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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.
5 nce-inducing inhibitor of the mitotic kinase Aurora A (AURKA) with an MDM2 antagonist activates p53 i
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
18 ially overlapping, nonredundant functions of Aurora A and Plk4 kinases contribute to initiate acentri
22 Using in vitro kinase assays, we show that Aurora A directly phosphorylates YY1 at serine 365 in th
25 ts uncover a novel mechanism that implicates Aurora A in the mitotic inactivation of transcription fa
29 imized by structure-based design to a potent Aurora A inhibitor (IC50 = 2 nM) with very high kinome s
36 cells showed reduced activation of Plk1 and Aurora A kinase at spindle poles and an impaired localiz
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-
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
48 to its activator protein TPX2, which impairs Aurora A localization at the mitotic spindle and induces
55 Moreover, aberrant expression of YAP and Aurora A signaling is highly correlated with triple-nega
59 on impairs activating autophosphorylation of Aurora A, a cell-cycle kinase critical for meiotic trans
61 rt the discovery of a selective inhibitor of Aurora A, a key regulator of cell division and potential
63 k1 promotes phosphorylation of human Plk1 by Aurora A, suggesting that this mechanism is conserved in
68 itosis, ATR localizes to centromeres through Aurora A-regulated association with centromere protein F
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.
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
91 s upstream activators polo-like kinase 1 and Aurora-A, targeted Hsp72 to the poles of cells with ampl
99 ora kinases, which include Aurora A (AURKA), Aurora B (AURKB) and Aurora C (AURKC), are serine/threon
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
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
118 ine 3 (H3T3ph) promotes proper deposition of Aurora B at the inner centromere to ensure faithful chro
121 dle association is important for active Ipl1/Aurora B complexes to preferentially destabilize misatta
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
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
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
148 fore anaphase onset by a mechanism involving Aurora B kinase, a key regulator of mitosis in a wide ra
150 er complex (CPC), whose enzymatic subunit is Aurora B kinase, promotes chromosome biorientation by de
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
164 show that this activity is regulated by Ipl1/Aurora B phosphorylation during cell cycle progression.
167 's affinity for microtubules is regulated by Aurora B phosphorylation on its N-terminal tail [12-15],
171 elay key events in anaphase, including AIR-2/Aurora B relocalization to the microtubules, in response
174 , detoxification of reactive oxygen species, aurora B signaling/apoptotic execution phase, the RAS si
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
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
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
190 ation also depends on the kinase activity of Aurora B, the catalytic subunit of the chromosomal passe
192 ow that PKCvarepsilon directly modulates the Aurora B-dependent abscission checkpoint by phosphorylat
195 re, we describe a novel pathway involving an Aurora B-PLK1 axis for regulation of MCAK activity in mi
197 both phosphorylated histone H3-positive, and Aurora B-positive cardiomyocytes in the post-LVAD hearts
203 l of shugoshin-2 from chromosome arms by the Aurora B/C kinase, an event crucial for the efficient re
205 ty of kinetochore attachment is regulated by Aurora B/Ipl1 kinase and this regulation is conserved fr
207 gulated by the conserved protein kinase Ipl1/Aurora-B and promotes the subsequent assembly of a kinet
209 atus, we reveal a spatially defined role for Aurora-B kinase in retarding the end-on conversion proce
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
217 facet of its regulation in epithelia, where Aurora-dependent phosphorylation triggers Lgl dissociati
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
231 rough pharmacologic and genetic studies that aurora kinase A (AURKA) represents a new therapeutic tar
235 data provide a promising rationale for using Aurora kinase A inhibition as a therapeutic modality of
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
245 proteins epithelial cell transforming 2 and Aurora kinase B (AurkB) are localized to stress granules
247 nt forms, interacts with the CPC core enzyme Aurora kinase B and staining of CPC components at centro
250 xhibit a twofold increase in transcripts for aurora kinase B, the centromeric cohesin ESCO2, DNMT1, t
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
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
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
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
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
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
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
284 tination of individual substrates, including Aurora kinases, with their degradation kinetics tracked
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
293 th the cartwheel protein TgSas-6 and a novel Aurora-related kinase, while an inner core closely align
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
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
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