ライフサイエンスコーパス: aurora

1 her TPX2 allosterically regulates the oldest Aurora.

2 al delivery of Polo-like kinase 1 (Plk1) and Aurora A (AurA) inhibitors attenuates kinase activity, p

3 ulatory allosteric pocket of the oncoprotein Aurora A (AurA) kinase, thereby offering the potential f

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

5 reveal a potential mechanistic link between Aurora A activation and changes in the intracellular red

6 the Aurora A activation loop is crucial for Aurora A activation by autophosphorylation.

7 that a conserved cysteine residue within the Aurora A activation loop is crucial for Aurora A activat

8 We identify deregulated Aurora A activity as a mechanism contributing to the pri

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

10 ted protein 1, residues 549-855 (SPICE1), as Aurora A and B kinases substrates in vitro.

11 rotein, such as small-molecule inhibitors of Aurora A and mTOR, are currently being evaluated in earl

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

13 Concurrent inhibition of Aurora A and PI3K signaling overcame PI3K inhibitor-indu

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

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

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

17 important not only for the activity of human Aurora A but also for that of fission yeast MAPK-activat

18 Furthermore, loss of TPX2 or Aurora A causes deprotection of stalled replication fork

19 Loss of TPX2 or Aurora A compromises DNA end resection, BRCA1 and Rad51

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

21 nding to the AURKA promoter, which increased Aurora A expression in resistant GSCs.

22 In this study, we identify the TPX2/Aurora A heterodimer, nominally considered a mitotic kin

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

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

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

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

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

28 Increased aurora A kinase (AAK) expression occurs in acute myeloid

29 -throughput drug screening revealed that the Aurora A kinase (Aurora A)/Polo-like kinase 1 (PLK1)/cyc

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

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

32 ental Cell, Zhao et al. (2019) show that the Aurora A kinase AIR-1 is the long-sought cue that downre

33 over that C. elegans zygotes depleted of the Aurora A kinase AIR-1 or lacking centrosomes entirely us

34 rect ancestors of two colocalizing proteins, Aurora A kinase and its allosteric activator TPX2 (targe

35 this study, x-ray crystal structures of the Aurora A kinase domain delineate redox-sensitive cystein

36 s residue promote autophosphorylation of the Aurora A kinase domain.

37 two MYCN-targeted small-molecule inhibitors, Aurora A kinase inhibitor alisertib (MLN8237) and mTOR i

38 olleagues demonstrate unequivocally that the Aurora A kinase inhibitor, alisertib, specifically neutr

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

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

41 edox modulation of the conserved Cys(290) of Aurora A may be an underappreciated regulatory mechanism

42 -deficient cells, as were phosphorylation of Aurora A on threonine 288, phosphorylation of Polo-like

43 By analyzing these mutants, we show that Aurora A phosphorylates the condensin I-dependent pool o

44 We find that TPX2/Aurora A plays a previously unrecognized role in DNA dam

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

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

47 the catalytic activity of the Ser/Thr kinase Aurora A was inhibited by the oxidation of a conserved c

48 screening revealed that the Aurora A kinase (Aurora A)/Polo-like kinase 1 (PLK1)/cyclin-dependent kin

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

50 , and cyclin B1 and phosphorylation of PLK1, Aurora A, and TPX2 were rescued by inhibition of the ana

51 ch was associated with delayed activation of Aurora A, Aurora B, and cyclin-dependent kinase 1 (CDK1)

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

53 Altogether, our findings of an Aurora A-mediated interaction of Merlin with alpha-tubul

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

55 is significantly reduced upon inhibition of Aurora A.

56 veloped to target specific subpopulations of Aurora A.

57 activation, independently of the effects of Aurora A.

58 The catalytic activity of human AURORA-A kinase (AURKA) regulates mitotic progression, a

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

60 cogenic networks including HIPPO-YAP/TAZ and AURORA-A/MYCN pathways.

61 under higher tension in vitro independent of Aurora activity.

62 The goals of AURORA are to achieve improved phenotypes, prediction to

63 Because auroras are produced mainly by electron precipitation an

64 The beta Aurora (Aurora3) localizes to centromeres and likely fun

65 Ska complex regulates, and is regulated by, Aurora B [13].

66 The Aurora B abscission checkpoint delays cytokinesis until

67 f Haspin and Bub1 activities fully abolished Aurora B accumulation at centromeres.

68 midzone and PLK1, while the other depends on Aurora B activity and centralspindlin at the equatorial

69 , how Haspin and Bub1 collaborate to control Aurora B activity at centromeres remains unclear.

70 gest that CDK11(p58) kinase activity opposes Aurora B activity to enable abscission to proceed and re

71 Aurora B also executes important functions in interphase

72 lly interacts with the checkpoint components Aurora B and ANCHR, and the abscission delay upon checkp

73 al telomere deprotection, regulated by TRF2, Aurora B and ATM.

74 Here we show that Aurora B and Bub1 at the centromere/kinetochore regulate

75 Thus, we propose that SET, Aurora B and Bub1 form a distance-dependent positive fee

76 We propose that the coincidence of Aurora B and CENP-C at inner kinetochores ensures the fi

77 of Sgo1, suggesting that Sgo1 can integrate Aurora B and PP2A activities to modulate Aurora B substr

78 ccount for the balanced co-overexpression of Aurora B and RepoMan in many cancers, which limits chrom

79 In addition, Aurora B and RepoMan independently promote cancer cell p

80 Thus, in meiosis, the requirements for Aurora B are distinct at centromeres and telomeres, illu

81 increases Dsn1 phosphorylation by enriching Aurora B at inner kinetochores, close to CENP-C.

82 revious work has shown KIF4A is activated by Aurora B at the anaphase central spindle.

83 ied and investigated discrete populations of Aurora B at the centromere/kinetochore region.

84 e spindle midzone, making it unavailable for Aurora B at the equatorial cortex.

85 ine 3 (H3T3ph) promotes proper deposition of Aurora B at the inner centromere to ensure faithful chro

86 ecular and cellular connections of the USP13-Aurora B axis, which potentially participates in the rew

87 The Aurora B chromosomal passenger complex (CPC) is a conser

88 dle association is important for active Ipl1/Aurora B complexes to preferentially destabilize misatta

89 evated expression of Ki67, p-histone H3, and Aurora B confirmed by immunocytochemistry compared with

90 In meiosis II, Aurora B controls KT-MT attachment but appears dispensab

91 also present evidence that USP13 instigates Aurora B deubiquitination and/or protect it from degrada

92 Our results give important insight into how Aurora B disrupts kinetochore-microtubule interaction in

93 nd, in addition, impairs the localization of Aurora B during anaphase, leading to induction of aneupl

94 Mechanistically, we show that elevated Aurora B expression in breast cancer cells activates AKT

95 Here we show that Aurora B expression is elevated in basal-like breast can

96 However, whether and how Aurora B governs telomere separation during meiosis has

97 It has long been debated how Aurora B halts this action when bi-orientation is establ

98 way during epithelial polarization and that Aurora B has a role in the formation of the apical surfa

99 nd that USP13-associates with and stabilizes Aurora B in cells, especially before their entry into mi

100 Abnormal modulation of Aurora B in interphase leads to cell cycle defects often

101 tance-dependent manner, thereby inactivating Aurora B in metaphase.

102 The co-up-regulation of RepoMan and Aurora B in tumors is inversely correlated with patient

103 Aurora B inactivation disrupts cytokinesis and causes de

104 These findings support that Aurora B induces EMT to promote breast cancer metastasis

105 Pharmacologic Aurora B inhibition might be a potential effective treat

106 in SCCRO-deficient cells with addition of an Aurora B inhibitor at the midbody stage suggests that Au

107 Aurora B is a serine/threonine kinase that has been impl

108 Hence, the co-up-regulation of RepoMan and Aurora B is associated with tumor aggressiveness but als

109 During (pro)metaphase, Aurora B is concentrated at the inner centromere by the

110 While localization of Aurora B is essential for faithful cell division, it is

111 Aurora B is overexpressed in many cancers but, surprisin

112 How Aurora B is recruited to and evicted from these regions

113 Although Aurora B is regarded as the "master regulator" of kineto

114 A critical target of Aurora B is the N-terminal "tail" domain of Hec1, which

115 inhibitor at the midbody stage suggests that Aurora B is the target of SCCRO-promoted Cul3(KLHL21) ac

116 esponsible for reciprocal activation between Aurora B kinase (AURKB) and MYC.

117 of the chromosome passenger complex proteins Aurora B kinase (AURKB) and Survivin in early mitosis.

118 , we found that local kinase activity of the Aurora B kinase (AURKB) subunit of the CPC caused disass

119 ETAA1, but not TOPBP1, results in decreased Aurora B kinase activity during mitosis.

120 at centromeric SET/TAF1 on Sgo2 up-regulates Aurora B kinase activity via PP2A inhibition in prometap

121 A key regulator of abscission timing is Aurora B kinase activity, which inhibits abscission and

122 CDK11(p58) kinase activity or inhibition of Aurora B kinase activity.

123 Aurora B kinase controls kinetochore assembly by phospho

124 The Ipl1/Aurora B kinase corrects improper attachments by phospho

125 To promote bi-orientation, Aurora B kinase disrupts aberrant kinetochore-microtubul

126 Aurora B kinase elicits a cascade of events starting wit

127 Recent evidence suggests that Aurora B kinase ensures proper chromosome segregation du

128 This modification triggers mobilization of Aurora B kinase from inner centromeres to kinetochore pr

129 Aurora B kinase has a critical role in regulating attach

130 ignaling and EMT that could be attenuated by Aurora B kinase inhibitor treatment.

131 d by mutations in kinetochore components and Aurora B kinase Ipl1.

132 Aurora B kinase is essential for faithful chromosome seg

133 er is diminished recruitment and activity of Aurora B kinase on chromosome arms.

134 Aurora B kinase phosphorylates kinetochore substrates to

135 Aurora B kinase plays essential roles in mitosis.

136 kinases, the Polo-like kinase TbPLK and the Aurora B kinase TbAUK1, and a cohort of trypanosome-spec

137 This de-phosphorylation antagonizes Aurora B kinase to modify the functions and interactions

138 that EWSR1/FLI1 impairs the localization of Aurora B kinase to the midzone (the midline structure lo

139 -294 hearts analyzed by Ki67, pH3, and AurB (Aurora B kinase) expression parallel to increased small

140 sting of Borealin, Survivin, INCENP, and the Aurora B kinase) is essential to achieve error-free chro

141 stablishing a kinetochore-associated pool of Aurora B kinase, a chromosomal passenger complex (CPC) s

142 s tension across the centromeres inactivates Aurora B kinase, and PP2A phosphatase dephosphorylates t

143 er complex (CPC), whose enzymatic subunit is Aurora B kinase, promotes chromosome biorientation by de

144 Aurora B kinase, which is essential for several aspects

145 Central to this regulation is Aurora B kinase, which phosphorylates kinetochore substr

146 of the outer kinetochore protein KKIP5 in an Aurora B kinase- and kinetochore-dependent, but ATM/ATR-

147 in cis by recruiting mitotic kinases such as Aurora B kinase.

148 ion, each component of which is regulated by Aurora B kinase.

149 res in early mitosis to activate its subunit Aurora B kinase.

150 ore-microtubule coupling and is regulated by Aurora B kinase.

151 c checkpoint, nor the phosphorylation of the Aurora B kinetochore substrates Hec1, Dsn1, and Knl1.

152 Conversely, Aurora B knock down by short-hairpin RNAs (shRNAs) suppr

153 Very little is however known about how Aurora B levels are regulated in interphase.

154 This raised the possibility that Aurora B localization at centromeres is dispensable for

155 This model predicts that Aurora B localization at centromeres is required for bi-

156 Here, we show that fission yeast Aurora B localizes at telomeres during meiosis I and pro

157 Aurora B localizes prominently to inner centromeres, and

158 Assessing if this PKCepsilon-Aurora B module provides a more widely exploited genome-

159 romotes the colocalization of EWSR1/FLI1 and Aurora B on the chromosomes during prophase and metaphas

160 However, chemical inhibition of either Aurora B or survivin does not target CPC specifically du

161 ntial target of cancer therapy by inhibiting Aurora B or survivin in different types of cancer includ

162 otective control for the cell cycle, we show Aurora B phosphorylation at S227 by PKCepsilon also occu

163 show that this activity is regulated by Ipl1/Aurora B phosphorylation during cell cycle progression.

164 ation during anaphase, assisted by a midzone Aurora B phosphorylation gradient - the 'ruler' model.

165 f Ndc80, including a 27-residue sequence and Aurora B phosphorylation sites, is both necessary and su

166 we identified a small, Bub1 kinase-dependent Aurora B pool that supported faithful chromosome segrega

167 y, suggesting that kinetochore enrichment of Aurora B promotes the phosphorylation of other kinetocho

168 While the Aurora B protein kinase destabilizes low-tension attachm

169 Aurora B recruitment accompanies histone H3 threonine-3

170 the conserved CTD SUMOylation sites perturbs Aurora B recruitment and checkpoint activation.

171 tinct molecular pathways are responsible for Aurora B recruitment to centromeres and kinetochores.

172 elay key events in anaphase, including AIR-2/Aurora B relocalization to the microtubules, in response

173 Molecular dynamics indicates that Aurora B S227 phosphorylation induces conformational cha

174 ocess involves PKCepsilon phosphorylation of Aurora B S227.

175 Expression of Aurora B S227A phenocopies inhibition of PKCepsilon in b

176 ate Aurora B and PP2A activities to modulate Aurora B substrate phosphorylation.

177 This suggests that Aurora B substrates at the kinetochore are not phosphory

178 ing the outer kinetochores [7, 8] and moving Aurora B substrates away from Aurora-B-localizing sites

179 R is activated at centromeres, it stimulates Aurora B through Chk1, preventing formation of lagging c

180 in or Bub1 activity is sufficient to recruit Aurora B to a distinct chromosomal locus.

181 ta indicate that SUMOylated Topo II recruits Aurora B to ectopic sites, constituting the molecular tr

182 we delineated the contributions of PLK1 and Aurora B to RhoA activation and cytokinesis initiation i

183 kinetochores during metaphase hyperactivates Aurora B via PP2A inhibition, and thereby rescues the fe

184 alization of CENP-A(Cse4), CENP-C(Mif2), and Aurora B(Ipl1) When the RNA interference system was intr

185 sphorylated by centromere-localized pools of Aurora B, and calls for a reevaluation of the current sp

186 ociated with delayed activation of Aurora A, Aurora B, and cyclin-dependent kinase 1 (CDK1).

187 reased incidence of aberrant localization of Aurora B, and greater levels of aneuploidy, compared wit

188 cyclin B1-associated CDK1, and indirectly by Aurora B, and is antagonized by PP1-mediated dephosphory

189 egulated by the same mechanisms that control Aurora B, including FOXM1-regulated expression and prote

190 ger complex (CPC), which includes the kinase Aurora B, is a master regulator of meiotic and mitotic p

191 bule attachments (K fibers) epistatically to Aurora B, the other major error-correcting kinase.

192 for USP13 to exert its stabilizing effect on Aurora B, their association is promoted by the Aurora B-

193 implications for the different functions of Aurora B, which promote the proper interaction between s

194 rrent spatial models for how tension affects Aurora B-dependent kinetochore phosphorylation.

195 -Cdk1 localized at the spindle midzone in an Aurora B-dependent manner, with incompletely separated c

196 Cyclin B1 degradation and mitotic exit in an Aurora B-dependent manner.

197 Importantly, Aurora B-dependent Ndc80 phosphorylation, a mark that ha

198 ted Ndc80 degradation, and demonstrates that Aurora B-dependent regulation of kinetochores extends be

199 n defects in CPC chromosomal recruitment and Aurora B-dependent spindle assembly, but not in spindle

200 survivin), which recruits Ipl1-Sli15 (yeast Aurora B-INCENP) to centromeres, can become dispensable

201 lation site (T343) responsible for mediating Aurora B-induced AKT/GSK3beta/Snail1 signaling and EMT t

202 rora B, their association is promoted by the Aurora B-mediated phosphorylation of USP13 at Serine 114

203 ule attachments that are not destabilized by Aurora B.

204 amatically increases Dsn1 phosphorylation by Aurora B.

205 ivation of Polo kinetochore targets Mps1 and Aurora B.

206 is12C by Dsn1 impedes its phosphorylation by Aurora B.

207 CENP scaffold and the catalytic subunit Ipl1/Aurora B.

208 of the checkpoint depends both on Haspin and Aurora B.

209 l of shugoshin-2 from chromosome arms by the Aurora B/C kinase, an event crucial for the efficient re

210 Moreover, inhibition of Aurora B/C kinases results in Kif4 mislocalization and c

211 ty of kinetochore attachment is regulated by Aurora B/Ipl1 kinase and this regulation is conserved fr

212 To understand how Aurora-B activity is counteracted, we compare the roles

213 Thus, we identify Aurora-B as a key upstream regulator of end-on conversio

214 This work reveals a role for Aurora-B in removing chromatin-associated RNAs during pr

215 igh RepoMan levels sensitize cancer cells to Aurora-B inhibitors.

216 mitosis is antagonistically regulated by the Aurora-B kinase and RepoMan (recruits PP1 onto mitotic c

217 atus, we reveal a spatially defined role for Aurora-B kinase in retarding the end-on conversion proce

218 Finally, we uncover a novel role for Aurora-B regulated Astrin-SKAP complex in ensuring the c

219 The Sli15/Ipl1(INCENP/Aurora-B) core-CPC interacted with COMA in vitro through

220 tability, which is not rescued by inhibiting Aurora-B, an attachment destabiliser, but is reversed by

221 is evicted from prophase chromosomes through Aurora-B-dependent phosphorylation of the SAF-A DNA-bind

222 d RNAs during prophase and demonstrates that Aurora-B-dependent relocalization of SAF-A during cell d

223 8] and moving Aurora B substrates away from Aurora-B-localizing sites at centromeres (spatial separa

224 0-Hz video sampling from the ground, Earth's aurora becomes a display for the resonant interactions.

225 o presented to Children's Hospital Colorado (Aurora, CO, USA) between March 1 and November 30, 2018,

226 AURORA conducts a large-scale (n = 5000 target sample) i

227 Phospho-mutant analysis shows that Aurora contributes to the microtubule bundling capacity

228 e in-depth analyses of the rich and evolving AURORA data.

229 The Aurora family of kinases and their downstream targets ar

230 addresses this question by studying dayside auroras from both hemispheres.

231 the wealth of data available on the role of Aurora in other kingdoms, knowledge on their function in

232 two decades ago, it was discovered that the aurora is also controlled by solar insolation.

233 reconnection in the magnetotail, the dayside aurora is closely associated with magnetic field merging

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

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

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

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

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

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

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

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

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

243 Aurora kinase A inhibition also destabilized MYCN, which

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

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

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

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

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

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

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

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

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

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

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

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

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

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

258 stream targets is important in understanding Aurora kinase function.

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

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

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

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

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

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

265 Aurora kinase inhibitors suppress this adaptive survival

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

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

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

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

270 Aurora kinase was upregulated and pCDK1 was downregulate

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

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

273 The aurora kinases (AURKs) comprise an evolutionarily conser

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

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

276 Aurora kinases are a family of serine/threonine kinases

277 Aurora kinases are key effectors of mitosis.

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

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

280 Aurora kinases create phosphorylation gradients within t

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

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

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

284 Aurora kinases play a major role in mitosis by regulatin

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

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

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

288 When Aurora kinases were inhibited together, lung cancer cell

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

290 is is the initial report of results from the AURORA multisite longitudinal study of adverse post-trau

291 o show that the surface-wave-driven sawtooth auroras occurred in more than 90% of geomagnetic storms

292 Despite this, preventing Aurora phosphorylation of the tail results in prematurel

293 that Ser-518 of Merlin is a substrate of the Aurora protein kinase A during mitosis and that its phos

294 We also describe the AURORA study, a specific example of current scientific e

295 cing Understanding of RecOvery afteR traumA (AURORA) Study.

296 e existence of substantial ice volume in the Aurora subglacial basin before continental-scale ice she

297 d glacial response to Pliocene warmth in the Aurora subglacial basin catchment.

298 ting and grounded below sea level within the Aurora subglacial basin, indicating that this catchment,

299 ta from the continental shelf seaward of the Aurora subglacial basin, that marine-terminating glacier

300 Unlike the nightside aurora, which is controlled mainly by magnetic field rec