ライフサイエンスコーパス: genome instability

1 rmation thereby amplifying the potential for genome instability.

2 ducing the formation of R-loops that lead to genome instability.

3 h would otherwise promote mutagenic NHEJ and genome instability.

4 ivation of post-replication repair (PRR) and genome instability.

5 viral replication, DDR activation, and host genome instability.

6 omatid breaks independent of p53, leading to genome instability.

7 eplicative mechanisms in CNV mutagenesis and genome instability.

8 significance in telomere dysfunction-induced genome instability.

9 aired, DNA double-strand breaks (DSBs) cause genome instability.

10 an inherited cancer disorder associated with genome instability.

11 ding to uracil misincorporation into DNA and genome instability.

12 two processes for protection against general genome instability.

13 be resolved before cell division to prevent genome instability.

14 sincorporated ribonucleotides, in preventing genome instability.

15 ors in driving R-loop-induced DNA damage and genome instability.

16 ase H2 complex as an important suppressor of genome instability.

17 ut checkpoint in Dpb11-depleted cells led to genome instability.

18 event abnormal mitotic spindle formation and genome instability.

19 tood but contributes significantly to B cell genome instability.

20 senchymal transition, stem cell pathways and genome instability.

21 able nature of genomes, which we refer to as genome instability.

22 istargeting represents an important risk for genome instability.

23 ion, which is associated with polyploidy and genome instability.

24 e are associated with replication stress and genome instability.

25 p62 levels, altered NF-kappaB signaling and genome instability.

26 ibutes to their survival, proliferation, and genome instability.

27 m arrested complexes, potentially triggering genome instability.

28 own about the direct consequences of plastid genome instability.

29 th deletions, chromosome translocations, and genome instability.

30 E degradation, abnormal DNA replication, and genome instability.

31 lar response to topo I-targeted drugs and to genome instability.

32 viral oncogene and drives proliferation and genome instability.

33 ring mitosis, which in turn can give rise to genome instability.

34 f cancer-specific liabilities resulting from genome instability.

35 onflicts lead to blockage of replication and genome instability.

36 ngation, pausing, termination, fidelity, and genome instability.

37 cessing by Smarcal1 and Mre11 predisposes to genome instability.

38 iation in nondividing cells can culminate in genome instability.

39 ers to replication and potential inducers of genome instability.

40 how imbalances in this equilibrium result in genome instability.

41 ew insights in Tax effects on DNA repair and genome instability.

42 nds of linear chromosomes, safeguard against genome instability.

43 errant chromosome segregation and heightened genome instability.

44 , a cancer predisposition syndrome driven by genome instability.

45 Mice deficient for SIRT6 exhibit genome instability.

46 ow increased hybrid formation and associated genome instability.

47 bility, that is, genome architecture incites genome instability.

48 es that trigger DNA double-strand breaks and genome instability.

49 er alterations, which may be mediated by the genome instability.

50 deficiency results in impaired HR repair and genome instability.

51 to prevent their accumulation and associated genome instability.

52 interaction with RNAPII, thereby preventing genome instability.

53 sources underlie age- and disease-associated genome instability.

54 tic cells due to their propensity to promote genome instability.

55 sitivity to ICLs, defects in ICL repair, and genome instability.

56 ession, bypass of cell-cycle checkpoints and genome instability.

57 spots, implicating the motif as a driver of genome instability.

58 ctive DNA damage responses that are prone to genome instability.

59 g oogenesis predisposes the female gamete to genome instability.

60 aused an inhibition of cell growth and viral genome instability.

61 uracil levels in nuclear DNA, and increased genome instability.

62 PC4 is sufficient to suppress G4-associated genome instability.

63 iption rate, tDNAs may be a potent source of genome instability.

64 Cytidine deaminase (CDA) deficiency leads to genome instability.

65 ng proteins as modulators of R-loop-mediated genome instability.

66 ear dysmorphia, nuclear envelope rupture and genome instability.

67 e rupture, nuclear compartment breakdown and genome instability.

68 on, leads to persistent replication gaps and genome instability.

69 DNA:RNA hybrids can lead to DNA damage and genome instability.

70 plication stress and eventually resulting in genome instability.

71 end resection at DSBs and telomeres prevents genome instability.

72 pmental defects, spontaneous cell death, and genome instability.

73 ize to chromosomal DNA, are potent agents of genome instability.

74 bonucleotide pools that cause DNA damage and genome instability.

75 in response to replication stress to prevent genome instability.

76 underlying cause of the transcription-linked genome instability.

77 esent evidence that MLL2 mutation results in genome instability.

78 ss of autophagy has been linked to increased genome instability.

79 recombination (HR), and its loss results in genome instability.

80 enously induced DNA damage sites, leading to genome instability.

81 tric chromosomes have been proposed to drive genome instability.

82 genotypes, represents a distinct subtype of genome instability.

83 progression to avoid replication stress and genome instability.

84 rstitial telomeric sequences (ITSs) promotes genome instabilities.

85 In addition, we find that genome instability, a hallmark of BRCA2 loss in other or

86 ls as a result of cell pathology and trigger genome instability, a hallmark of cancer and a number of

87 Genome instability, a hallmark of cancer progression, is

88 r alteration (CNA) is a major contributor to genome instability, a hallmark of cancer.

89 cleotides from DNA results in an increase in genome instability, a phenomenon that has been character

90 lt in significant fitness costs arising from genome instability, accelerated ageing and disease.

91 reased ZBTB4 expression correlates with high genome instability across many frequent human cancers.

92 or Sgs1/BLM in suppressing R-loop-associated genome instability across species.

93 in many eukaryotic genomes and are linked to genome instabilities and disease in humans.

94 omic DNA (>1,000,000 per cell), resulting in genome instability and a p53-dependent DNA-damage respon

95 promoter CpG islands that presumably lead to genome instability and aberrant expression of tumor supp

96 lts propose a mechanism for progerin-induced genome instability and accelerated replicative senescenc

97 een linked to transcription, replication and genome instability and are implicated in cancer and othe

98 hybrids, referred to as R-loops, can promote genome instability and cancer development.

99 of DNA helicases that is needed to suppress genome instability and cancer predisposition.

100 genes are responsible for the phenotypes of genome instability and cancer predisposition.

101 d identifies genes implicated in aneuploidy, genome instability and cancer susceptibility.

102 man skin from ultraviolet (UV) light-induced genome instability and cancer, as demonstrated by the de

103 Defects in this regulation can induce genome instability and cancer.

104 II (TOP2) activity are a potential source of genome instability and chromosome translocation.

105 g among repeated genes is a potent driver of genome instability and evolution.

106 e with other factors to increase genetic and genome instability and favor transformation.

107 le elements (TEs) are a tremendous source of genome instability and genetic variation.

108 athway, and this contributes to the observed genome instability and growth defects.

109 ty (MSI) is an important indicator of larger genome instability and has been linked to many genetic d

110 MCM protein deficiency results in genome instability and high rates of cancer in mouse mod

111 Importantly, inactivation of ERK8 results in genome instability and is associated with cell transform

112 genomic aberration that is often induced by genome instability and is associated with diseases such

113 ts in DNA damage response pathways result in genome instability and lead to carcinogenesis, but may a

114 ironmental stress conditions lead to general genome instability and mask the Sir2-mediated recombinat

115 We demonstrate that both the genome instability and mortality of MRE11(-/-) and MRE11

116 ling characteristic of cancer cells, akin to genome instability and mutation.

117 significant correlations of BRCA score with genome instability and neoadjuvant chemotherapy.

118 cations for how endocycles may contribute to genome instability and oncogenesis.

119 esis, caspase-3 activation may contribute to genome instability and play a pivotal role in tumor form

120 hat a defect in this regulation may increase genome instability and promote tumorigenesis.

121 mage repair and checkpoint responses prevent genome instability and provide a barrier to the developm

122 ing chromosome organization, and visualizing genome instability and rearrangement.

123 uggest that PMUs are involved in phytoplasma genome instability and recombination.

124 NA/DNA structure, has been linked to induced genome instability and regulated gene expression.

125 to DNA leads to severe consequences, such as genome instability and replication stress.

126 eplication forks can result in cell death or genome instability and resulting transformation to malig

127 Thus, mitochondrial genome instability and ROS enhance intestinal tumorigene

128 erevisiae, cells lacking RTT107 or SLX4 show genome instability and sensitivity to DNA replication st

129 Loss of DEK induces genome instability and sensitizes cells to DNA double st

130 haplotype diversity and that may also affect genome instability and sequence evolution.

131 hase, the critically short telomeres lead to genome instability and telomerase is further up-regulate

132 -bridge-breakage cycles, which further drive genome instability and thereby contribute to the transfo

133 ved feature in cancer that may contribute to genome instability and to tumour cell invasion.

134 resulted in delayed DNA repair and increased genome instability and transformation independent of p53

135 DR inactivation in these conditions promotes genome instability and tumor progression, but the underl

136 g-term silencing of BRCA1, thereby promoting genome instability and tumor progression.

137 sult in DNA rereplication, which can lead to genome instability and tumorigenesis.

138 vered, implicating HMGA2 in the promotion of genome instability and tumorigenesis.

139 that genome-wide DNA hypomethylation induces genome instability and tumors in animals caution against

140 strand breaks (DSBs) can lead to cell death, genome instability, and carcinogenesis.

141 used to measure the frequency of large-scale genome instability, and deeper sequencing of eight singl

142 ble element activity can lead to detrimental genome instability, and hosts have evolved mechanisms to

143 ingle-stranded DNA are potent instigators of genome instability, and RPA and Mre11-Sae2 play importan

144 e mechanisms that give rise to these extreme genome instabilities are likely different.

145 Cellular mechanisms preventing genome instability are crucial to human health because g

146 The mechanisms responsible for ITS-mediated genome instability are not understood in molecular detai

147 t the mechanisms by which R-loops compromise genome instability are poorly understood.

148 the myriad mechanisms that can give rise to genome instability are still to be fully elucidated.

149 on cell growth, cell cycle progression, and genome instability as a mechanism for cancer initiation.

150 We review the causes of genome instability as well as how it results in hyper-re

151 man MLL2 knockout cells are characterized by genome instability as well.

152 tion for RB in HR, which could contribute to genome instability associated with RB loss.

153 replicate across lesions, thereby preventing genome instability at the cost of increased point mutati

154 rds to the orientation-specific elevation in genome instability at the guanine-rich sequence.

155 upport for a function of Top1 in suppressing genome instability at the guanine-run containing sequenc

156 Replication fork pausing drives genome instability, because any loss of paused replisome

157 le element Ty1 of S. cerevisiae is a form of genome instability, because the transposition events ind

158 A base damage is an important contributor to genome instability, but how the formation and repair of

159 t surveillance pathway that protects against genome instability by blocking cell growth.

160 ements are known to be major contributors to genome instability by generating Alu-mediated copy-numbe

161 mitochondrial dysfunction stimulates nuclear genome instability by inhibiting the production of ISC-c

162 Plk4 autoregulation thus guards against genome instability by limiting centrosome duplication to

163 surveillance mechanism that protects against genome instability by preventing cell growth after centr

164 nd together define a pathway that suppresses genome instability by recruiting the SMC5/6 cohesion com

165 However, genome instability can be enhanced by exposure to extern

166 idea that subtle enhancements of endogenous genome instability can exceed the tolerance of cancer ce

167 The increased mutation load associated with genome instability can lead to neuronal dysfunction and

168 re are deficiencies in DNA repair machinery, genome instability can manifest.

169 curs in stable diploid G1 phase cells before genome instability can occur.

170 plication is critical for cell division, and genome instability can result if duplication is not rest

171 not GIS genes, but suppressed the increased genome instability caused by individual query mutations.

172 esponse (DDR) are often tumor prone owing to genome instability caused by oncogenic challenges.

173 before signs of tumorigenesis indicated that genome instability caused tumorigenesis.

174 Trinucleotide repeats are a source of genome instability, causing replication fork stalling, c

175 DNA transcription, replication, and repair, genome instability, cellular senescence, and stem-cell d

176 urvival, improved chemotherapy response, and genome instability compared with BRCA wild-type.

177 e-deficient cells, and its depletion worsens genome instability, compromising cell survival.

178 s a rare recessive disorder characterized by genome instability, congenital malformations, progressiv

179 Genome instability contributes to cancer development and

180 Such high levels of genome instability could well be a factor in age-related

181 Genome instability, defined as higher than normal rates

182 r emphasis on the role of transcription as a genome instability determinant.

183 Fanconi anaemia (FA) is a genome instability disease caused by defects in the FA D

184 ll as novel disease models and mechanisms of genome instability disorders.

185 in response to diethylnitrosamine-induced or genome instability-driven metabolic stress in a murine m

186 Cells from Bloom's syndrome patients display genome instability due to a defective BLM and the downre

187 lts in mitochondrial dysfunction and nuclear genome instability due to an increase in uracil misincor

188 element transposition causes mutagenesis and genome instability during hybrid dysgenesis.

189 a correlation between retrotransposition and genome instability during yeast aging.

190 Genome instability, epigenetic remodelling and structura

191 function holds promise to maximally exploit genome instability for hereditary and sporadic cancer th

192 Genome instability has long been implicated as the main

193 ntext, 53BP1 deficiency, although leading to genome instability, has only modest effects on V(D)J rec

194 e-strand breaks (DSBs) are a major source of genome instability; however, recent studies from Lee et

195 fied highly transcribed genes as a source of genome instability; however, the degree to which large-s

196 associated with DNA damage accumulation and genome instability; however, the mechanisms underlying R

197 hesis is a prominent source of mitochondrial genome instability; however, the precise molecular deter

198 ther defects in these pathways contribute to genome instabilities in vivo.

199 t cGAS localizes to micronuclei arising from genome instability in a mouse model of monogenic autoinf

200 talled replication forks are major causes of genome instability in all organisms.

201 se, POLIB, act as safeguards against plastid genome instability in Arabidopsis (Arabidopsis thaliana)

202 istic insights into the processes that cause genome instability in BRCA1/2-deficient cells.

203 lt-NHEJ pathway that not only contributes to genome instability in cancer cells but may also be a the

204 arrangement given its likely contribution to genome instability in cancer cells.

205 DNA replication stress promotes genome instability in cancer.

206 bout genes involved in DNA damage repair and genome instability in cancer.

207 e mutant of CDC6 promotes re-replication and genome instability in cells lacking the CDT1 inhibitor G

208 to uracil (U) in DNA is a constant source of genome instability in cells.

209 ted that cigarette smoke condensate leads to genome instability in human bronchial epithelial cells.

210 ncided with substantially elevated levels of genome instability in Mcm4chaos3/chaos3;Fancc-/- cells,

211 A protracted period of genome instability in neoallopolyploids may increase opp

212 A widely used approach for assessing genome instability in plants makes use of somatic homolo

213 y, which could cause aberrant DSB repair and genome instability in pre-B cells.

214 Finally, we discuss the genetics of genome instability in relation to longevity to address t

215 ion and also relieves replication stress and genome instability in RER-defective cells.

216 loinsufficient (HI) genes that guard against genome instability in Saccharomyces cerevisiae.

217 ndings identify ZGA as a source of intrinsic genome instability in the germline and suggest that geno

218 ts detrimental effects, and thereby prevents genome instability in the transcribed region of genes.

219 ations, and these low-copy repeats can cause genome instability in this region.

220 Additionally, genome instability in Top1-deficient yeasts is not compl

221 mutations in RAD51 itself may contribute to genome instability in tumor cells, either directly throu

222 ggered the activation of autophagy to reduce genome instability in tumor foci.

223 new potential mechanism for mutagenesis and genome instability in XPV individuals.

224 Genome instability in yeast and mammals is caused by RNA

225 ing the formation of micronuclei, markers of genome instability, in mouse erythrocytes.

226 tant role in the cell-intrinsic responses to genome instability, including a transient cell cycle arr

227 they can be used with confidence to measure genome instability, including the complete sequences of

228 Telomere disruption typically results in genome instability induced by telomere fusions.

229 ogether, these results indicate that plastid genome instability induces an oxidative burst that favor

230 ential for replisome inactivation, and hence genome instability, inside cells.

231 gulatory connections may be connected to the genome instability involved in several human diseases, i

232 Genome instability is a hallmark of cancer cells.

233 Genome instability is a recurring feature of tumorigenes

234 -1 and ciprofloxacin-treated plants, plastid genome instability is associated with increased reactive

235 Genome instability is associated with mitotic errors and

236 tability are crucial to human health because genome instability is considered a hallmark of cancer.

237 Identifying the causes of genome instability is crucial to understanding genome dy

238 GEN1 depletion extend beyond mitosis, since genome instability is observed throughout all phases of

239 This explains how extensive genome instability is prevented in eukaryotic cells whos

240 As altered Cse4/CENP-A activity leads to genome instability, it is pivotal to understand the mech

241 ms bone marrow progenitor cells and promotes genome instability, leading to development of chronic my

242 ur data indicate that, upon Sub1-disruption, genome instability linked to co-transcriptionally formed

243 cases, RecQ4, BLM, and WRN suppress distinct genome instability-linked diseases with severe phenotype

244 charomyces cerevisiae system to characterize genome instability mediated by yeast telomeric (Ytel) re

245 To prevent genome instability, mitotic exit is delayed until all ch

246 Due to genome instability, most cancers exhibit loss of regions

247 a timely converging fork or Mus81 may propel genome instability observed in cancer.

248 Genome instability occurs early in the development of mo

249 lated PCNA during DNA replication, while the genome instability of an elg1Delta mutant suggests timel

250 clinical rectal tumor samples, likely due to genome instability of precancerous and/or early cancer c

251 nd break repair (DSBR) provides insight into genome instability, oncogenesis and genome engineering,

252 rminus is essential to prevent initiation of genome instability permissive for tumorigenesis.

253 i1-dependent SUMO chain formation causes the genome instability phenotypes of SUMO-targeted ubiquitin

254 n of normal DNA replication leads to rampant genome instability primarily in the form of chromosomal

255 e relentless and heterogeneous nature of the genome instability processes, are likely to confound tre

256 yndrome (RJALS), a disorder characterized by genome instability, progeria and early onset hepatocellu

257 se 3alpha, Bloom helicase, and RecQ-mediated genome instability protein 1 and 2 can partially disenta

258 ches to develop interventions that attenuate genome instability, reduce disease risk, and increase li

259 uding inflammation, invasion and metastasis, genome instability, resistance to chemo/radiotherapy, an

260 Also, genome instability resulting from an excess of DDB2 pers

261 eostasis and suggest a mechanistic basis for genome instability resulting from deregulated DNA replic

262 transcription is associated with eukaryotic genome instability, resulting in increased rates of mito

263 ethylation can be a potential contributor to genome instability seen in myeloma.

264 st that the origin of replication-associated genome instability should be re-evaluated.

265 ngle-base substitutions, LOH, or large-scale genome instability signatures characteristic of BRCA1/2-

266 NA replication involves the inherent risk of genome instability, since replisomes invariably encounte

267 t the PRDM9 locus also influences aspects of genome instability-specifically, a megabase-scale rearra

268 le-stranded breaks (a 13-mer associated with genome instability) strongly correlate with densities of

269 MAP1S levels triggers autophagy to suppress genome instability such that both the incidence of dieth

270 The identity of all Genome Instability Suppressing (GIS) genes is not curren

271 Fanconi anemia (FA) is a rare familial genome instability syndrome caused by mutations in FA ge

272 Fanconi anemia (FA) is a genome instability syndrome characterized at least in pa

273 Fanconi anemia (FA) is a genome instability syndrome characterized by bone marrow

274 Fanconi anemia (FA) is a recessive genome instability syndrome characterized by heightened

275 nd crosslinks (ICLs) are associated with the genome instability syndrome Fanconi anemia (FA).

276 Fanconi anemia (FA) is a genome instability syndrome that has been associated wit

277 in patient cells, CS is widely considered a genome instability syndrome.

278 restriction-like therapy for human progeroid genome instability syndromes and possibly neurodegenerat

279 The assay detects low levels of genome instability that cannot be readily identified by

280 n of DNA damage checkpoint function leads to genome instability that in turn can predispose cellular

281 fy carcinogen susceptibility as an origin of genome instability that is regulated by nuclear architec

282 lustered DNA damage repair appear to promote genome instability that may lead to carcinogenesis.

283 s renders them vulnerable to DSBs, promoting genome instability that may lead to carcinogenesis.

284 A anaphase bridges are a potential source of genome instability that may lead to chromosome breakage

285 en not properly processed, can contribute to genome instability that underlies aging and disease deve

286 earrangements resulting from region-specific genome instability, that is, genome architecture incites

287 and break repair in suppression of oncogenic genome instability, the genomic elements required for ch

288 Telomere attrition can promote genome instability, thereby stimulating initiation of ea

289 s cerevisiae, loss of mtDNA leads to nuclear genome instability, through a process of cell-cycle arre

290 ediated fusions that would otherwise promote genome instability to fuel tumorigenesis.

291 for BLM-associated polypeptide/RecQ-mediated genome instability) to form the BTB (BLM-Topo IIIalpha-B

292 cells contributes to cell proliferation and genome instability, two aspects promoting melanoma initi

293 t arise during transcription pausing lead to genome instability unless they are resolved efficiently.

294 transposons in aging-associated increases in genome instability using the Saccharomyces cerevisiae ch

295 coincides with the orientation where higher genome instability was observed.

296 results define Top1 as a source of DSBs and genome instability when ribonucleotides incorporated by

297 e dispensable for Sgs1's role in suppressing genome instability, whereas the zinc-binding domain and

298 egulated expression of AID causes widespread genome instability, which alone is insufficient to induc

299 or of elevated recombination activity and of genome instability, which is a hallmark of cancer.

300 ween adults and children are associated with genome instability, which is much more frequent in adult