ライフサイエンスコーパス: mitotic

1 esence of paclitaxel synergistically induced mitotic abnormalities in nearly 100% of cells and comple

2 phenotype, which is associated with reduced mitotic activity and lower expression of PLETHORA 1 (PLT

3 The mitotic activity of root apical meristem (RAM) is critic

4 As this mosaic grows by mitotic addition of new photoreceptors at the rim of the

5 c event affiliated with childhood B-ALL, the mitotic and chromosomal defects associated with HyperD B

6 ree systems that recapitulate distinct inter-mitotic and G1 phases and a continuous transition from p

7 e were established using this system on both mitotic and meiotic chromosomes.

8 We identify key regulatory factors for both mitotic and meiotic enhancers, revealing a molecular log

9 hlear organoid and explant cultures to model mitotic and nonmitotic mechanisms of hair cell generatio

10 tor-like cells and to produce hair cells via mitotic and nonmitotic mechanisms.

11 n, inferring that 55 (74%) embryos possessed mitotic aneuploidies and 23 (31%) embryos possessed meio

12 t pattern cortical Galphai, LGN, and nuclear mitotic apparatus protein (NuMA) [3, 7-18].

13 otting the presence of galectin-8 within the mitotic apparatus.

14 Reducing mitotic arrest by reversin treatment prevented accumulat

15 The gradual weakening of SAC during mitotic arrest enables APC/C(CDC20) to degrade cyclin B1

16 PyST is known to induce mitotic arrest followed by extensive cell death in mamma

17 icity of TH588, in line with the notion that mitotic arrest is required for ROS buildup and oxidation

18 to the colchicine site of tubulin to induce mitotic arrest through a microtubule cytoskeleton-based

19 ed predominantly in those cells that undergo mitotic arrest upon PyST expression.

20 g PLK1 inhibition with nocodazole (to induce mitotic arrest) had synergistic antitumor effects in vit

21 ack control of APC/C to SAC during prolonged mitotic arrest.

22 trocyte morphogenesis from stem cell to post-mitotic astrocyte in vivo, identifies a role for Fgf rec

23 ange oRG cellular morphology, migration, and mitotic behavior, but do not affect proliferation or cel

24 Overall, our results provide insights into mitotic bioenergetics and suggest that cell division is

25 yclinB1 activity, thus preventing cells from mitotic catastrophe and cell death.

26 eads to centrosome depletion, which triggers mitotic catastrophe in cells that exhibit amplicon-direc

27 hromosomal abnormalities, ultimately causing mitotic catastrophe in PARP inhibitor treated HR-profici

28 ant role of UNC5B in small-T antigen-induced mitotic catastrophe that also requires PP2A.IMPORTANCE U

29 ss their interplay with cellular senescence, mitotic catastrophe, and autophagy.

30 cancer cells become PARPi sensitive, undergo mitotic catastrophe, and die.

31 sion before repair is completed resulting in mitotic catastrophe.

32 cycle progression, and both replication and mitotic catastrophe.

33 is compromised for approximately half of all mitotic CDK substrates, with substrates affected general

34 for phosphorylation of a distinct subset of mitotic Cdk1 substrates that are essential to complete c

35 arvation, Schizosaccharomyces pombe exit the mitotic cell cycle and become irreversibly committed to

36 veloped a novel computational model of human mitotic cell cycle, integrating diverse cellular mechani

37 ulation of cytokinesis," "G1/S transition of mitotic cell cycle," "DNA recombination," and "telomere

38 helming down-regulation of genes involved in mitotic cell division but an up-regulation of genes invo

39 ynchronous mitotic domains leads to aberrant mitotic cell division orientations.

40 Sugt1 both disrupts kinetochore assembly in mitotic cells due to the mislocalization of two componen

41 Mitotic cells must form a single nucleus during telophas

42 We present a model in which KV mitotic cells strategically place their cytokinetic brid

43 (mPT), which is especially important in post-mitotic cells such as cardiomyocytes and neurons.

44 Our results indicate that a subset of mitotic cells within a population can experience discret

45 peractivity alters centrosome positioning in mitotic cells, affecting oriented cell division and prom

46 ed a distinct population of ITGA6(+)ITGB4(+) mitotic cells, whose offspring further segregated into a

47 n interactome in spread interphase and round mitotic cells.

48 n-dependent regulation of PPP holoenzymes in mitotic cells.

49 ittle is known about their functions in post-mitotic cells.

50 or cell nuclei, with high expression in some mitotic cells.

51 We identify that mitotic centriole over-elongation is dependent on mitoti

52 of CENP-A chromatin to establish and sustain mitotic centromere function in Drosophila.

53 both C. elegans and zebrafish [2, 3], where mitotic centrosome area scales more closely with changes

54 We find that the mitotic centrosome, a structure that assembles the mitot

55 ion is needed at kinetochores to silence the mitotic checkpoint (a.k.a. spindle assembly checkpoint [

56 KT-MT attachments, it did not compromise the mitotic checkpoint, nor the phosphorylation of the Auror

57 In addition to establishing mitotic chromosome architecture, condensin-mediated long

58 Condensin complexes are essential for mitotic chromosome assembly and segregation during cell

59 c chromosomes and important for establishing mitotic chromosome condensation.

60 Mitotic chromosome reorganization is marked by the gener

61 must resist microtubule-mediated forces for mitotic chromosome segregation.

62 The inner centromere is a region on the mitotic chromosome that serves as a platform for mitotic

63 cellular-molecular mechanisms underlying the mitotic/chromosome defects predicated to be early pathog

64 erase IIalpha (TOP2A) is a core component of mitotic chromosomes and important for establishing mitot

65 undation for thinking about the evolution of mitotic chromosomes as they prepare for anaphase segrega

66 A long-standing conundrum is how mitotic chromosomes can compact, as required for clean s

67 ted roles in mitosis including 1) connecting mitotic chromosomes to spindle microtubules to establish

68 We demonstrated that Grh remains bound to mitotic chromosomes, a property shared with other pionee

69 ads to an increase in the size of individual mitotic chromosomes, consistent with de-condensation.

70 ds to accumulation of SAF-A-RNA complexes on mitotic chromosomes, defects in metaphase chromosome ali

71 te whether 'one-sided' complexes can compact mitotic chromosomes, organize interphase domains, and ju

72 h scales, from the 10 nm sized nucleosome to mitotic chromosomes, whilst jostling within the crowded

73 he distinct appearance of heterochromatin on mitotic chromosomes.

74 PICH specifically disperses SUMO2/3 foci on mitotic chromosomes.

75 The 2 mitotic clocks were decelerated in SZ related to antitum

76 of APC/C is necessary to establish a unique mitotic collapse with sustained CDK1 activity, consisten

77 aryotic cell cycle and point to a coordinate mitotic control of lipid metabolism.

78 r Ana3 nor Rcd4 participates directly in the mitotic conversion of centrioles to centrosomes, but bot

79 Copy number alterations often occur in mitotic crises, and lead to simultaneous gains of chromo

80 romosomal events resulting from interhomolog mitotic cross-overs.

81 easure the frictional forces produced by the mitotic crosslinking protein PRC1 that resist microtubul

82 rther mitotic marker analysis re-stated that mitotic cycle continues until stage 5.

83 the hydrophobic patch, on the fission yeast mitotic cyclin Cdc13 as a potential mechanism to correct

84 Two mitotic cyclin types, cyclin A and B, exist in higher eu

85 1 and IGS2 physically interact with GSCs and mitotic cysts to control GSC maintenance and cyst format

86 The mitotic deacetylase complex (MiDAC) is a recently identi

87 umber and mitotic delay, further implicating mitotic defects in interneuron loss.

88 for improving patient outcomes by enhancing mitotic defects induced by taxanes alone.

89 Mitotic defects often trigger apoptosis, impairing cell

90 ctasia mutated (ATM), and exhibited multiple mitotic defects.

91 loss fails to rescue interneuron number and mitotic delay, further implicating mitotic defects in in

92 Reeler mutations that shifted neuronal post-mitotic development were sufficient to alter glial layer

93 male gametophyte development, the asymmetric mitotic division of an undetermined unicellular microspo

94 DNA methylation, is stably propagated during mitotic division.

95 tease activity is required for supernumerous mitotic divisions of the mat3-4 cells.

96 ed to predict: chronological age, mortality, mitotic divisions, or telomere length.

97 rather mitotic progression was impaired and mitotic DNA synthesis triggered.

98 disrupting the establishment of asynchronous mitotic domains leads to aberrant mitotic cell division

99 ell division such as chromosome segregation, mitotic duration and cytokinesis.

100 dent induction of aneuploidy associated with mitotic dysfunction and the identification of the phosph

101 tablished cell lines probably underestimates mitotic dysfunction in advanced human cancers.

102 cular logic for the concurrent activation of mitotic enhancers and suppression of meiotic enhancers i

103 changes in Cdk1 activity are permissive for mitotic entry and exit but that the changes in PP2A-B55

104 We conclude that the nucleus accelerates mitotic entry and propose that it acts as a pacemaker fo

105 Thus, the spatial pattern of mitotic entry can differentially regulate tissue shape t

106 ose that high Polo-kinase activity following mitotic entry directs the RZZ complex to minimize premat

107 f YTHDF2 in HeLa cells leads to the delay of mitotic entry due to overaccumulation of negative regula

108 nation, which relies on apical constriction, mitotic entry in an artificially contractile ectoderm in

109 While premature mitotic entry inhibits mesoderm invagination, which reli

110 The model starts at mitotic entry initiated by the activities of Cyclin-depe

111 tive live-cell imaging, we demonstrated that mitotic entry reverses apical contractility by interferi

112 ELK and indicate that MELK inhibition delays mitotic entry, likely via transient G(2)/M checkpoint ac

113 orm a feedforward regulatory loop to promote mitotic entry.

114 eraction between CDK1 and PP2A in regulating mitotic entry.

115 Loss of cyclin A in G2-phase prevents mitotic entry.

116 , whether and how MCAK activity required for mitotic error correction is regulated by alpha-tubulin d

117 Mitotic error correction relies on the kinesin-13 MCAK,

118 y was required and sufficient to correct the mitotic errors caused by excessive alpha-tubulin detyros

119 ing hepatocytes to estimate the frequency of mitotic errors during regeneration.

120 in nontumorigenic prostate epithelial cells, mitotic errors ensued, producing aneuploid, and multinuc

121 bnormalities in human blastocysts arise from mitotic errors in around 70% of cases.

122 ues during chronic damage without generating mitotic errors, and aneuploidy is not commonly observed

123 fitness, changes in gene expression, or more mitotic errors.

124 proteins that were significantly enriched on mitotic ESC chromosomes.

125 The final barrier to mitotic establishment corresponds to nuclear envelope br

126 Strikingly, a subset of mitotic events results in a short pulse of ERK inactivit

127 important role in the regulation of several mitotic events, and in hematological malignancies, AURKA

128 sphatase occurs only after completion of key mitotic events.

129 Disrupting UHRF1 degradation at mitotic exit accelerates G1-phase cell cycle progression

130 atase Cdc14, whose activity is essential for mitotic exit and completion of the cell cycle.

131 on switch coordinating E2F8 degradation with mitotic exit and the activation of APC/C(Cdh1).

132 Mitotic exit and the re-initiation of transcription are

133 sion cycle protein 20 (CDC20), and ends upon mitotic exit mediated by APC/C bound to CDC20 homolog 1

134 The Mitotic Exit Network (MEN), a budding yeast Ras-like sig

135 g the early stages of mitosis(8), but during mitotic exit the brushes collapse and Ki-67 promotes chr

136 Here we show that Hog1 delays mitotic exit when cells are stressed during metaphase.

137 NuMA affects chromatin decondensation at the mitotic exit, and nuclear shape in interphase.

138 During mitotic exit, however, centrosomes are deformed and frac

139 Deficiencies in RepID, CRL4 or RBBP7 delay mitotic exit, increase genomic instability and enhance s

140 At mitotic exit, such trapping of Lem2-Nur1 on heterochroma

141 B drives the bulk of changes observed during mitotic exit.

142 biquitinates the SAC mediator BUB3 to enable mitotic exit.

143 zing cell survival upon stress by regulating mitotic exit.

144 tform to test hypotheses about regulation of mitotic exit.

145 "adaptor" BicD2, both in neurons and in non-mitotic fibroblasts.

146 cen mRNA localization to centrosomes ensures mitotic fidelity.

147 tromeres epigenetically and is essential for mitotic fidelity.

148 of several parameters such as the density of mitotic figures, and BrdU and proliferating cell nuclear

149 inetochore must harness, transmit, and sense mitotic forces, as a lack of tension signals incorrect c

150 hly flexible, a feature important for CENP-A mitotic functions.

151 tivation of a FOXM1-CDK1 circuit that drives mitotic gene expression and DNA damage.

152 failure of this process dramatically alters mitotic gene expression.

153 oceeds, the Pax6 expression changes from the mitotic germinal zone in the ventricular zone to become

154 describe the protocols developed to produce mitotic gynogenes, and from these the first clonal lines

155 taining mitotic H3K4me1 or locally retaining mitotic H3K27ac are associated with cell type-specific g

156 Enhancers globally retaining mitotic H3K4me1 or locally retaining mitotic H3K27ac are

157 e detailed comparisons between molecular and mitotic histories.

158 ic mice are important tools for tracking the mitotic history of murine HSCs in label dilution experim

159 d somatically expressed MEILB2-BRME1 impairs mitotic HR.

160 Rdh54 help to define their functions during mitotic HR.

161 hat kindlin-2 maintains spindle integrity in mitotic human cells.

162 A patients, TGF-beta1 levels correlated with mitotic index, Breslow index and melanoma growth rate, a

163 CDKA1, the ortholog of the yeast and animal mitotic inducer CDK1, regulates the critical size for co

164 assical chemotherapeutics and the potency of mitotic kinase inhibitors to generate a class of high-pr

165 fly neural stem cells (neuroblasts) that the mitotic kinase Polo and its centriolar protein substrate

166 tion system to discover that Cdk1, the major mitotic kinase that drives the cell cycle, phosphorylate

167 nd it reveals a scaffolding role for the key mitotic kinase, Cyclin B1:CDK1, which ultimately helps t

168 oring protein Gravin restricts the action of mitotic kinases and cell-cycle effectors to defined mito

169 Inhibitors of essential mitotic kinases exemplify this paradigm shift, but intol

170 Aurora kinases (AURKA and AURKB) are mitotic kinases with an important role in the regulation

171 uction of diverse cytokines, and shutdown of mitotic kinases, resulting in cell cycle arrest.

172 One such target is the mitotic kinesin KIF11, which can be inhibited with ispin

173 e CPC subunits, survivin and INCENP, and the mitotic kinesin-like protein 2 (MKLP2) in targeting to t

174 We have recently demonstrated that a 'mitotic' kinesin-6 (Pavarotti in Drosophila) effectively

175 SCNT, the transferred nucleus first enters a mitotic-like state (premature chromatin condensation).

176 However, our further mitotic marker analysis re-stated that mitotic cycle con

177 increased numbers of CD45(+) leukocytes and mitotic markers (phosphorylated histone H(3) and phospho

178 ls to re-enter cell division by establishing mitotic microtubule arrays.

179 n-8, pericentrin compactness is lessened and mitotic microtubule length is shortened, as demonstrated

180 tein that localizes to the division site and mitotic microtubules and plays a critical role in divisi

181 Therefore, we aimed to establish a mitotic model by transiently expressing D-type cyclins i

182 moesin, the only ERM in Drosophila, controls mitotic morphogenesis and epithelial integrity.

183 Post-mitotic neuronal migration in the developing cerebral co

184 and specific transcriptional changes in post-mitotic neurons that delineate hierarchical regulatory s

185 rs2 null NSCs can still transition into post-mitotic neurons, but fail to undergo terminal differenti

186 ns and damaged organelles are vital for post-mitotic neurons.

187 ween microtubule-sliding in mitosis and post-mitotic neurons.

188 ion, and axo-dendritic specification in post-mitotic neurons.

189 that does not exchange with NPCs even after mitotic NPC breakdown.

190 IPs (Dll1+) extensively targeted contacts to mitotic NSCs (Notch active), revealing a substrate for c

191 d how this process contributes to subsequent mitotic nuclear envelope (NE) remodeling remains unclear

192 tissue architecture during growth influence mitotic nuclear migration.

193 Basal displacement of mitotic nuclei in the retinal neuroepithelium was observ

194 clear bodies, ensuring its availability upon mitotic onset.

195 hromosome was previously observed to adopt a mitotic organisation distinct from that of surrounding m

196 primarily due to aneuploidies of meiotic or mitotic origin.

197 he frog egg helped identify the cyclin-based mitotic oscillator and how this approach quickly merged

198 s the Wnt5a (-/-) phenotype, perturbing post-mitotic pathfinding and leading to apoptosis.

199 We describe an unexpected mitotic peak in the abundance of ergosterol and thiamine

200 n to abDGCs develops during a prolonged post-mitotic period and running scales both SST and PV synapt

201 The delay was observed throughout all mitotic phases in live cell imaging using GFP-labeled H2

202 However, because of the prominent mitotic phenotype upon NuMA loss, its precise function i

203 Genetic complementation of mitotic phenotypes identifies a novel KLTF peptide motif

204 K1, ATG13, ATG14, and TFEB, we show that the mitotic phosphorylation of these autophagy regulators, i

205 s with a newly evolved H2A variant lacking a mitotic phosphorylation site.

206 ic centriole over-elongation is dependent on mitotic Polo-like kinase 1, which we uncover as a novel

207 norhabditis elegans zygote, we show that the mitotic Polo-like kinase PLK-1 phosphorylates the lamin

208 und no lagging chromosomes or micronuclei in mitotic polyploid cells.

209 ons could play prominent roles in regulating mitotic processes.

210 ecies during mitosis in cancer by disturbing mitotic progression and simultaneously inhibiting the hy

211 A, cyclin B and Greatwall kinase coordinate mitotic progression by increasing levels of Cdk1-depende

212 itor restored taxane sensitivity by inducing mitotic progression errors and apoptosis.

213 over that Magoh deficiency delays progenitor mitotic progression in a dosage-sensitive fashion, with

214 ccumulation of genomic 8-oxodG and perturbed mitotic progression in cancer cells, which can be exploi

215 icient fibroblasts exhibit a marked delay in mitotic progression that can be rescued by lentiviral tr

216 on fork progression was observed, but rather mitotic progression was impaired and mitotic DNA synthes

217 y of human AURORA-A kinase (AURKA) regulates mitotic progression, and its frequent overexpression in

218 kinase activity might not grossly impact on mitotic progression, while treatment with MRE11A inhibit

219 or NBN did not show a significant slowing of mitotic progression.

220 rate, inhibiting CDH1 activity and promoting mitotic progression.

221 en two broad growth and survival strategies: mitotic proliferation or meiotic differentiation into a

222 n of meiotic enhancers in the somatic and/or mitotic proliferation phases.

223 t simulates temporal changes in 12 different mitotic proteins and associated protein complexes in mul

224 The phosphorylation of mitotic proteins is bistable, which contributes to the d

225 n B can enter mitosis and phosphorylate most mitotic proteins, because of parallel PP2A:B55 phosphata

226 d multiple mechanisms of degradations of the mitotic proteins.

227 growth phase, Breslow thickness, ulceration, mitotic rate, regression, and lymphovascular invasion we

228 ts highlight the importance of primary tumor mitotic rate.

229 s correlated with nocturnal hypoxemia and CM mitotic rate.

230 om DNA methylation maintenance errors during mitotic rather than during meiotic cell divisions.

231 f Wnt signaling and Chk1 expression leads to mitotic re-entry and the concomitant upregulation of Dpp

232 ested tracheoblasts and are downregulated at mitotic re-entry.

233 alk." An example is human Pin1, an essential mitotic regulator consisting of a Trp-Trp (WW) domain fl

234 t analogy, an interaction between the master mitotic regulator cyclin B1 and the spindle checkpoint c

235 It is a known mitotic regulator, and it is well-described that KIF11 i

236 APC/C activity promotes proteolysis of other mitotic regulators.

237 lin B1-Cdk is the primary kinase that drives mitotic remodeling; here we show that it is targeted to

238 incorporation of 8oxodG into the DNA during mitotic replication and increased toxicity.

239 Taken together, our data unravel a mitotic role of RAD50 that can be separated from its kno

240 here has been a growing appreciation for non-mitotic roles for KIF11.

241 to pattern the cortex during the process of mitotic rounding is sufficient to translate interphase s

242 correlate with cardiomyocyte inefficiency in mitotic rounding, a process which is key to successful c

243 ignaling to alter cell mechanics and enhance mitotic rounding, so that Ras(V12)-expressing cells are

244 We performed SisterC on mitotic Saccharomyces cerevisiae cells.

245 tic chromosome that serves as a platform for mitotic signaling and possesses unique biophysical prope

246 e assembly checkpoint (SAC), thus undergoing mitotic slippage due to defective AURKB and impaired SAC

247 Mitotic slippage involves cells exiting mitosis without

248 A further level of control of the timing of mitotic slippage is through p31(comet)-mediated suppress

249 1, cumulating in the cell exiting mitosis by mitotic slippage.

250 outer radial glial cells (oRGs) and undergo mitotic somal translocation (MST) during division.

251 erived oRG-like cells undergo characteristic mitotic somal translocation behavior previously only obs

252 Notably, the two mitotic SPBs are affected in an asymmetric manner such t

253 permatocyte, followed by the change from the mitotic spermatogonia to early meiotic spermatocyte.

254 c centrosome, a structure that assembles the mitotic spindle [1], is notably large in the zebrafish e

255 e polarized orientation of the S. cerevisiae mitotic spindle and primes the invariant inheritance of

256 trioles organize the microtubule network and mitotic spindle and, as basal bodies, nucleate cilia and

257 motor proteins that play important roles in mitotic spindle assembly [1].

258 The essential functions required for mitotic spindle assembly and chromosome biorientation an

259 protein that we previously found to control mitotic spindle assembly and chromosome dynamics.

260 our study highlight that kindlin-2 regulates mitotic spindle assembly and that this process is pertur

261 neuroblasts and human cancer cells to study mitotic spindle assembly in polyploid cells, we found th

262 at range from retrograde axonal transport to mitotic spindle assembly(1,2).

263 egregation during cell division is driven by mitotic spindle attachment to the centromere region on e

264 is extensively reorganized so that a bipolar mitotic spindle can be correctly assembled.

265 Mitotic spindle length, for example, varies several-fold

266 The tail is essential for mitotic spindle localization, which becomes severely red

267 nein motor function/localization that alters mitotic spindle orientation, chromosomal segregation, an

268 The microtubules that form the mitotic spindle originate from microtubule-organizing ce

269 Factors that regulate mitotic spindle positioning remain unclear within the co

270 Sperm-associated Antigen 5 (SPAG5) is a mitotic spindle protein.

271 The KSP inhibitor targets the mitotic spindle through mechanisms independent of microt

272 ular functions including organization of the mitotic spindle to ensure faithful chromosome segregatio

273 velope enables chromosome segregation by the mitotic spindle(1).

274 ate chromosomes in mitosis, cells assemble a mitotic spindle, a molecular machine with centrosomes at

275 centromeric chromatin to microtubules of the mitotic spindle, enabling sister chromatid segregation i

276 KIF15 and MAD1L1 suggest a possible role of mitotic spindle-assembly genes in IPF susceptibility.

277 ures ranging from contractile bundles to the mitotic spindle.

278 eiotic spindle assembly but is toxic for the mitotic spindle.

279 ubule cytoskeleton and form the poles of the mitotic spindle.

280 pull on astral microtubules to position the mitotic spindle.

281 lum, the subpellicular microtubules, and the mitotic spindle.

282 rating animal cells are able to orient their mitotic spindles along their interphase cell axis, setti

283 Kinesin-5 motors organize mitotic spindles by sliding apart microtubules.

284 atment leads to disorientation of Plasmodium mitotic spindles during the asexual reproduction and res

285 til all chromosomes are properly attached to mitotic spindles.

286 ia infectious spread (de novo infection) and mitotic spread (infected cell proliferation), creating a

287 The relative contributions of infectious and mitotic spread to HTLV-1 persistence are unknown, and wi

288 We estimate the ratio of infectious to mitotic spread using a hybrid model of deterministic and

289 , whereas a decrease in active Polo in later mitotic stages allows the formation of stable amphitelic

290 Here, we examined the late mitotic stages NPCs in vivo and mouse embryonic fibrobla

291 prolonged mitosis due to extension of early mitotic stages.

292 kinases and cell-cycle effectors to defined mitotic structures.

293 ng mitosis and pathologically activating the mitotic surveillance pathway in the developing brain.

294 d mitosis was rescued by inactivation of the mitotic surveillance pathway.

295 s commit rapidly proliferating cells to post-mitotic terminal differentiation.

296 Cells in largely non-mitotic tissues such as the brain are prone to stochasti

297 However, the mechanisms that underlie mitotic transcriptional regulation are unclear.

298 Thus, TRIM37 is an essential determinant of mitotic vulnerability to PLK4 inhibition.

299 s, but what determines the spatial origin of mitotic waves remains unclear.

300 ators and influence the emergent behavior of mitotic waves.