ライフサイエンスコーパス: aurora

1 eriods (in the case of broadband or Alfvenic aurora).

2 slower equatorward movement of the substorm aurora.

3 produce strong electric currents and bright aurora.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

69 activation towards its centrosomal substrate Aurora A.

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

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

72 is significantly reduced upon inhibition of Aurora A.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

93 But what modulates these currents and aurora and controls dissipation of the energy released i

94 gnetosheath, formation of widespread diffuse aurora, and enhancement of pick-up ions.

95 Plant Auroras are functionally divided into two clades.

96 In contrast, Earth's less intense auroras are generally caused by wave scattering of magne

97 The alpha Auroras (Aurora1 and Aurora2) associate with the spindle

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

99 ora kinases, which include Aurora A (AURKA), Aurora B (AURKB) and Aurora C (AURKC), are serine/threon

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

101 The 'NoCut', or Aurora B abscission checkpoint can be activated if DNA i

102 d trans-phosphorylation that is critical for Aurora B activation.

103 lization contributes to CPC functions beyond Aurora B activation.

104 ts microtubule-binding capability to promote Aurora B activity in cells and stimulates Aurora B catal

105 reveal co-existence of distinct high and low Aurora B activity states, sustained by a two-component k

106 show that protein phosphatase 1 counteracts Aurora B activity to enable Ska kinetochore accumulation

107 We propose that Ska promotes Aurora B activity to limit its own microtubule and kinet

108 In cells with reduced Aurora B activity, there is a decrease in the frequency

109 an essential CPC component required for full Aurora B activity.

110 strate of Aurora B, but is also required for Aurora B activity.

111 ad in cancers, which causes an impairment in Aurora B activity.

112 Overexpression of Aurora B also results in a reduced DNA damage response a

113 y exchanging centromere Borealin pool, while Aurora B and Mps1 play minimal roles in maintaining CPC

114 in line with an inverse correlation between Aurora B and p21(Cip1) expression in human leukemias.

115 a genome protection mechanism that relies on Aurora B and the ESCRT-III subunit CHMP4C to delay absci

116 ger complex (CPC), containing mitotic kinase Aurora B as a catalytic subunit, ensures faithful chromo

117 ent abscission checkpoint by phosphorylating Aurora B at S227.

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

119 Ubiquitination-promoted turnover of Aurora B at the midbody was deficient in SCCRO- and KLHL

120 te Aurora B activity in cells and stimulates Aurora B catalytic activity in vitro.

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

122 Inhibition of the kinase Aurora B does not change the distribution despite signif

123 bles abscission, bypassing the PKCvarepsilon-Aurora B exit pathway.

124 Aurora B facilitates KT-MT dynamics by phosphorylating k

125 ger complex (CPC), without abolishing global Aurora B function.

126 Overexpression of Aurora B in cultured cells induces defective chromosome

127 These studies reveal a novel role of Aurora B in maintaining genomic integrity by promoting t

128 Here, we describe a new role for Aurora B in telomere dispersion and disjunction during f

129 ucidated, yet signaling pathways upstream of Aurora B in this context remain poorly understood.

130 Long-term overexpression of Aurora B in vivo results in aneuploidy and the developme

131 on the new H3 is significantly reduced after Aurora B inhibition, suggesting a cross-talk between H3S

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

133 Our results demonstrate that Aurora B inhibits both direct interaction with the micro

134 Aurora B is overexpressed in human tumors although wheth

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

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

137 bule and kinetochore binding is curtailed by Aurora B is the spindle and kinetochore-associated (Ska)

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

139 ediated primarily by the centromere-enriched Aurora B kinase (ABK), typically occurs near spindle pol

140 elays of nuclear envelope reassembly require Aurora B kinase activity.

141 two holoenzymes are dynamically regulated by Aurora B kinase during mitosis.

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

143 control the assembly of these pathways, with Aurora B kinase promoting KMN network recruitment to CEN

144 cytokinesis initiation factor 1 (CIF1), and aurora B kinase that acts in concert at the new FAZ tip

145 ted the localization of polo-like kinase and aurora B kinase to the new FAZ tip, thus revealing the m

146 Aurora B kinase was more commonly overexpressed than AAK

147 Aurora B kinase, a key regulator of cell division, local

148 fore anaphase onset by a mechanism involving Aurora B kinase, a key regulator of mitosis in a wide ra

149 Analysis of AAK, Aurora B kinase, MYC, BCL-2, phosphatidylinositol 3-kina

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

151 It is a key target of Aurora B kinase, which destabilizes erroneous attachment

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

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

154 The duration of this block is controlled by Aurora B kinase.

155 NP is responsible for binding and activating Aurora B kinase.

156 on force and kinetochore phosphorylation by Aurora B kinase.

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

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

159 Thus, overexpression of Aurora B may contribute to tumor formation not only by i

160 Aurora B phosphorylates both Ska1 and Ska3 to inhibit th

161 the CPC becomes particularly important when Aurora B phosphorylates kinetochore targets to eliminate

162 In one mechanism, the centromeric kinase Aurora B phosphorylates Mis12C and strengthens its bindi

163 Aurora B phosphorylates PLK1 on Thr210 to activate its k

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

165 is more complicated than predicted from the Aurora B phosphorylation gradient model.

166 Aurora B phosphorylation of Dam1p C terminus weakens dir

167 's affinity for microtubules is regulated by Aurora B phosphorylation on its N-terminal tail [12-15],

168 theoretical model for spatial regulation of Aurora B phosphorylation.

169 Aurora B regulates cytokinesis timing and plays a centra

170 Dsn1 phosphorylation by Ipl1/Aurora B relieves this autoinhibition, enabling MIND to

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

172 This decrease in Aurora B results in diminished binding of the chromokine

173 as does expression of a non-phosphorylatable Aurora B S227A mutant.

174 , detoxification of reactive oxygen species, aurora B signaling/apoptotic execution phase, the RAS si

175 The inhibitor furthermore does not induce Aurora B specific effects in cells.

176 This phosphorylation invokes a switch in Aurora B specificity, with increased phosphorylation of

177 er, depletion of the ESCRT-III component and Aurora B substrate CHMP4C enables abscission, bypassing

178 tromere-associated kinesin localization, and Aurora B T-loop phosphorylation at kinetochores.

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

180 monstrate that PKCvarepsilon signals through Aurora B to exit the abscission checkpoint and complete

181 itment of the tension checkpoint kinase Ipl1/Aurora B to inner centromeres in metaphase but is not re

182 Importantly, targeting Aurora B to microtubules by UBASH3B is necessary for the

183 n this pathway and is sufficient to localize Aurora B to microtubules prior to anaphase.

184 ould act as a flexible "dog leash," allowing Aurora B to phosphorylate dynamic substrates localized i

185 ntegrates this and other signals upstream of Aurora B to regulate when the final step in the physical

186 we show that Ska is not only a substrate of Aurora B, but is also required for Aurora B activity.

187 (INCENP), Survivin, Borealin, and the kinase Aurora B, contributes to the activation of the mitotic c

188 ssembly depends on multiple mitotic kinases (Aurora B, Mps1, and Plx1) and is suppressed by protein p

189 UBASH3B interacts with ubiquitylated Aurora B, one of the main kinases regulating chromosome

190 ation also depends on the kinase activity of Aurora B, the catalytic subunit of the chromosomal passe

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

192 ow that PKCvarepsilon directly modulates the Aurora B-dependent abscission checkpoint by phosphorylat

193 Aurora B-orchestrated PLK1 kinase activity was examined

194 We propose that bistability of an Aurora B-phosphatase system underlies formation of spati

195 re, we describe a novel pathway involving an Aurora B-PLK1 axis for regulation of MCAK activity in mi

196 We reason that the Aurora B-PLK1 signaling at the kinetochore orchestrates

197 both phosphorylated histone H3-positive, and Aurora B-positive cardiomyocytes in the post-LVAD hearts

198 rotubule attachment in a manner dependent on Aurora B.

199 on the spindle, indicating misregulation of Aurora B.

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

201 ntribute to activation of the mitotic kinase Aurora B.

202 omere and provides the binding site for Ipl1/Aurora B.

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

204 eated with Hesperadin, a potent inhibitor of Aurora B/C kinases.

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

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

207 gulated by the conserved protein kinase Ipl1/Aurora-B and promotes the subsequent assembly of a kinet

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

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

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

211 Here the authors show that Aurora-B regulates end-on conversion in human cells and

212 om extensive emerged coastal deposits of the Aurora Basin.

213 eating marine embayments into the Wilkes and Aurora basins that were conducive to high diatom product

214 clude Aurora A (AURKA), Aurora B (AURKB) and Aurora C (AURKC), are serine/threonine kinases required

215 ld admitted to Children's Hospital Colorado (Aurora, CO, USA) with acute flaccid paralysis with spina

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

217 facet of its regulation in epithelia, where Aurora-dependent phosphorylation triggers Lgl dissociati

218 regulation antagonistically affect the alpha Aurora double mutant phenotypes.

219 The Aurora family of serine/threonine kinases is essential f

220 AbbVie Pharmaceuticals, Aurora Foundation, Boston Claude D Pepper Older American

221 Jupiter's relatively steady main aurora has a power density that is so much larger than E

222 s (59.9-60.1 years in Lansing, Michigan, and Aurora, Illinois, vs 77.0-79.6 years in Marquette, Michi

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

224 helterin component, rescued cell death after Aurora inhibition by promoting the loading of condensin

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

243 7, and 5azadC, which are known to target the Aurora kinase and DNA methylation pathways.

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

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

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

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

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

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

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

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

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

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

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

255 Aurora kinase genes were enriched in STAT5BN642H-express

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

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

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

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

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

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

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

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

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

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

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

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

268 The aurora kinases (AURKs) comprise an evolutionarily conser

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

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

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

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

273 Aurora kinases are key effectors of mitosis.

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

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

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

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

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

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

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

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

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

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

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

285 lar proteins, particularly substrates of the aurora kinases.

286 2 nM) with very high kinome selectivity for Aurora kinases.

287 mitosis in a distribution that overlaps with Aurora kinases.

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

289 ost of the planet, Mars is likely to exhibit auroras more globally than Earth.

290 ons of hot electrons (in the case of diffuse aurora) or by the turbulent or stochastic downward accel

291 ss more than 1,000 times that of the Earth's aurora, over a region with a strong magnetic anomaly whe

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

293 th the cartwheel protein TgSas-6 and a novel Aurora-related kinase, while an inner core closely align

294 Planetary auroras reveal the complex interplay between an atmosphe

295 eport the discovery of low-altitude, diffuse auroras spanning much of Mars' northern hemisphere, coin

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 lant homolog of TPX2 have been identified as Aurora substrates in plants.