ライフサイエンスコーパス: breakage

1 s (free volume collapse and endothermic bond breakage).

2 d breaks (DSBs) result from replication-fork breakage.

3 h one another in the apparent absence of DNA breakage.

4 reakage as the archetypical mode of symmetry breakage.

5 n, which generates an abasic site for strand breakage.

6 chanical strength and are prone to permanent breakage.

7 catalysis does not involve bond formation or breakage.

8 ts associated with cellular responses to DNA breakage.

9 actin filaments, causing their buckling and breakage.

10 ated in a clinically relevant manner without breakage.

11 ng camptothecin, that cause replication fork breakage.

12 if1, slow DNA replication, and stimulate DNA breakage.

13 to prevent replication fork stalling and DNA breakage.

14 phase bridge formation and ultimately to DNA breakage.

15 nuclear foci that demarcate sites of genome breakage.

16 existence of regions that are susceptible to breakage.

17 t can form a new cap and resume growth after breakage.

18 lates water insertion prior to hydrogen bond breakage.

19 ient to protect microtubules from mechanical breakage.

20 ant increase in the frequency of microtubule breakage.

21 guingly limits recombination induced by fork breakage.

22 hyphae in both fungi with serious folds and breakage.

23 rs may predispose certain genomic regions to breakage.

24 n constraining recombination induced by fork breakage.

25 at speeds up to 5 mum/s without the risk of breakage.

26 the enzyme's star activity or to random DNA breakage.

27 d pronounced susceptibility to single-strand breakage.

28 g membrane availability and necessitating NE breakage.

29 on, as tissue failure still occurred by cell breakage.

30 romoting survival following replication fork breakage.

31 tence length and increased susceptibility to breakage.

32 he elongated mitotic spindle as the cause of breakage.

33 , local infiltration (3.0%), leakage (1.5%), breakage (1.4%), phlebitis (1.2%), and thrombosis (0.5%)

34 eplication fork reversal protects forks from breakage after poisoning of Topoisomerase 1.

35 We hypothesize that even though there are breakages among neighboring capsomers, RNA-capsid protei

36 ect of 2.44 +/- 0.22 for the C-H vs C-D bond breakage and a secondary isotope effect corresponding to

37 pates in multiple steps of DNA single-strand breakage and base excision repair.

38 y the depletion of Mcm10 leads to chromosome breakage and cell cycle checkpoint activation.

39 ells are particularly vulnerable to this DNA breakage and cells defective in rejoining of S-phase DSB

40 at Fcy1-mediated deamination is one cause of breakage and contractions in the presence of R-loops.

41 Oncogene-induced DNA breakage and DDR activation instead occurred upon persis

42 bsequently increased reactivity towards bond breakage and decomposition.

43 that CIN in terms of ICL-induced chromosomal breakage and defective chromatid cohesion is frequently

44 technologies to monitor and detect catheter breakage and disconnects is promising.

45 ction is important for preventing chromosome breakage and elucidate a DNA repair mechanism that is cr

46 ding cell wall incorporating strain-enhanced breakage and enzyme-mediated crosslink kinetics.

47 PSII repair and reassembly involve the breakage and formation of disulfide bonds among PSII pro

48 sformations are directed by cooperative bond breakage and formation, resulting in expansion or contra

49 In plants and animals, chromosomal breakage and fusion events based on conserved syntenic g

50 and intragenomic rearrangements, chromosome breakage and fusion, rDNA changes, and loss of repeat se

51 d label-free manner without any need of cell breakage and has great potential for both diagnostic and

52 We describe procedures for the efficient breakage and homogenization of every larval stage, inclu

53 psis-like pattern generated after chromosome breakage and illegitimate rejoining.

54 generate reactive oxygen or cause direct DNA breakage and is only minimally mutagenic.

55 cally to the transposon ends and carries out breakage and joining at the 3' ends, and TnsA, which car

56 recognizes the transposon ends and mediates breakage and joining is heteromeric.

57 lated nuclease, markedly limited chromosomal breakage and led to further accumulation of reversed for

58 displayed a higher magnitude of chromosomal breakage and micronucleus formation than the wild-type o

59 cation making DNA more susceptible to strand breakage and mutations.

60 ficiency results in elevated chromosomal/DNA breakage and permanent genome rearrangements.

61 DNA strand breakage and perturbation of cell-cycle progression cont

62 ween rapidly segregating centromeres without breakage and providing a spatiotemporal window for their

63 amage and ameliorated spontaneous chromosome breakage and radials in human FA patient-derived cells.

64 tion could precipitate widespread chromosome breakage and rearrangement in the course of malignancy.

65 or chromosome arms undergo massive local DNA breakage and rearrangement.

66 rough a series of carefully orchestrated DNA breakage and rejoining events.

67 transposase of these elements catalyzes DNA breakage and rejoining reactions required for transposit

68 e elastic-fluid model to the kinetics of DNA breakage and repair by assuming that the local volume fr

69 Coordination of DNA breakage and repair during the cell cycle is critical to

70 and dynamic resource useful for studying DNA breakage and repair mechanisms, and for analyzing the ge

71 romosomal lesions through repeated cycles of breakage and repair of such lesions.

72 hat ultrasonication was responsible for cell breakage and subsequent lycopene release in a highly vis

73 some overduplication, aneuploidy, chromosome breakage and the formation of micronuclei by targeting c

74 ed replication forks are sites of chromosome breakage and the formation of toxic recombination interm

75 t protects bacteria from double-stranded DNA breakage and TLD.

76 ions predispose genome regions to chromosome breakage and translocations.

77 modifications as facilitators of chromosome breakage and translocations.

78 n oxidative DNA adduct formation, DNA strand breakage, and cell death.

79 le sites (CFSs) are hot spots of chromosomal breakage, and CFS breakage models involve perturbations

80 gns of growth failure, increased chromosomal breakage, and NK cell deficiency.

81 upporting replicative models for spontaneous breakage, and providing the first true breakage rates.

82 suggesting that incomplete replication, fork breakage, and repair occur widely in polytene cells.

83 Expanded CAG repeats are prone to breakage, and repair of the breaks can cause repeat cont

84 at replication forks independently of their breakage, and to be antagonized by poly (ADP-ribose) pol

85 ng mechanisms that repair these forms of DNA breakage are largely unknown.

86 is best compatible with flow-based symmetry breakage as the archetypical mode of symmetry breakage.

87 , redox-neutral and photoreductive Fe-N bond breakage as well as photooxidative N-N bond breakage occ

88 transport renders the spindle susceptible to breakage, as observed in cells with a variety of defects

89 nt to PCNA or in helicase-deficient mutants, breakage at a CAG/CTG repeat increases.

90 hyde, associated with widespread chromosomal breakage at a concentration not producing breaks in pare

91 f goethite and hematite, was abandoned after breakage at Cueva Anton, 60 km inland.

92 These findings provide evidence that breakage at expanded CAG repeats occurs due to R-loop fo

93 DNA breakage at fragile sites is associated with regions tha

94 r, there has been no direct evidence linking breakage at fragile sites to the formation of a cancer-s

95 logical RNR activity and reduced chromosomal breakage at fragile sites.

96 tion via a mec1 mutation leads to chromosome breakage at replication forks initiated from virtually a

97 Such breakage at single-strand interruptions results in artif

98 ecise plant genome editing by catalyzing DNA-breakage at specific targets to stimulate targeted mutag

99 cally, while MEC1 cells exhibited chromosome breakage at stress-response transcription factors, mec1

100 at the 3' ends, and TnsA, which carries out breakage at the 5' ends of Tn7.

101 chromosomal translocation typically involves breakage at the bcl-2 major breakpoint region (MBR) to c

102 n addition, we find hotspots of subtelomeric breakage at the end of chromosomes 9q and 22q; these sit

103 mec1 cells predominantly suffered chromosome breakage at transporter genes, many of which are the sub

104 data, extracting the rates of single-strand breakage at two dye staining ratios and measuring the da

105 rambling was likely attributed to an initial breakage between the light (Cys 214) and heavy (Cys 223)

106 culate that telomeric aggregates and ongoing breakage-bridge-fusion cycles lead to disturbed cytokine

107 rm anaphase bridges, resulting in chromosome breakage by an unknown mechanism.

108 f histone marks sensitizes genome regions to breakage by endonuclease challenge or irradiation and pr

109 y to examine their gemifloxacin-mediated DNA breakage by Streptococcus pneumoniae topo IV and gyrase.

110 ollectively, these data implicate chromosome breakage by TOP2 as an endogenous threat to gene transcr

111 lternative DNA structure formation and a DNA breakage cell assay were used to validate the computatio

112 we recorded no evidence of healing and when breakage characteristics were typical of fresh bone.

113 We show that gene breakage commonly inactivates the tumour suppressors RB1

114 breaks are abundant forms of endogenous DNA breakage, contributing to hereditary ataxia and underlyi

115 ochastic DNA damage to the time-resolved DNA breakage data, extracting the rates of single-strand bre

116 rated that BRCA1 recruitment to areas of DNA breakage depended on RAP80 and the RNF8/RNF168 E3 ubiqui

117 me maintenance are linked to rare chromosome breakage disorders.

118 ask that often results in untimely electrode breakage due to crashing against a substrate.

119 often occur at genomic sites susceptible to breakage during DNA replication, including regions with

120 ns-arginine into the catalytic site and bond breakage during hydrolysis are monitored in real time.

121 us and DNA damage-induced nicks are prone to breakage during PFGE.

122 ng the growth of new fibrils and the role of breakage events in cytotoxicity.

123 e of seeding, nucleation, growth, and fibril breakage events.

124 pseudocapillary networks because of numerous breakage events.

125 ny autonomous IgH targeted by programmed DNA breakage, factors predisposing broken DNA ends to transl

126 sts a sequence-independent mechanism for DNA breakage followed by telomere healing, with the formatio

127 loci that are especially susceptible to DNA breakage following conditions of partial replication str

128 pi systems, which assist phosphate-C1' bond breakage following FMN reduction, leading to formation o

129 HM) for antibody affinity maturation and DNA breakage for antibody class switch recombination (CSR) v

130 reduced susceptibility to DNA double-strand breakage for IR makes double-strand breaks (DSBs) in bde

131 chaperone protein, catalyzes disulfide bond breakage, formation, and rearrangement.

132 e in logistic regression models) and of aCFS breakage frequencies (explaining approximately 45% of th

133 We also analyzed aCFS breakage frequencies as a function of their genomic land

134 ents show that this damage is not due to DNA breakage from mechanical stress on chromatin in the defo

135 Breakage-fusion-bridge (BFB) cycle is a series of chromo

136 DNA amplification, most notably seen in the breakage-fusion-bridge (BFB) cycle.

137 te, which subsequently undergoes a series of breakage-fusion-bridge (BFB) cycles.

138 Breakage-fusion-bridge (BFB) is a mechanism of genomic i

139 It is thought to arise through a breakage-fusion-bridge (BFB) mechanism.

140 inute chromosome formation (MYC and MDM2) or breakage-fusion-bridge (KRAS, MDM2 and RFC3).

141 plex chromosomal rearrangements initiated by breakage-fusion-bridge cycles and completed by simultane

142 In sporadic iAMP21, breakage-fusion-bridge cycles are typically the initiati

143 Breakage-fusion-bridge cycles followed by chromothripsis

144 15;21)c to be constitutionally dicentric and breakage-fusion-bridge cycles generate dicentric chromos

145 Perpetuation of breakage-fusion-bridge cycles in CML progenitors was med

146 result in fusions which initiate chromosomal breakage-fusion-bridge cycles, causing genomic instabili

147 rearranged, and corroded through hundreds of breakage-fusion-bridge cycles.

148 they generate new DSBs downstream of IgH via breakage-fusion-bridge cycles.

149 of telomeric fusions indicative of multiple breakage-fusion-bridge cycles.

150 a rapid increase in DNA content and trigger breakage-fusion-bridge cycles.

151 t seal end-to-end fusions, in the absence of breakage-fusion-bridge cycles.

152 duplications have been attributed solely to breakage-fusion-bridge cycles.

153 epeatedly generates palindromic DNA, such as Breakage-Fusion-Bridge cycles.

154 ic chromosomes and c-myc amplification via a breakage-fusion-bridge mechanism.

155 omosome damage, repair, and damage through a breakage-fusion-bridge mechanism.

156 ases of amplifications are compatible with a breakage-fusion-bridge mechanism.

157 duplication such as tandem duplications and breakage/fusion/bridge (B/F/B) cycles.

158 We observed ICL-induced chromosomal breakage in 9 of 17 (53%) HNSCC cell lines derived from

159 tes stalled fork degradation and chromosomal breakage in BRCA2-defective cells.

160 -called "mustard oil bomb," in which vacuole breakage in cells harboring myrosinase and glucosinolate

161 The data illuminate spontaneous DNA breakage in E. coli and human cells and illustrate the v

162 nvestigated fork progression and chromosomal breakage in human cells in response to a panel of sublet

163 The ability to catalyze covalent bond breakage in isolated small molecules using compressive f

164 e failure during ripening was mainly by cell breakage in Kanzi apples and, in contrast, by cell separ

165 s in chromatin changes induced by chromosome breakage in mammalian cells and their implications for g

166 Although our understanding of dormancy breakage in mature seeds is well advanced, relatively li

167 Dicentric chromosomes undergo breakage in mitosis, resulting in chromosome deletions,

168 ion of FANCM was responsible for chromosomal breakage in one cell line, whereas in two other cell lin

169 nity of these motifs, and they were prone to breakage in Pif1-deficient cells, whereas non-G4 Pif1-bi

170 are reported to be especially vulnerable to breakage in sir2Delta mutants.

171 endonuclease 1, introducing a single-strand breakage in the hairpin loop.

172 (SET to a sigma* orbital concerted with C-Cl breakage) in alkanes compared to stepwise OS-SET (SET to

173 is thus provided for further analysis of the breakage-independent recognition of homology that underl

174 oxidation and supercoiled plasmid DNA strand breakage inhibition induced by both peroxyl and hydroxyl

175 sition owing to the similarity of sigma-bond breakage into a delocalized pi-system.

176 , over the studied speed range, the junction breakage is caused purely by the growth of the gap betwe

177 use genetic models indicate that chromosomal breakage is common at sites of transcriptional turbulenc

178 uce radiation damage levels to hydrogen bond breakage is demonstrated.

179 We explore how chromosome breakage is integrated with meiotic progression and how

180 Under quiescent conditions where fibril breakage is minimal, faster growing fibrils have a selec

181 By contrast, no chromosome breakage is observed with alleles containing pairs of Ac

182 ly nonlinear and/or asymmetric, and C-H bond breakage is partially rate-limiting for all reactions.

183 phosphate is bound is not observed, and bond breakage is the rate-limiting step.

184 e DNA secondary structures can result in DNA breakage leading to cancer and other diseases.

185 heavy-light chain linkage suggests that the breakage may result from electron transfer from Cys(231)

186 Yet the breakage mechanism is not well understood, and the exper

187 e hot spots of chromosomal breakage, and CFS breakage models involve perturbations of DNA replication

188 omputationally that water cage formation and breakage near the hydrophobic groups control the fusion

189 se, are neither associated with chromosomal breakage nor with significant DDR activation.

190 breakage as well as photooxidative N-N bond breakage occur on a time scale well below a few hundred

191 ed bone and molar fragments, indicating that breakage occured while fresh.

192 of bone, molar and stone refits suggest that breakage occurred at the site of burial.

193 nical treatments, our studies show that bond breakage occurs mainly due to the erosion of rigid clust

194 tinum(0), a complete silicon-phosphorus bond breakage occurs, yielding the unprecedented dinuclear pl

195 o IDDS system in three other cases including breakage of a catheter, pump malfunction and arachnoid a

196 t contribution are involved in formation and breakage of a common intermediate.

197 on are remotely coupled to the formation and breakage of a disulfide bond over a distance of >14 A.

198 -mercaptopropanehydrazide cargo by formation/breakage of a disulfide bond, while dynamic hydrazone ch

199 this study, we show that the elongation and breakage of a filament of a colloidal fluid under tensil

200 ng the activation pathway accompanied by the breakage of a number of key interactions stabilizing the

201 contribution that roughly corresponds to the breakage of a single hydrogen bond.

202 bilin chromophore and, in certain cases, the breakage of a thioether linkage to a conserved cysteine

203 n small amounts of fluoride are added during breakage of Al flocs, there can be significant improveme

204 ergo an energy dissipation mechanism through breakage of bonds when strain is applied, while retainin

205 egions of unreplicated DNA can result in the breakage of DNA during mitosis, which in turn can give r

206 for nucleotide excision repair suggest that breakage of DNA strands triggers reorganization of the n

207 An imbalance of the normal microbial flora, breakage of epithelial barriers or dysfunction of the im

208 derivatized polyether track by the formation/breakage of ester linkages.

209 he conserved carboxy tail of FtsZ leading to breakage of FtsZ filaments.

210 It is proposed that the formation and breakage of GaAs-O-Si bonding bridges are responsible fo

211 s in the region 1175-1157cm(-1), linked with breakage of glycosidic bonds, were the most useful for d

212 The breakage of GroES symmetry requires the stochastic hydro

213 of the following conformational changes: the breakage of H-bond interactions between the backbone nit

214 ydrogen-bond scalar couplings, it seems that breakage of hydrogen bonds in the ion pairs occurs on a

215 s system (CNS) mainly in young adults, and a breakage of immune tolerance to CNS self-antigens has be

216 striking association between the binding and breakage of intersubunit salt bridges in the EC domain.

217 The earliest breakage of left-right symmetry occurs as the result of

218 Possible mechanisms for the breakage of molecular crystals under high-intensity ultr

219 We discuss how breakage of nicked DNA may be mechanistically linked to

220 Although breakage of nicked subchromosomal fragments is field str

221 ns, the stochastic hydrolysis of ATP and the breakage of nucleotide symmetry also occur within the en

222 res the stochastic hydrolysis of ATP and the breakage of nucleotide symmetry.

223 Additionally, the two step action ((i) breakage of polymer-water hydrogen bonding and (ii) poly

224 of peptide desorption and/or water-mediated breakage of pore connections.

225 With respect to the breakage of symmetry, it is induced by asynchronous expa

226 In contrast to Ras . GAP catalysis, the bond breakage of the beta-gamma-phosphate but not the Pi rele

227 binding of NO to the heme and the resulting breakage of the bond between the heme iron and histidine

228 in and GAF domain dynamically transition via breakage of the C10/Cys-494 thioether bond, opposite rot

229 hyde, and the aldehydes corresponding to the breakage of the carboncarbon double bonds: propanal, hex

230 The late breakage of the compensatory mechanism at work in the wa

231 The movement of H6 is associated with breakage of the E247-R135 and R135-E134 salt bridges and

232 ssion complex is completed by remodeling and breakage of the ESCRT-III polymer assisted by VPS4.

233 vulnerable to radical attacks that result in breakage of the heavy-light chain linkage and cleavage o

234 one of these substitutions could inhibit the breakage of the heavy-light chain linkage suggests that

235 Still, it is unknown how the breakage of the iron-His bond translates into NO-depende

236 having a key role in NO activation following breakage of the iron-His bond.

237 ture, and position of its atoms, governs the breakage of the molecule and, as a result, determines th

238 erol:PUFA ratio of the sperm membrane caused breakage of the neck and acrosome region and immotility

239 attack on the phosphorous atom that leads to breakage of the phosphodiester bond.

240 Interestingly, breakage of the phosphodiester bonds at the AID-initiate

241 l to current changes during quasi-controlled breakage of the pipet tip.

242 pumping in the system, which results in the breakage of the time-reversal symmetry.

243 The breakage of this strained bond upon Zn(2+) dissociation

244 n, class switching, increased cell turnover, breakage of tolerance, and a loss of the capacity to gen

245 ic class switching, increased cell turnover, breakage of tolerance, increased immature/transitional B

246 BLM fails to correct the elevated chromosome breakage of transfected BLM-deficient cells.

247 an spontaneously regenerate, their temporary breakage offers a limited time window when hair cells ar

248 ure, or only in response to a challenge like breakage or actin overexpression.

249 nt mitomycin C but do not exhibit chromosome breakage or cell cycle arrest after diepoxybutane treatm

250 into molecular vibrational modes, leading to breakage or formation of individual bonds.

251 nome instability that may lead to chromosome breakage or nondisjunction during mitosis.

252 There was no prosthesis loosening, breakage, or infection leading to removal after a mean f

253 lements of the theory, we found that the MBR breakage process is indeed highly dependent on DNA methy

254 hondrial samples is often considered to be a breakage product of the F(1)F(O) ATP synthase during sam

255 we determined the structures and chromosome breakage properties of 15 maize p1 alleles: each allele

256 e strongly nonlinear dependence of crosslink breakage rate on crosslink elongation.

257 Breakage rates were calculated by analyzing the capsular

258 neous breakage, and providing the first true breakage rates.

259 Analysis of the chromosomal breakage regions suggests a sequence-independent mechani

260 regulating the number of rotations during a breakage-religation cycle.

261 hese results to experimentally generated DNA breakage-repair by sequencing seven transgenic animals,

262 In all cases, dicentric breakage requires anaphase exit, ruling out stretching b

263 Instead, breakage requires cytokinesis.

264 of cell cycle activity and DNA double-strand breakage, respectively, associated with neuron death.

265 When DNA breakage results in a 3'-PO4 terminus, the end is consid

266 fragmentation occurs at conserved chromosome breakage sequences, generating macronuclear chromosomes.

267 This breakage should allow TALEs to access superhelically-bro

268 nts for -4G, -2A and -1T bases preceding the breakage site (between -1 and +1) and enzyme-unique or d

269 c modifications can be introduced around the breakage site during its repair by two major DNA damage

270 nrestrained fork progression and chromosomal breakage, suggesting fork remodeling as a global fork sl

271 The irreversible nature of floc breakage suggests that some form of specific, chemical i

272 Warsaw breakage syndrome (WABS) is caused by defective DDX11, a

273 Nijmegen breakage syndrome 1 (NBS1) is a component of the MRE11 c

274 ing directly to DNA breaks requires Nijmegen breakage syndrome 1 (NBS1).

275 11 (Mre11)/DNA repair protein Rad50/Nijmegen breakage syndrome 1 proteins] to sites of DNA damage whe

276 Here, we have identified a chromosome breakage syndrome associated with severe lung disease in

277 th a unique genetic disorder known as Warsaw breakage syndrome characterized by cellular defects in g

278 th a unique genetic disorder known as Warsaw breakage syndrome characterized by cellular defects in s

279 turn triggers direct binding to the Nijmegen breakage syndrome gene product, Nbs1.

280 other hand, the mutant protein from a Warsaw breakage syndrome patient failed to unwind these triplex

281 SMCE3 with an autosomal recessive chromosome breakage syndrome that leads to defective T and B cell f

282 oderma pigmentosum/Cockayne syndrome, Warsaw breakage syndrome, and dyskeratosis congenita, respectiv

283 ed activation of the repair protein Nijmegen Breakage Syndrome-1 but not p53.

284 the chromosomal instability disorder Warsaw breakage syndrome.

285 CID, XLA, ataxia-telangiectasia and Nijmegen-breakage-syndrome and thus facilitates effective newborn

286 h SCID, XLA, ataxia-telangiectasia, Nijmegen-breakage-syndrome, common variable immunodeficiency, imm

287 e loss, micronuclei formation and chromosome breakage that are further elevated by replication stress

288 llenic hydroarylation/N1-C4 beta-lactam bond breakage to afford dihydro-oxepino[4,5-b]indole-4-carbox

289 R.PabI from a hyperthermophile, ascribed the breakage to high temperature while another showed its we

290 ome-disentangling machine auto-regulates DNA breakage to prevent the aberrant formation of mutagenic

291 Remarkably, cells specifically utilize fork breakage to rescue stalled replication and avoid lethali

292 to increased OS rigidity and thus increased breakage, ultimately contributing to retinal degeneratio

293 fork degradation, but increases chromosomal breakage, uncoupling fork protection, and chromosome sta

294 gions of the genome that exhibit chromosomal breakage under conditions of mild replication stress, ar

295 Chemical bond formation and breakage underlie the lives of cells, but as this specia

296 phosphorylation is essential to prevent DNA breakage upon replication stress and cells harboring SIR

297 city; blocks resection; and demonstrates DNA breakage via APOBEC3A cytosine deaminase.

298 The activation energy of double bond breakage was relatively low ( approximately 25 kJ/mol) a

299 mice showed hypersensitivity and chromosomal breakage when treated with mitomycin C, a DNA interstran

300 omerase (topo) IV inducing site-specific DNA breakage within a bent DNA gate engaged in DNA transport