structural mechanism to inhibit AURKA activity and mitotic localization.

146 Moreover, HIF-1alpha inhibited AURKA expression by inhibiting beta-catenin transcriptio

147 Instead, AURKA preferentially interacts with heterogeneous nuclea

148 ost mitotic cells express two AURK isoforms (AURKA and AURKB), mammalian germ cells also express a th

149 Aurora A kinase (AURKA) activation, related in part to AURKA amplificatio

150 reveal that the presence of Aurora-A Kinase (AURKA) in the nucleus and metastatic dissemination are m

151 Aurora A kinase (AURKA) is overexpressed in 96% of human cancers and is c

152 study, we demonstrated that aurora-A kinase (AURKA) is required to mediate TGF-B-induced expression o

153 catalytic activity of human AURORA-A kinase (AURKA) regulates mitotic progression, and its frequent o

154 The centrosomal Aurora-A kinase (AURKA) regulates mitotic progression, and overexpression

155 Aurora kinases (AURKA and AURKB) are mitotic kinases with an important r

156 Aurora kinases, AURKA, AURKB, and AURKC, are serine/threonine kinases th

157 Among these, a role for basal body-localized AURKA in regulating ciliary disassembly in interphase ce

158 c events, and in hematological malignancies, AURKA and AURKB hyperexpression are found in patients wi

159 Mechanically, AURKA-mediated phosphorylation of LKB1 impairs LKB1 inte

160 hanism, cells exposed to AurkinA mislocalise AURKA from mitotic spindle microtubules.

161 kinases required for the control of mitosis (AURKA and AURKB) and meiosis (AURKC).

162 e as the target for a new class of dual-mode AURKA inhibitors, with implications for the chemical bio

163 Expression of MYCN, AURKA, TGFBR1, and TGFBR2 was directly inhibited by miR-

164 -dependent genes induced by nuclear AURKA (N-AURKA), including migration/invasion, survival/death, an

165 r specimens revealed a correlation between N-AURKA presence and decreased patient survival.

166 we identify associations in black women near AURKA, CAPN13, PIK3CA, and SERPINB5 via TWAS that are un

167 Our findings unveil a new AURKA-SDCBP-EGFR axis that is involved in ESCC progressi

168 Nuclear AURKA activates transcription of "hypoxia-induced genes"

169 r targeting both the cytoplasmic and nuclear AURKA function to effectively eliminate BCSCs, so as to

170 tiple HIF-dependent genes induced by nuclear AURKA (N-AURKA), including migration/invasion, survival/

171 ys in cancer metastasis, identifying nuclear AURKA as a crucial upstream regulator of the HIF1 transc

172 ction and transcriptional network of nuclear AURKA in BCSCs remain unknown.

173 Here, we report that nuclear AURKA can be recruited by Forkhead box subclass M1 (FOXM

174 asmic AURKA activity and disrupt the nuclear AURKA/FOXM1-positive feedback loop, respectively, result

175 genetic resistance through the activation of AURKA by its coactivator TPX2 emerges in response to chr

176 Treatment-induced activation of AURKA is associated with resistance to EGFR inhibitors i

177 ogically, the amplification or activation of AURKA-induced impairment of the LKB1/AMPK signaling path

178 w that phospho-Bora is a direct activator of AURKA kinase activity.

179 re, we show that NEDD9, a known activator of AURKA, is directly involved in AURKA stability.

180 entified unexpected nonmitotic activities of AURKA.

181 Moreover, binding of AURKA to DROSHA transcript further strengthens the bindi

182 The coexpression of AURKA together with TAp73 inhibited the activation of th

183 ence analysis demonstrated colocalization of AURKA and GSK-3beta proteins and a significant increase

184 Lastly, combination of AURKA and MEK inhibitors induces a deleterious effect on

185 ion in quiescent cells, where degradation of AURKA is required to maintain the primary cilium.

186 We show that genetic depletion of AURKA, or its inhibition by allosteric but not catalytic

187 Finally, mutated derivatives of AURKA impaired for CaM binding and/or CaM-dependent acti

188 -3p expression, leading to downregulation of AURKA.

189 l lines were used to evaluate the effects of AURKA inhibition and overexpression on migration and adh

190 The effects of AURKA overexpression associated with poor clinical outco

191 d RNA interference to examine the effects of AURKA overexpression in human bladder cancer cells.

192 Elevated expression of AURKA adversely affects prognosis in estrogen receptor (

193 In our UAB TNBC cohort, the expression of AURKA and AURKB was significantly higher in TNBC tumors

194 The expression of AURKA is increased upon androgen stimulation in LNCaP-AR

195 hese findings suggest that the expression of AURKA is regulated by androgen in prostate cancer cells

196 Conversely, enforced expression of AURKA resulted in increased migration, adhesion and acti

197 Patients with high expression of AURKA were associated with shorter overall survival.

198 We correlated increased expression of AURKA with increased levels of tumor necrosis factor-alp

199 newly discovered transactivating function of AURKA, sensitizing resistant BCSC to kinase inhibition.

200 n, and overexpression and hyperactivation of AURKA commonly promotes genomic instability in many tumo

201 ng silencing of miR-4715-3p and induction of AURKA in UGCs.

202 Inhibition of AURKA also reduced growth of xenograft tumors from human

203 mediated depletion or chemical inhibition of AURKA induces apoptosis and cell death in vitro and in x

204 Inhibition of AURKA or reconstitution of miR-4715-3p inhibited GPX4 an

205 l or RNA interference-mediated inhibition of AURKA significantly reduced ovarian carcinoma cell migra

206 In addition, selective inhibition of AURKA suppressed cuSCC cell proliferation, induced apopt

207 Inhibition of AURKA using siRNA produced similar results, suggesting a

208 -497, as well as pharmacologic inhibition of AURKA, a miR-497 target, suppress tumor growth in xenogr

209 ar senescence is caused by the inhibition of AURKA.

210 In contrast, pharmacologic inhibition of AURKA/B or knockdown of AURKA/B pathway components incre

211 at alisertib, a pharmacological inhibitor of AURKA, causes primary cilia formation and cellular senes

212 LN8237 (Alisertib), a selective inhibitor of AURKA, induced polyploidization and expression of mature

213 tional small-molecule selective inhibitor of AURKA, reduced nuclear staining of nuclear factor-kappaB

214 et of CHD1 and suppressed the interaction of AURKA with the coactivator TPX2, thereby rendering cance

215 The knockdown of AURKA reversed the phosphorylation of GSK-3beta and the

216 ologic inhibition of AURKA/B or knockdown of AURKA/B pathway components increased paclitaxel and IR s

217 Cs, respectively) results in lower levels of AURKA and decreased proliferation, and NANOG and AURKA e

218 c mucosa of patients had increased levels of AURKA protein and nuclear NF-kappaB, compared with healt

219 e majority of tumors have elevated levels of AURKA protein, few have AURKA gene amplification, implyi

220 alyzed by immunohistochemistry for levels of AURKA.

221 The mechanism of AURKA activation involves interactions with multiple par

222 findings unveil the activation mechanism of AURKA that is critical for mitotic entry.

223 resh insight into the catalytic mechanism of AURKA, and identify a key structural feature as the targ

224 Overexpression of AURKA and activation of its downstream pathway was enric

225 eta at Ser 9 following the overexpression of AURKA in AGS cells.

226 rays, we found significant overexpression of AURKA in gastrointestinal tumor tissues compared with no

227 Overexpression of AURKA is common in cancer, resulting in acquisition of a

228 Overexpression of AURKA led to down-regulation of the TAp73-induced activa

229 s demonstrated significant overexpression of AURKA with downregulation of miR-4715-3p.

230 putative binding sites on the 3UTR region of AURKA.

231 binding of miR-4715-3p on the 3UTR region of AURKA.

232 induced AR binding in the intronic region of AURKA.

233 define Ca(2+)/CaM as important regulators of AURKA activation in mitotic and nonmitotic signaling.

234 this study, we have investigated the role of AURKA in regulating glycogen synthase kinase (GSK)-3beta

235 We investigated the roles of AURKA in inflammation and gastric tumorigenesis.

236 Although most studies of AURKA focus on its role in mitosis, some recent work ide

237 KIFC1 was identified as a new substrate of AURKA, and new TPX2-interacting protein.

238 ur findings provide rationale for the use of AURKA inhibitors in treatment of metastatic tumors and p

239 We tested the effects of alisertib or AURKA overexpression or knockdown in 10 upper gastrointe

240 beta-catenin levels in cells overexpressing AURKA.

241 ses we show that genetic and pharmacological AURKA inhibition elicits metabolic reprogramming mediate

242 d a leading significant increase of phosphor-AURKA/B/C, AURKA, AURKB, and PLK1, which fall into the m

243 , these findings demonstrate that LIN28B-RAN-AURKA signaling drives neuroblastoma oncogenesis, sugges

244 ation of either degrader efficiently reduced AURKA levels in vivo in a neuroblastoma xenograft mouse

245 nsive transcription inhibitor iCRT14 reduced AURKA levels and rescued ciliary defects, inducing a sig

246 icient to disrupt binding and led to reduced AURKA protein levels.

247 C oncogenic circuit, wherein SRSF1 regulates AURKA 5' UTR alternative splicing, enhancing AURKA prote

248 define a role for beta-catenin in regulating AURKA and formation of primary cilia in the setting of V

249 at posttranscriptional mechanisms regulating AURKA protein levels are significant.

250 mplex-dependent mechanism, thereby relieving AURKA expression from let-7i suppression.

251 However, suppression of RNF4, AURKA, or PLK1 returned the reinitiation of replication

252 Treatment with MLN8237, a selective AURKA inhibitor, promoted polyploidization and different

253 Alisertib, a selective AURKA inhibitor, upregulates ERalpha and restores endocr

254 Both compounds retained rapid and selective AURKA degradation with improved pharmacokinetic properti

255 More specifically, AURKA is ubiquitously expressed in most advanced-stage R

256 strategy that simultaneously targets SRSF1, AURKA, and MYC oncogenes.

257 Here, we uncover an SRSF1-AURKA-MYC oncogenic circuit, wherein SRSF1 regulates AUR

258 In addition, RNA stimulated AURKA kinase activity and stabilized its conformation.

259 responses to EGFR inhibitors by suppressing AURKA-driven residual disease and acquired resistance.

260 RKA, in a PHD-independent reaction targeting AURKA for degradation in quiescent cells, where degradat

261 expression level was significant higher than AURKA in patients, and predicted a poorer prognosis with

262 Moreover, we provide evidence that AURKA binds to SDCBP and phosphorylates it at the Ser131

263 Here, we provide further evidence that AURKA is significantly overexpressed in AR-positive CRPC

264 We also found that AURKA is down-regulated and primary cilia formation is e

265 We show here that AURKA activation at the basal body in ciliary disassembl

266 We report here that AURKA expression is driven by beta-catenin transcription

267 Taken together, our results indicate that AURKA regulates TAp73-dependent apoptosis and highlight

268 NMT promoter luciferase assays revealed that AURKA's effects on NNMT were caused by PAX3-mediated tra

269 In addition, we show that AURKA and FOXM1 participate in a tightly coupled positiv

270 Here we show that AURKA translocates to the nucleus and causes distinct on

271 The AURKA/MDM2 combination therapy shows adequate bioavailab

272 ed Tyr-Ser-Tyr motif from TPX2, blocking the AURKA-TPX2 interaction.

273 tic kinase Aurora A, which is encoded by the AURKA gene.

274 We also show that the FISH test for the AURKA gene copy number in urine yielded a specificity of

275 otes inclusion of an Alu-derived exon in the AURKA 5' UTR, resulting in splicing-dependent mRNA accum

276 apoptosis and highlight the potential of the AURKA inhibitor MLN8054 in treating cancers that are def

277 -ubiquitin ligase RNF4 and activation of the AURKA-PLK1 pathway.

278 f AurkinA, a novel chemical inhibitor of the AURKA-TPX2 interaction, which acts via an unexpected str

279 stabilization induced by inactivation of the AURKA/PLK1 pathway does not affect translation, indicati

280 the results in this study indicates that the AURKA and AURKB overexpression are important findings in

281 Finally, we demonstrated that the AURKA inhibitor AKI603 and FOXM1 inhibitor thiostrepton

282 We conclude that the AURKA/GSK-3beta interaction is important in regulating b

283 ing STAT3 phosphorylation and binding to the AURKA promoter, which increased Aurora A expression in r

284 Our study unveils the AURKA-induced oncogenic m(6)A modification as a key regu

285 gnition subunit of APC/C ubiquitin ligase to AURKA.

286 Binding of NEDD9 to AURKA is critical for AURKA stabilization, as mutation o

287 inase (AURKA) activation, related in part to AURKA amplification and variants, is associated with dow

288 d predict the sensitivity of the patients to AURKA inhibitors based on NEDD9 expression.

289 cts are associated with a better response to AURKA inhibition in advanced prostate cancer.

290 EDD9 in tumor cells increases sensitivity to AURKA inhibitors.

291 by rendering cancer cells more vulnerable to AURKA inhibitors.

292 disease relapse and selected 10, i.e. TOP2A, AURKA, CKS2, CCNB2, CDK1 SLC19A1, E2F8, E2F1, PRC1, KIF1

293 ed additional targets including ZIC1, TOP2A, AURKA, and IGF-1R, which could form the basis of future

294 aemia (ALL) patients and the efficacy of two AURKA and AURKB designed inhibitors (GW809897X and GW806

295 quitinate HIFalpha is unable to ubiquitinate AURKA.

296 y, VHL mono-, rather than poly-ubiquitinates AURKA, in a PHD-independent reaction targeting AURKA for

297 ivated the Akt pathway, thereby upregulating AURKA expression through activation of the beta-catenin/

298 More importantly, the sites at which AURKA phosphorylates SDCBP are crucial for the EGFR sign

299 fibrosis in PMF and that targeting them with AURKA inhibitors has the potential to provide therapeuti

300 Treatment with AURKA-selective small molecule inhibitor MLN8054 led to