ライフサイエンスコーパス: catastrophe

1 er without suffering from the 'superposition catastrophe'.

2 replication in a process known as the 'dimer catastrophe'.

3 hment and/or mitotic podocyte death (mitotic catastrophe).

4 it may lead to aberrant mitosis (ie, mitotic catastrophe).

5 tion stress and oncogene-induced replication catastrophe.

6 mitosis, resulting in cell death by mitotic catastrophe.

7 ng the possibility of a future public health catastrophe.

8 mediator of CDK2 inhibition-driven anaphase catastrophe.

9 antagonized CDK2 inhibitor-mediated anaphase catastrophe.

10 ic dissection remains the most common aortic catastrophe.

11 ic arrest then led to cell death via mitotic catastrophe.

12 itosis where they ultimately died by mitotic catastrophe.

13 d for cell cycle progression undergo mitotic catastrophe.

14 exhibit prolonged mitosis and die of mitotic catastrophe.

15 nthrax had the potential to cause a national catastrophe.

16 int, and potentially a regulation point, for catastrophe.

17 agrees with that needed to cancel the polar catastrophe.

18 DNA replication, ultimately causing mitotic catastrophe.

19 ath, both of which are indicative of mitotic catastrophe.

20 system, leading to hypermutability and error catastrophe.

21 rs of nuclear vesicles indicative of mitotic catastrophe.

22 ction occurring to counteract a polarization catastrophe.

23 leads to a dramatic increase in microtubule catastrophe.

24 ip and ultimately contributes to microtubule catastrophe.

25 osis induced in vivo in part through mitotic catastrophe.

26 iminates Ras-activated cells through mitotic catastrophe.

27 ls from centrosome reduplication and mitotic catastrophe.

28 al impact over North America caused a global catastrophe.

29 checkpoint activation and resultant mitotic catastrophe.

30 " at the growing MT plus end that suppresses catastrophe.

31 Website following the 2011 tsunami-initiated catastrophe.

32 wild-type tumors arrested, avoiding mitotic catastrophe.

33 h the activation of stathmin and microtubule catastrophe.

34 ore than two centrosomes and undergo mitotic catastrophe.

35 fratentorial consequence of a supratentorial catastrophe.

36 population structure for extinction or error catastrophe.

37 d the frequency of radiation-induced mitotic catastrophe.

38 tic endoreduplication checkpoint and mitotic catastrophe.

39 ed ROS levels, culminating in a bioenergetic catastrophe.

40 cal crosslinking and by reducing rates of MT catastrophe.

41 at nearly all occur during a single cellular catastrophe.

42 ty of MT plus end movement by suppressing MT catastrophe.

43 ading to premature mitotic entry and mitotic catastrophe.

44 Cells live on the edge of a proteostasis catastrophe.

45 transition and results in increased mitotic catastrophe.

46 MLH1 promotes interstrand cross-link repair catastrophe.

47 that ultimately drove cells into replication catastrophe.

48 cleation and anchoring rather than promoting catastrophe.

49 and heat shock-induced death, and in mitotic catastrophe.

50 f RBM3 downregulation, cells undergo mitotic catastrophe.

51 GTP cap and an increase in the frequency of catastrophe.

52 ckpoints, resulting in cell death by mitotic catastrophe.

53 d environmental problems following a nuclear catastrophe.

54 rminal GDP-bound subunits without undergoing catastrophe.

55 ing about the molecular events that initiate catastrophe.

56 l concentration, at the expense of increased catastrophe.

57 haviors deliver organisms away from imminent catastrophe.

58 dance of replication catastrophe and mitotic catastrophe.

59 thways to counter this looming public health catastrophe.

60 rough mitosis, marked aneuploidy and mitotic catastrophe.

61 exchangeable nucleotide led to less frequent catastrophe.

62 on leading to apoptosis, defined as anaphase catastrophe.

63 tubule growth and increases the frequency of catastrophe.

64 ends where they reinforce growth and inhibit catastrophe.

65 forced expression of KLF14 leads to mitotic catastrophe.

66 vate extinction risk and signal an impending catastrophe.

67 g microtubule ends and on the time course of catastrophes.

68 as by reducing the frequency of microtubule catastrophes.

69 A suppresses microtubule growth and inhibits catastrophes.

70 slowing growth and, consequently, promoting catastrophes.

71 ly, primarily by decreasing the frequency of catastrophes.

72 persistent microtubule growth by suppressing catastrophes.

73 y, but they polymerize slower and have fewer catastrophes.

74 een gods and good governments in the face of catastrophes.

75 rescue and pauses, as well as in suppressing catastrophes.

76 afflicted with this "... most formidable of catastrophes."

77 hat promotes sudden depolymerization, termed catastrophe [1-4].

78 7 million) worldwide are driven to financial catastrophe-32.8 million (32.4-33.1 million) from the co

79 ng of the microtubule cytoskeleton by making catastrophe a first-order random process.

80 ac myocytes resulted in induction of mitotic catastrophe, a previously unreported event in cardiac my

81 t, dimerization is necessary for the EB anti-catastrophe activity in cells; this explains why the EB1

82 disorder Perry syndrome abrogates this anti-catastrophe activity.

83 These infrequent transitions, termed "catastrophes", affect numerous cellular processes but th

84 the haploid inducer, consistent with genomic catastrophes affecting a single, laggard chromosome comp

85 Mre11 appear to cooperate to prevent mitotic catastrophe after DNA replication arrest.

86 point function, leading to increased mitotic catastrophe and a modest increase in radiation sensitivi

87 sulting in centrosome reduplication, mitotic catastrophe and abrogation of cell proliferation.

88 omeric DNA end fusions, resulting in mitotic catastrophe and apoptosis; and 4) induction of chromosom

89 ly enter mitosis and ultimately face mitotic catastrophe and apoptotic cell death.

90 doubt on the existence of a Kauzmann entropy catastrophe and associated ideal glass transition.

91 opy, the generally accepted notions of polar catastrophe and cation intermixing for the metallic inte

92 Inactivation of SAE2 leads to mitotic catastrophe and cell death upon Myc hyperactivation.

93 transcription process, can lead to cellular catastrophe and disease.

94 e SAM domain is necessary to prevent meiotic catastrophe and ensure female fertility.

95 lete absence of Mtrm results in both meiotic catastrophe and female sterility.

96 Mechanisms of CDK2-mediated anaphase catastrophe and how activated KRAS enhances this effect

97 gation, multipolarity, misalignment, mitotic catastrophe and loss of spindle checkpoint, that are acc

98 reak formation, and avoidance of replication catastrophe and mitotic catastrophe.

99 own or overexpression coincided with mitotic catastrophe and multinucleation that are typically obser

100 pression, however, did not lead to metabolic catastrophe and rapid death of growth factor-deprived ce

101 e assembly checkpoint, and triggered mitotic catastrophe and reduced cell viability.

102 Control over MT catastrophe and rescue by Kip3 defines the length and li

103 tes MT dynamics by increasing frequencies of catastrophe and rescue events.

104 lternating between growth and shortening via catastrophe and rescue events.

105 nesin-8 motor Kip3 alternately mediates both catastrophe and rescue of the bud MT.

106 Our findings have implications for both catastrophe and rescue of the dynamic microtubule end, a

107 fter they are incorporated into the lattice; catastrophe and rescue result from stochastic fluctuatio

108 bud neck is maintained by spatial control of catastrophe and rescue, which extends MT lifetime >25-fo

109 he tip spontaneously progresses through both catastrophe and rescue.

110 in the depths of these cracks influence both catastrophe and rescue.

111 c KIF3CC as a unique promoter of microtubule catastrophe and substantiate its physiological role in c

112 rmalities lead to cell death through mitotic catastrophe and that cell death occurred also from inter

113 normal mitotic spindle formation and mitotic catastrophe and that deregulated FOXM1 and KIF20A expres

114 les, it is essential to prevent both meiotic catastrophe and the female sterility observed in mtrm/mt

115 ities which exhibit Anderson's orthogonality catastrophe and the Kondo effect.

116 GDP in the lattice dictates the frequency of catastrophe and the severity of rapid shrinking.

117 s in these conditions could induce metabolic catastrophe and therefore prove an effective antitumor t

118 pathways simultaneously resulted in mitotic catastrophe and tumor apoptosis and markedly reduced the

119 ondrial respiration, leading to bioenergetic catastrophe and tumour cell death.

120 d in nature, sometimes leading to unexpected catastrophes and disasters in seemingly normal condition

121 immunity and tolerance toward various immune catastrophes and inflammation.

122 ocytes becoming binucleate (mitotic podocyte catastrophe) and subsequent wrinkling of glomerular capi

123 every 8 nm, inhibits BtubAB mini microtubule catastrophe, and increases rescue.

124 ion of glycosomal enzymes, causing metabolic catastrophe, and it kills the parasite.

125 ng to four events, including growth, rescue, catastrophe, and pause.

126 fts induces premature mitotic entry, mitotic catastrophe, and reduction of tumor growth.

127 effects on microtubule dynamics: it induces catastrophes, and it increases growth velocity, as does

128 orphism-array profiling to show that genomic catastrophes are frequent in EAC, with almost a third (3

129 otubule growth times supported the view that catastrophes are microtubule age dependent.

130 inst repeated doses, and introducing mitotic catastrophe (as opposed to arbitrary delayed cell-death)

131 expression results in G2 arrest and mitotic catastrophe associated with failure of premitotic cytopl

132 This model shows a denaturation catastrophe at temperatures of 49-55 degrees C, roughly

133 n of Kip3, whereas the motor domain mediates catastrophe at the bud tip.

134 bition of Par3 and Trio restores microtubule catastrophe at the cell contact and rescues CIL and neur

135 of the cell, with an increase in microtubule catastrophe at the collision site during CIL.

136 ural crest migration by reducing microtubule catastrophe at the site of cell-cell contact and abrogat

137 opular illustration of ecological and social catastrophe attributed to deforestation.

138 Our focus on catastrophe avoidance provides a unique perspective for

139 paclitaxel and peloruside A, induce not only catastrophes but also rescues and can reverse the aging

140 les that includes not only the statistics of catastrophes but also the statistics of rescues.

141 llective goal, aimed at reducing the risk of catastrophe, but act as if they were blind to this risk.

142 d cell death by selectively limiting mitotic catastrophe, but not apoptosis.

143 injury, MDM2 drives podocyte loss by mitotic catastrophe, but the function of MDM2 in resting podocyt

144 ion by which animals can evacuate ecological catastrophes, but remain poorly studied in marine system

145 icrotubules are thought to be protected from catastrophe by a GTP-tubulin "cap": GTP-tubulin subunits

146 ns lead us to propose that stathmin promotes catastrophe by binding to and acting upon protofilaments

147 ur results suggest that stathmin can promote catastrophe by direct action on protofilament structure

148 ational modeling suggests that dynein delays catastrophe by exerting tension on individual protofilam

149 Furthermore, Par3 promotes microtubule catastrophe by inhibiting the Rac-GEF Trio, as double in

150 Eribulin amplifies a natural pathway toward catastrophe by promoting the arrest of protofilament elo

151 rophes, suggesting that in cells EBs prevent catastrophes by counteracting other microtubule regulato

152 -cycle checkpoints safeguard cells from such catastrophes by impeding cell-cycle progression when mis

153 It would be maladaptive to learn about catastrophes by trial and error alone.

154 But this yield catastrophe can be mitigated by using highly non-stoichi

155 The metabolic catastrophe caused by loss of Slc7a5 reflected the requi

156 The catastrophe caused massive destruction of homes and buil

157 tosis as a result of early mitotic entry and catastrophe compared to DDR-D cells.

158 ppraisal of the in situ pathology of mitotic catastrophe compared with other proposed types of podocy

159 sitions through phases of growth, pause, and catastrophe, continuously exploring and adapting to the

160 ut not in wild-type cells leading to mitotic catastrophe, defective cell division and apoptosis.

161 ent, which have been shown to induce mitotic catastrophe-dependent senescence.

162 on and underwent proliferative and metabolic catastrophe early after encountering antigen.

163 e a survival mechanism against environmental catastrophes even when they are rare.

164 Thus, the likelihood of a catastrophe event may be intimately linked to the aging

165 units at the microtubule tip, resulting in a catastrophe event.

166 ame time, Kif15 motors cooperate to suppress catastrophe events at polymerizing microtubule plus-ends

167 icrotubule-associated proteins could promote catastrophe events in part by modifying microtubule tip

168 are two separate factors that contribute to catastrophe events in the 3D simulation: the GTP-tubulin

169 To investigate microtubule catastrophe events, we performed 3D mechanochemical simu

170 oot hair tip growth by promoting microtubule catastrophe events.

171 soluble tubulin and its ability to act as a catastrophe factor by directly binding to the microtubul

172 l imaging, that p150(Glued) is a potent anti-catastrophe factor for microtubules.

173 Thus, dynactin acts as an anti-catastrophe factor that extends microtubule growth poste

174 o the microtubule plus-end, acts as a potent catastrophe factor through an increase in microtubule ca

175 pse remodeling, and its function involves MT catastrophe factors including kinesin-13/KLP-7 and spast

176 strophe is different from the well-described catastrophe factors kinesin-13 MCAK and kinesin-8 Kip3/K

177 e propose that Prc1E and Kif4, together with catastrophe factors, promote "anti-parallel pruning" tha

178 Thus, both kinesins are catastrophe factors; Kip3 mediates fine control of micro

179 llular ATP-inducing cell death by "metabolic catastrophe." Finally, xenograft analysis confirmed the

180 SLX4 complex is critical to prevent mitotic catastrophe following common fragile site expression.

181 otubules with these mutations have decreased catastrophe frequencies and increased average lifetimes

182 Microtubules with betaIIB have catastrophe frequencies approximately threefold lower th

183 eated by B-lattice seeds, yet have increased catastrophe frequencies at both ends.

184 These chimeras have catastrophe frequencies similar to that of the correspon

185 , microtubule growth rate distributions, and catastrophe frequencies, we found that all tested mutant

186 ch perturbs microtubule growth by increasing catastrophe frequency and inhibits axon extension during

187 bules in ark1-1 root hairs exhibited reduced catastrophe frequency and slower growth velocities, both

188 the absence of the kinesins, the microtubule catastrophe frequency depends on the age of the microtub

189 , and by increasing the switching frequency (catastrophe frequency) from growth to shortening at plus

190 he factor through an increase in microtubule catastrophe frequency, and does so by elimination of the

191 increases MT rescue frequency, decreases MT catastrophe frequency, and moderately decreases MT disas

192 on for its effects on microtubule growth and catastrophe frequency, which cause microtubules to be mo

193 with dramatically reduced shrinking rate and catastrophe frequency.

194 d fluorescent protein) increased microtubule catastrophe frequency.

195 dynamic microtubules (MTs) by reducing their catastrophe frequency.

196 ncreasing the growth rate and decreasing the catastrophe frequency.

197 he global population is at risk of financial catastrophe from surgery.

198 These findings suggest that genomic catastrophes have a significant role in the malignant tr

199 molog of Xenopus gene which Prevents Mitotic Catastrophe (hPMC2).

200 Mitotic catastrophe implies that mitotic podocytes eventually de

201 s massive ssDNA accumulation and replication catastrophe in a fraction of early S-phase cells.

202 disease, constitute an ongoing public health catastrophe in both the developed and, more recently, th

203 on of FF could selectively trigger metabolic catastrophe in glioblastoma cells.

204 us Chk1- and MK2 inhibition leads to mitotic catastrophe in KRAS-mutant cells.

205 es show centrosome reduplication and mitotic catastrophe in osteosarcoma cells inducibly expressing a

206 te for telomerase and the source of telomere catastrophe in Rtel1(-/-) cells.

207 The sudden environmental catastrophe in the wake of the end-Cretaceous asteroid i

208 lines, ATRi selectively induced replication catastrophe in those harboring high APOBEC3A and/or APOB

209 n patterns have been suggested to foreshadow catastrophes in a wide variety of systems.

210 andemic of 1918 was one of the worst medical catastrophes in human history.

211 mplified models of dynamic microtubules, the catastrophes in this model arise owing to fluctuations i

212 ure according to the baseline probability of catastrophe, in agreement with theoretical predictions.

213 lowed by stochastic switching events termed "catastrophes," in which microtubules suddenly undergo ra

214 In interphase, it promotes microtubule catastrophe; in mitosis, it contributes to anaphase chro

215 2 years of their rule in Germany resulted in catastrophes including World War II, the most destructiv

216 s ATM-dependent and mediated through mitotic catastrophe independently of apoptosis.

217 model is that stathmin promotes microtubule catastrophe indirectly, and does so by sequestering tubu

218 Extinction catastrophe induced by promutagenic nucleosides has been

219 ell cycle checkpoint activation, and mitotic catastrophe-induced apoptotic cell death.

220 of discordant microtubules through frequent catastrophe-inducing collisions among microtubules.

221 straints against which theoretical models of catastrophe induction can be tested.

222 We found that EBs promote microtubule catastrophe induction in the presence of all MTAs tested

223 aints on the possible molecular mechanism of catastrophe induction.

224 We propose that catastrophe inhibition by SLAIN2 and CLASP1 supports mes

225 However, SLAIN2-dependent catastrophe inhibition determines microtubule resistance

226 kinesin Kip2 is a microtubule polymerase and catastrophe inhibitor in vitro that uses its processive

227 n two centrosomes and, indicative of mitotic catastrophe, irregularly shaped nuclei or multiple micro

228 the age of the microtubule, indicating that catastrophe is a multistep process.

229 refore, the ATP-promoted KIF3CC mechanism of catastrophe is different from the well-described catastr

230 s for sudden loss of the GTP cap, leading to catastrophe, is not known.

231 r the end of a growth phase, an event called catastrophe, is still not understood.

232 king protein (+TIP) SLAIN2, which suppresses catastrophes, is not required for 2D cell migration but

233 ese increasingly large fires are 'ecological catastrophes.' Landscape-scale severe burning was catast

234 or pushing a viral population over its error catastrophe limit, as observed before in cell culture st

235 or rate of viral replication above the error catastrophe limit.

236 WGS of 22 EAC cases show that catastrophes may lead to oncogene amplification through

237 y are hallmarks of radiation-induced mitotic catastrophe (MC), a common phenomenon occurring in tumor

238 g microtubule stability through a novel anti-catastrophe mechanism regulated by tissue-specific isofo

239 ansition can be explained through the "polar catastrophe" mechanism arising from the divergence of th

240 bridging, nuclear fragmentation, and mitotic catastrophe, mirroring the effects of HDACi on cancer ce

241 red overspill evolution providing a tool for catastrophe mitigation and future planning.

242 Here we have developed the original dimer catastrophe model by incorporating copy number variance

243 Employing a modified "polar catastrophe" model, we demonstrate that the nanowire het

244 ith nocodazole were found to undergo mitotic catastrophe more readily when endogenous caspase-2 was r

245 However, after cold-induced catastrophe, MT regrowth is accelerated in San-siRNA cel

246 ing metaphase, ultimately leading to mitotic catastrophe, multinucleation, and the loss of stemness.

247 million years ago one of the largest cosmic catastrophes occurred in our solar system since the accr

248 Mitotic catastrophe occurs when cells enter mitosis with damaged

249 th temperature coincides with a denaturation catastrophe of its proteome.

250 mediate chromosome congression by promoting catastrophe of long kinetochore microtubules (kMTs).

251 nd centrosome protein CP110 induced anaphase catastrophe of lung cancer cells.

252 microtubules, dynein delayed barrier-induced catastrophe of microtubules.

253 era, Indonesia, caused the greatest volcanic catastrophe of the last 100 kyr, climactically erupting

254 ers multipolar spindle formation and mitotic catastrophe, offering an attractive therapeutic approach

255 A damage before cells display severe mitotic catastrophe or apoptosis.

256 ends and are sufficient to either trigger a catastrophe or induce slow and erratic microtubule growt

257 In the absence of catastrophe or large fertility reductions (to fewer than

258 eyond the threshold of viability, extinction catastrophe or lethal mutagenesis, was proposed over a d

259 y at the plus ends of long MTs, promoting MT catastrophes or pausing.

260 IR) by inducing apoptosis, necrosis, mitotic catastrophe, or permanent growth arrest.

261 normal aging of a cell, followed by a short catastrophe phase in which noise increased.

262 Recently, a chromosome catastrophe phenomenon termed chromothripsis, in which n

263 f stathmin to tubulin or microtubules or its catastrophe-promoting activity.

264 tically toward the steady-state level of the catastrophe-promoting configurations.

265 Rac1 distribution and parameters such as the catastrophe-promoting constant and tubulin association r

266 For catastrophe-promoting stathmin, we do not find bistabili

267 We investigate both tubulin sequestering and catastrophe promotion as mechanisms for MT growth inhibi

268 a global decrease in stathmin levels, an MT catastrophe protein, in activated macrophages using both

269 s so by elimination of the dependence of the catastrophe rate on microtubule lifetime.

270 Moreover, KIF3CC accelerates the catastrophe rate without altering the microtubule growth

271 -stathmin-MT pathway in which the growth and catastrophe rates of MTs are regulated by cytosolic stat

272 hese results have important consequences for catastrophe regulation in cells, as microtubule-associat

273 hanistic model for the phenomenon of mitotic catastrophe, relying on a combination of unregulated, mu

274 In the absence of Klp5/6, microtubule catastrophe/rescue frequency and dynamicity are suppress

275 ted cells that then arrest or die by mitotic catastrophe, revealing a new role for Myc in the profici

276 e effect of surgical conditions on financial catastrophe should be quantified so that any financial r

277 e lattice of MTs within the bud, yet induces catastrophe spatially near the bud tip.

278 form invasive pseudopods because it prevents catastrophes specifically at their tips.

279 s a priori for handling wastes from combined catastrophes such as those recently observed in Japan.

280 th that resembles a necrotic form of mitotic catastrophe suggesting that CD95 protects cancer cells f

281 ration, inhibition of apoptosis, and mitotic catastrophe, suggesting an important potential mechanism

282 ied tubulin, EBs promote rather than inhibit catastrophes, suggesting that in cells EBs prevent catas

283 ong decrease in the microtubule frequency of catastrophes, suggesting that KIF3C functions as a micro

284 gh their action on microtubule ends, because catastrophe suppression does not require the EB domains

285 step inhibition described by a mathematical catastrophe that results in growth hysteresis, character

286 Finally, we describe the fitness catastrophes that result from the prevailing evolutionar

287 The compounded impacts of the catastrophes that resulted from the Great East Japan Ear

288 question is how regulatory proteins modulate catastrophe, the conversion from growth to shortening.

289 Catastrophe-the switch from growing to shrinking-occurs

290 ia the long-hypothesized mechanism of "error catastrophe." The findings also support a role for prion

291 Employing the catastrophe theory principles we show that these states

292 y, instability mechanisms, chaos theory, and catastrophe theory, offer potent models that can be appl

293 tes mitotic transition and increases mitotic catastrophe, thereby inhibiting glioma development and p

294 idelity, despite error rates above the error catastrophe threshold.

295 The probability for a catastrophe to occur increases with microtubule age, put

296 Importantly, mitotic catastrophe was also confirmed in isolated adult cardiac

297 d state, which displays hallmarks of mitotic catastrophe, was prevented by expression of either the E

298 the distribution of maximum lengths prior to catastrophe, whereas MCAK promotes rapid restructuring o

299 promoting microtubule growth and suppressing catastrophe, whereas, in contrast, EB2 does not play a d

300 falciparum malaria has been a global health catastrophe, yet much about the CQ resistance (CQR) mech