ライフサイエンスコーパス: Aurora-B

1 Aurora B directly phosphorylated Ska1 and Ska3 in vitro,

2 Aurora B facilitates KT-MT dynamics by phosphorylating k

3 Aurora B functions to correct improper kinetochore-micro

4 Aurora B is a mitotic checkpoint kinase that plays a piv

5 Aurora B is an essential mitotic kinase, which is involv

6 Aurora B is overexpressed in human tumors although wheth

7 Aurora B kinase phosphorylates kinetochore proteins duri

8 Aurora B kinase regulates the proper biorientation of si

9 Aurora B kinase was more commonly overexpressed than AAK

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

11 Aurora B knockdown inhibited Mad2 phosphorylation in mit

12 Aurora B phosphorylates both Ska1 and Ska3 to inhibit th

13 Aurora B phosphorylates histone H3S28 at active promoter

14 Aurora B phosphorylates PLK1 on Thr210 to activate its k

15 Aurora B phosphorylation at S196 in the neck opens MCAK

16 Aurora B phosphorylation of Dam1p C terminus weakens dir

17 Aurora B promotes this process in a manner that is codep

18 Aurora B regulates cytokinesis timing and plays a centra

19 Aurora B therefore ensures that suppression of microtubu

20 Aurora B-orchestrated PLK1 kinase activity was examined

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

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

23 cts in CPC centromere targeting and aberrant Aurora B activity.

24 Chromatin obstructions activated Aurora B(AIR-2) at the spindle midzone, which is needed

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

26 ription and that the cell cycle arrest after Aurora B inhibition depends on p53 and pRB tumor suppres

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

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

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

30 h appropriate kinetochore orientation and an Aurora B-like activity.

31 ic spindle in early mitosis is guarded by an Aurora B kinase-dependent error correction mechanism [1,

32 chore orientation effect and corrected by an Aurora B-like activity, whereas in anaphase, it is corre

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

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

35 EB proteins and explain the importance of an Aurora B phosphorylation gradient for the spatiotemporal

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

37 Thus, an Aurora B gradient appears to mediate a surveillance mech

38 und that kinetochore protein NUF2/HIM-10 and Aurora B/AIR-2 kinase are less abundant on mitotic chrom

39 , with Polo promoting stable attachments and Aurora B promoting detachment.

40 s exhibit overexpression of Mad2, BubR1, and Aurora B, but only overexpression of Aurora B phenocopie

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

42 omere triggers dissociation of condensin and Aurora B from the centromere, thereby stabilizing the bi

43 metaphase and controlled dynein/dynactin and Aurora B activities in kinetochores, chromosome segregat

44 MPS1 localization further required HEC1 and Aurora B activity.

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

46 Bub3, and the kinases Bub1, Mph1 (Mps1), and Aurora B.

47 We added probes for NUMA and Aurora B to reveal microtubule polarity.

48 horylation in Xenopus egg extracts, Plk1 and Aurora B both promote this modification in human cells.

49 tubules) requires the activities of Polo and Aurora B kinases, with Polo promoting stable attachments

50 This crosstalk may enable Polo and Aurora B to achieve a balance wherein microtubule mis-at

51 eres of two key cell cycle kinases, Polo and Aurora B, are critical for ensuring that the two sister

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

53 Ring1B and Aurora B bind to a wide range of active promoters in res

54 ver of regulatory phosphorylation on another Aurora B substrate MKlp1 was observed, suggesting that P

55 1)-protein phosphatase 2A (PP2A) antagonizes Aurora B and Cdk1 partly by dephosphorylating Sororin an

56 onserved proteins known in mammals/yeasts as Aurora B/Ipl1, INCENP/Sli15, Survivin/Bir1, and Borealin

57 During mitotic spindle assembly, Aurora B kinase is part of an error correction mechanism

58 A midzone-associated Aurora B gradient was found to monitor chromosome positi

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

60 romeric histone H2A, attenuation of KT-based Aurora B kinase activity, and lethal chromosome congress

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

62 lization contributes to CPC functions beyond Aurora B activation.

63 for efficient complex formation with Bim1p, Aurora B/Ipl1p-dependent phosphorylation of Bim1p down-r

64 Haspin inhibitors did not block Aurora B localization to the spindle midzone in anaphase

65 ates of EB3 phosphorylation on serine 176 by Aurora B.

66 uploidy and the stress pathways activated by Aurora B inhibition and also support the use of Aurora B

67 is dynamic regulation of Mad1 association by Aurora B is only uncovered when CENP-I is depleted, cons

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

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

70 the inner centromere and are destabilized by Aurora B phosphorylation, whereas kinetochores under ten

71 Biorientation is ensured by Aurora B kinase (Ipl1), a member of the four-subunit chr

72 tion of histone H3 at serine-10 (H3S10ph) by Aurora B on chromosome arms but, in Aurora B reactivatio

73 le depolymerization activity is inhibited by Aurora B-dependent phosphorylation, but the mechanism of

74 d Ndc80, independently of phosphorylation by Aurora B kinase, and this regulation was required for ac

75 on force and kinetochore phosphorylation by Aurora B kinase.

76 KIF4A phosphorylation by Aurora B stimulates the maximal microtubule-dependent AT

77 inhibits abscission upon phosphorylation by Aurora B.

78 ntly, the antagonistic regulation of Polo by Aurora B and Map205 in cytokinesis reveals that interdom

79 Here we show that phosphorylation of Polo by Aurora B is required for cytokinesis.

80 e postulate that condensin I is recruited by Aurora B(AIR-2) to aid in the resolution of chromatin ob

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

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

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

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

85 ted that these interactions are regulated by Aurora B.

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

87 tion with microtubules and its regulation by Aurora B.

88 , the delayed fission kinetics is rescued by Aurora-B inhibition.

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

90 ctivity that accompanies anaphase and causes Aurora B translocation away from centromeres [7-12] and

91 sed H3T3ph, resulting in loss of centromeric Aurora B and reduced phosphorylation of centromere and k

92 The chromosomal passenger complex containing Aurora B can be found on a subset of spindle microtubule

93 l passenger protein complex (CPC) containing Aurora B kinase, borealin, INCENP, and survivin, which o

94 tricted negative feedback loop counteracting Aurora B in anaphase.

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

96 uld be recognized as erroneous, would elicit Aurora B-dependent destabilization of kinetochore-microt

97 g chemically induced dimerization to enhance Aurora B activity at metaphase kinetochores.

98 end-tracking protein, is required to enrich Aurora B at inner centromeres in a microtubule-dependent

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

100 s, whereas two key midzone assembly factors, Aurora B and Kif4, act as they do in midzones.

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

102 te that the KNL1 N terminus is essential for Aurora B activity at kinetochores.

103 elucidated the antineoplastic mechanism for Aurora B kinase inhibitors in cancer cells with WT p53.

104 Moreover, ULP-4 is necessary for Aurora B(AIR-2) extraction from chromatin and relocation

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

106 zes to kinetochores and is also required for Aurora B-serine 331 phosphorylation in nocodazole or unp

107 findings establish KNL1 as a requirement for Aurora B activity at kinetochores and for wild-type kine

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

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

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

111 Aurora-A differs from Aurora-B/C at three positions in the ATP-binding pocket

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

113 Furthermore, Aurora B transiently interacts with HDAC3 at the kinetoc

114 Furthermore, Aurora B/Ipl1 directly phosphorylates She1, and this mod

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

116 B at the central spindle, rather than global Aurora B activity, regulates KIF4A accumulation at the c

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

118 We present the structure of the human Aurora B kinase domain in complex with the C-terminal Au

119 n distinguishing human Aurora A versus human Aurora B kinase in vivo.

120 n anti-acetyl lysine antibody, we identified Aurora B as an acetylated protein in PC3 prostate cancer

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

122 nsient but significant reduction (P=0.02) in Aurora B acetylation during early mitosis.

123 10ph) by Aurora B on chromosome arms but, in Aurora B reactivation assays, recovery of H3S10ph was de

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

125 with corresponding significant decreases in Aurora B phosphorylation of Ndc80/Hec1.

126 aining foci on the outside, and plus ends in Aurora B-containing foci on the inside.

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

128 inally, we demonstrate that this increase in Aurora B activity causes premature collapse of the mitot

129 about the mechanisms by which an increase in Aurora B kinase activity can impair mitotic progression

130 ncrease (P<0.01 and P<0.05, respectively) in Aurora B acetylation as compared to siLuc or vehicle-tre

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

132 Interestingly, increased Aurora B activity also leads to problems with chromosome

133 a yeast model, we demonstrate that increased Aurora B activity as a result of the overexpression of t

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

135 1-depleted cells, suggesting KNL1 influences Aurora B activity through an additional pathway.

136 Aurora dependency in SCLC primarily involved Aurora B, required its kinase activity, and was independ

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

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

139 The conserved kinases Mps1 and Ipl1/Aurora B are critical for enabling chromosomes to attach

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

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

142 determine that evolutionarily conserved Ipl1/Aurora B contributes to phosphorylation of Cse4, as leve

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

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

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

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

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

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

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

150 The conserved kinase Aurora B phosphorylates the major microtubule-binding ki

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

152 The mitotic kinase Aurora B is concentrated at the anaphase central spindle

153 functional properties of the mitotic kinase Aurora B.

154 ntribute to activation of the mitotic kinase Aurora B.

155 by a mechanism involving the protein kinase Aurora B, which destabilizes kinetochore microtubules (k

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

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

158 i15 is required for activation of the kinase Aurora B/Ipl1 and can occur in trans.

159 Here we show that the mitotic kinases Aurora B and Cyclin-dependent kinase 1 (Cdk1) destabiliz

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

161 hosphorylation of centromere and kinetochore Aurora B substrates.

162 icantly from that seen in the Xenopus laevis Aurora B:INCENP complex currently used as a model for st

163 0 and histone H3 phospho-Thr3) that localize Aurora B.

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

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

166 , the budding yeast homolog of the mammalian Aurora B kinase, triggers shedding of a kinetochore prot

167 otes Aurora B activity through Bub1-mediated Aurora B targeting.

168 expression of a phosphomimetic S331E mutant Aurora B rescued chromosome alignment or segregation in

169 Although Plx1, and not Aurora B, is critical for H3T3 phosphorylation in Xenopu

170 endent manner by overwhelming the ability of Aurora B to mediate error correction.

171 These results suggest that activation of Aurora B kinase by clustering either on chromatin or on

172 the centromere and governs an activation of Aurora B kinase judged by phosphorylation of Ser-7 in CE

173 We conclude that the dual activities of Aurora B and CENP-I generate a molecular switch that mai

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

175 controlling the localization and activity of Aurora B kinase through phosphorylation of histone H2A a

176 the centromeric localization and activity of Aurora B kinase, a known regulator of k-MT attachment st

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

178 regulation and the first molecular basis of Aurora B regulation in melanoma cells.

179 ion of the CPC without affecting the bulk of Aurora B activity in HeLa cells.

180 nger complex (CPC) in animals, consisting of Aurora B kinase and three evolutionarily conserved prote

181 se chromosome misalignment and a decrease of Aurora B-mediated Ndc80 phosphorylation at kinetochores.

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

183 o PFI-1 showed significant downregulation of Aurora B kinase, thus attenuating phosphorylation of the

184 Moreover, knocking down the expression of Aurora B effectively reduced the sensitivity of cancer c

185 RZZ dissociation functions independently of Aurora B, which regulates their association.

186 ension are pulled away from the influence of Aurora B, stabilizing their microtubule attachments.

187 Pharmacologic inhibition of Aurora B in cancer cells with WT p53 increased p53 prote

188 t that activation of p21 after inhibition of Aurora B is correlated with increased chromosome missegr

189 induction of p21 by p53 after inhibition of Aurora B is dependent on the p38 MAPK, which promotes tr

190 We also demonstrate that inhibition of Aurora B results in down-regulation of E2F-mediated tran

191 Inhibition of Aurora B results in stabilization of p53 and induction o

192 avior (caused by, for example, inhibition of Aurora B).

193 in a p38-dependent manner upon inhibition of Aurora B.

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

195 aneuploid cells synergize with inhibitors of Aurora B to inhibit colony formation and oncogenic trans

196 Lack of Aurora B kinase function results in the inability to cor

197 esults provide insight into the mechanism of Aurora B regulation and the first molecular basis of Aur

198 the TPR domain was the critical mediator of Aurora B control over MPS1 localization, as its deletion

199 Mislocalization of Aurora B correlated with dephosphorylation of CENP-A and

200 on the spindle, indicating misregulation of Aurora B.

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

202 Overexpression of Aurora B in cultured cells induces defective chromosome

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

204 cogenic hyperactivation or overexpression of Aurora B may compromise the tumor suppressor function of

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

206 R1, and Aurora B, but only overexpression of Aurora B phenocopies mitotic defects observed in ARF(-/-

207 We show that an MKlp2-dependent pool of Aurora B at the central spindle, rather than global Auro

208 This pool of Aurora B phosphorylates substrates including the kinesin

209 re independently dictates the recruitment of Aurora B kinase, kinase activity on a kinetochore substr

210 s following mitotic exit, and recruitment of Aurora B kinase, male germ cell Rac GTPase-activating pr

211 explanation for the common up-regulation of Aurora B in human cancers.

212 theoretical model for spatial regulation of Aurora B phosphorylation.

213 Regulation of Aurora B/Ipl1 kinase activity and localization is critic

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

215 aspin inhibitors reveal centromeric roles of Aurora B in chromosome movement and spindle checkpoint s

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

217 orylation of Ser-7 in CENP-A, a substrate of Aurora B.

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

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

220 However, ectopic targeting of Aurora B to kinetochores does not fully rescue Aurora B

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

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

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

224 ora B inhibition and also support the use of Aurora B inhibitors in combination therapy for treatment

225 rotubule attachment in a manner dependent on Aurora B.

226 1, yet the consequences of KNL1 depletion on Aurora B phospho-regulation remain unknown.

227 calponin homology domain of HEC1 but not on Aurora B-dependent phosphorylation of the HEC1 tail.

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

229 le for BubR1-associated PP2A-B56 in opposing Aurora B and suggest that BubR1-bound PP2A-B56 integrate

230 ma and -epsilon play a general role opposing Aurora B at the central spindle.

231 zation to the spindle midzone in anaphase or Aurora B function in cytokinesis.

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

233 tors, such as compound 28c, of Aurora-A over Aurora-B.

234 he expression of phospho-histone H3, phospho-Aurora B, and Ki-67 was also suppressed in the HOI-07 tr

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

236 that Chk2 stabilizes Mps1 and phosphorylates Aurora B-serine 331 to prevent mitotic exit when most ki

237 ent abscission checkpoint by phosphorylating Aurora B at S227.

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

239 d to explore the novel scaffold of potential Aurora B inhibitors.

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

241 kinetochores, suggesting that KNL1 promotes Aurora B activity through Bub1-mediated Aurora B targeti

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

243 role in chromosome segregation by recruiting Aurora B.

244 The kinetochore protein KNL1 recruits Aurora B-counteracting phosphatases and the Aurora B-tar

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

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

247 rora B to kinetochores does not fully rescue Aurora B activity in KNL1-depleted cells, suggesting KNL

248 Restoring Aurora B to near-normal levels rescues mitotic phenotype

249 together, we identified HOI-07 as a specific Aurora B inhibitor, which deserves further investigation

250 addition to regulating attachment stability, Aurora B controls microtubule dynamics through phosphory

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

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

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

254 This compound suppressed Aurora B kinase activity in lung cancer cells, evidenced

255 t PP2A-B56gamma can dephosphorylate the T799 Aurora B site on KIF4A and thereby counteract the Aurora

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

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

258 Here, we found that Aurora B phosphorylates PKM2, but not PKM1, at T45; this

259 We found that Aurora B phosphorylation of Dsn1 promotes the interactio

260 We show here that Aurora B kinase phosphorylates Polo on its activation lo

261 Together, these results indicate that Aurora B is more active in its deacetylated state and fu

262 We propose that Aurora B phosphorylation antagonizes the interaction bet

263 Collectively, our findings, showing that Aurora B is a potential target in melanoma cells, partic

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

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

266 The Aurora B kinase coordinates kinetochore-microtubule atta

267 e compound library were screened against the Aurora B structure and one compound, (E)-3-((E)-4-(benzo

268 nd stress-activated kinases (MSK1/2) and the Aurora B kinase.

269 Aurora B-counteracting phosphatases and the Aurora B-targeting factor Bub1, yet the consequences of

270 ochore assembly and is phosphorylated by the Aurora B kinase.

271 n the Ndc80 complex is phosphorylated by the Aurora B kinase.

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

273 a B site on KIF4A and thereby counteract the Aurora B- and microtubule-stimulated ATPase activity of

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

275 Accordingly, CHMP4C functioned in the Aurora B-dependent abscission checkpoint to prevent both

276 ssing only mutant forms of KIF4A lacking the Aurora B phosphorylation site overextended the anaphase

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

278 ity as a result of the overexpression of the Aurora B and inner centromere protein homologs triggers

279 cells remain sensitive to the effect of the Aurora B inhibitor.

280 n of kinetochores through recruitment of the Aurora B kinase.

281 ectedly reveals a dimeric arrangement of the Aurora B:INCENP complex, which was confirmed to exist in

282 We show that the Aurora B kinase and the polycomb protein Ring1B have ess

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

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

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

286 on rendered MPS1 localization insensitive to Aurora B inhibition.

287 eacetylation acts as a rheostat to fine-tune Aurora B activity during mitotic progression.

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

289 romosome segregation depends critically upon Aurora B phosphorylation of Ndc80/Hec1.

290 HOI-07 potently inhibited in vitro Aurora B kinase activity in a dose-dependent manner, wit

291 together, our results suggest that, in vivo, Aurora B releases kinetochores via at least two mechanis

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

293 yeast and human cells under conditions where Aurora B activity is compromised.

294 Whether Aurora B and p53 are coordinately regulated during the c

295 However, whether Aurora B is regulated by acetylation is not known.

296 It is unknown whether Aurora B phosphorylation promotes release directly, by i

297 se data are consistent with a model in which Aurora B activity relieves a TPR-dependent inhibitory co

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

299 We find that the Ndc80 complex with Aurora B phosphomimetic mutations is defective at promot

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