ライフサイエンスコーパス: catastrophe

1 er without suffering from the 'superposition catastrophe'.

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

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

4 ore repair is completed resulting in mitotic catastrophe.

5 ed ROS levels, culminating in a bioenergetic catastrophe.

6 that ultimately drove cells into replication catastrophe.

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

8 rogression, and both replication and mitotic catastrophe.

9 ckpoints, resulting in cell death by mitotic catastrophe.

10 d environmental problems following a nuclear catastrophe.

11 rminal GDP-bound subunits without undergoing catastrophe.

12 ing about the molecular events that initiate catastrophe.

13 ng microtubule pausing typically followed by catastrophe.

14 l concentration, at the expense of increased catastrophe.

15 haviors deliver organisms away from imminent catastrophe.

16 dance of replication catastrophe and mitotic catastrophe.

17 thways to counter this looming public health catastrophe.

18 exchangeable nucleotide led to less frequent catastrophe.

19 on leading to apoptosis, defined as anaphase catastrophe.

20 tubule growth and increases the frequency of catastrophe.

21 ends where they reinforce growth and inhibit catastrophe.

22 forced expression of KLF14 leads to mitotic catastrophe.

23 vate extinction risk and signal an impending catastrophe.

24 nuclease cleavage, resulting in replication catastrophe.

25 tion stress and oncogene-induced replication catastrophe.

26 mitosis, resulting in cell death by mitotic catastrophe.

27 mediator of CDK2 inhibition-driven anaphase catastrophe.

28 antagonized CDK2 inhibitor-mediated anaphase catastrophe.

29 ic dissection remains the most common aortic catastrophe.

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

31 itosis where they ultimately died by mitotic catastrophe.

32 d for cell cycle progression undergo mitotic catastrophe.

33 exhibit prolonged mitosis and die of mitotic catastrophe.

34 nthrax had the potential to cause a national catastrophe.

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

36 agrees with that needed to cancel the polar catastrophe.

37 personally and professionally by this global catastrophe.

38 DNA replication, ultimately causing mitotic catastrophe.

39 system, leading to hypermutability and error catastrophe.

40 -derived polioviruses, and counteracts error catastrophe.

41 rs of nuclear vesicles indicative of mitotic catastrophe.

42 ction occurring to counteract a polarization catastrophe.

43 leads to a dramatic increase in microtubule catastrophe.

44 ip and ultimately contributes to microtubule catastrophe.

45 osis induced in vivo in part through mitotic catastrophe.

46 ls from centrosome reduplication and mitotic catastrophe.

47 al impact over North America caused a global catastrophe.

48 checkpoint activation and resultant mitotic catastrophe.

49 to chromothripsis, a form of extreme genomic catastrophe.

50 apoptotic cell death in S-phase and mitotic catastrophe.

51 ts are important determinants of microtubule catastrophe.

52 bility transition pore (mPTP), is a cellular catastrophe.

53 tion and exacerbated ribavirin-induced error catastrophe.

54 nprotected ssDNA has been termed replication catastrophe.

55 modelled as proliferation-dependent mitotic catastrophe.

56 off-rate to specifically suppress minus-end catastrophe.

57 es, and vulnerability to anaphase or mitotic catastrophe.

58 of action of BETi in TNBC, that is, mitotic catastrophe.

59 ls lacking cyclin F leads to DNA replication catastrophe.

60 tubulin biochemistry improved predictions of catastrophe.

61 use persistent fork stalling and replication catastrophe.

62 nal accommodation can improve predictions of catastrophe.

63 ated DNA to enter mitosis leading to mitotic catastrophe.

64 ginning of evolution, even before the oxygen catastrophe.

65 nt RNA replication mechanisms, namely, error catastrophe.

66 d aberrant mitosis and cell death by mitotic catastrophe.

67 utations in viral RNA genomes leads to error catastrophe.

68 a mechanism for viruses to counteract error catastrophe.

69 poliovirus to evade ribavirin-induced error catastrophe.

70 iminates Ras-activated cells through mitotic catastrophe.

71 rough mitosis, marked aneuploidy and mitotic catastrophe.

72 ng the possibility of a future public health catastrophe.

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

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

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

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

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

78 as by reducing the frequency of microtubule catastrophes.

79 A suppresses microtubule growth and inhibits catastrophes.

80 ruct structural reforms intended to mitigate catastrophes.

81 ules combine very fast growth and infrequent catastrophes.

82 ed to consider long-term consequences of the catastrophes.

83 sticity, vital rate covariance, and periodic catastrophes.

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

85 7 million) worldwide are driven to financial catastrophe-32.8 million (32.4-33.1 million) from the co

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

87 disorder Perry syndrome abrogates this anti-catastrophe activity.

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

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

90 s render picornaviruses susceptible to error catastrophe, an overwhelming accumulation of mutations i

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

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

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

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

95 further depleting NAD+ to cause an energetic catastrophe and cell death.

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

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

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

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

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

101 ease in cell death resulted from a metabolic catastrophe and knockout cells displayed severely distur

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

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

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

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

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

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

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

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

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

111 he tip spontaneously progresses through both catastrophe and rescue.

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

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

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

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

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

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

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 lity is governed by the costs of the "coding-catastrophe", and can be explained by a concurrent decli

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

124 interplay with cellular senescence, mitotic catastrophe, and autophagy.

125 ells become PARPi sensitive, undergo mitotic catastrophe, and die.

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

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

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

129 eased the amount of polymer assembled before catastrophes, and decreased the frequency of microtubule

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

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

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

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

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

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

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

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

138 mutants is a consequence of replication fork catastrophes at centromeres.

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

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

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

142 e virus resistant to ribavirin-induced error catastrophe, but only when RNA recombination was at wild

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

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

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

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

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

153 n the immediate death and suffering that the catastrophes cause for fellow humans, rather than on the

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

155 birth-and-death process by the occurrence of catastrophes: cell rupture events that affect all bacter

156 iple effects of its loss: G2 arrest, mitotic catastrophe, chromosome mis-segregation / aneuploidy due

157 ion, confirming that ribavirin-induced error catastrophe coincides with defects in sexual RNA replica

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

159 DNA damage, chromosomal breaks, and mitotic catastrophe compared with monotherapy.

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

161 I summarize evidence for such 'catastrophe compassion', discuss its roots, and consider

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

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

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

165 Replication catastrophe depends on accumulation of the transcription

166 The occurrence of this stochastic yield catastrophe does not depend on model details but is gene

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

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

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

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

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

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

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

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

175 oot hair tip growth by promoting microtubule catastrophe events.

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

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

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

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

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

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

182 by which picornaviral RDRPs influence error catastrophe: fidelity of RNA synthesis and RNA recombina

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

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

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

186 Microtubules with betaIIB have catastrophe frequencies approximately threefold lower th

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

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

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

190 nt with an increased rate of acceleration of catastrophe frequency with microtubule age, perhaps via

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

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

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

194 ncreasing the growth rate and decreasing the catastrophe frequency.

195 with dramatically reduced shrinking rate and catastrophe frequency.

196 d fluorescent protein) increased microtubule 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 Mitotic catastrophe implies that mitotic podocytes eventually de

200 picornaviruses to counteract and avoid error catastrophe.IMPORTANCE Positive-strand RNA viruses produ

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

202 icro-level failures cascade to a macro-level catastrophe in a tissue or organs remain largely unexplo

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

204 centrosome depletion, which triggers mitotic catastrophe in cells that exhibit amplicon-directed over

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

206 nvestigate replication stress-driven mitotic catastrophe in human cells and identify that replication

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

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

209 al abnormalities, ultimately causing mitotic catastrophe in PARP inhibitor treated HR-proficient cell

210 scusses the clinical implications of mitotic catastrophe in podocyte health during diabetic kidney di

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

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

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

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

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

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

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

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

219 2 years of their rule in Germany resulted in catastrophes including World War II, the most destructiv

220 the concentration dependence of microtubule catastrophe incorrectly.

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

222 Extinction catastrophe induced by promutagenic nucleosides has been

223 rgeting mechanism originating from metabolic catastrophe induced in the cells by removal of ADPGK.

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

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

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

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

228 Catastrophe induction with vinblastine prevented microtu

229 aints on the possible molecular mechanism of catastrophe induction.

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

231 However, SLAIN2-dependent catastrophe inhibition determines microtubule resistance

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

233 Mitotic catastrophe is a broad descriptor encompassing unclear m

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

235 A combination of vital rate alteration with catastrophes is the most realistic solution to the forag

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

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

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

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

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

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

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

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

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

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

246 re-enter the cell cycle and undergo mitotic catastrophe, modulated via the Hippo pathway but indepen

247 , X. tropicalis microtubules grow slower and catastrophe more frequently.

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

249 When such catastrophes occur, centromeres become susceptible to nu

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

251 isely predictable; (ii) the probability of a catastrophe occurring in any one year increases as the l

252 Mitotic catastrophe occurs when cells enter mitosis with damaged

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

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

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

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

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

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

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

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

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

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

263 cytokinesis and ultimately underwent mitotic catastrophe, phenotypes that were rescued by heterologou

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 scale of this pandemic compare to another US catastrophe: racial inequality?

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

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

272 ple, decrease in growth rate, or increase in catastrophe rate, as the soluble subunit pool decreases.

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

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

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

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

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

278 trate how replication stress-induced mitotic catastrophe signals cell death with implications for can

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

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

281 unity, fine-tuning is critical to preventing catastrophes such as autoimmunity, chronic inflammation,

282 e allocation of resources during health care catastrophes, such as the COVID-19 pandemic.

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

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

285 of UNC5B in small-T antigen-induced mitotic catastrophe that also requires PP2A.IMPORTANCE UNC5B, PP

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

287 The molecular mechanisms behind microtubule catastrophe, the switch from growth to rapid shrinking,

288 Catastrophe-the switch from growing to shrinking-occurs

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

290 Employing the catastrophe theory principles we show that these states

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

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

293 This catastrophe triggered a clarion call for the immediate d

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

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

296 echanisms counteract ribavirin-induced error catastrophe, we selected for ribavirin-resistant poliovi

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

298 be uniquely bad relative to near-extinction catastrophes, which allow for recovery.

299 PEAMOtecan kills glioma cells by mitotic catastrophe with p53 mutant/knockdown cells being more s

300 owever, they do not think that an extinction catastrophe would be uniquely bad relative to near-extin