コーパス検索結果 (１語後でソート)
通し番号をクリックするとPubMedの該当ページを表示します
1 he formation of micronuclei, a clear sign of genome instability.
2 process that produces gene amplification and genome instability.
3 rmation thereby amplifying the potential for genome instability.
4 th deletions, chromosome translocations, and genome instability.
5 ress can stall replication forks, leading to genome instability.
6 ding to uracil misincorporation into DNA and genome instability.
7 ved and how, when unresolved, they can cause genome instability.
8 cessing by Smarcal1 and Mre11 predisposes to genome instability.
9 deficiency results in impaired HR repair and genome instability.
10 sources underlie age- and disease-associated genome instability.
11 uracil levels in nuclear DNA, and increased genome instability.
12 PC4 is sufficient to suppress G4-associated genome instability.
13 iption rate, tDNAs may be a potent source of genome instability.
14 Cytidine deaminase (CDA) deficiency leads to genome instability.
15 ng proteins as modulators of R-loop-mediated genome instability.
16 ear dysmorphia, nuclear envelope rupture and genome instability.
17 e rupture, nuclear compartment breakdown and genome instability.
18 on, leads to persistent replication gaps and genome instability.
19 op1) in absence of RER induces mutations and genome instability.
20 DNA:RNA hybrids can lead to DNA damage and genome instability.
21 plication stress and eventually resulting in genome instability.
22 end resection at DSBs and telomeres prevents genome instability.
23 pmental defects, spontaneous cell death, and genome instability.
24 ize to chromosomal DNA, are potent agents of genome instability.
25 bonucleotide pools that cause DNA damage and genome instability.
26 in response to replication stress to prevent genome instability.
27 underlying cause of the transcription-linked genome instability.
28 esent evidence that MLL2 mutation results in genome instability.
29 ss of autophagy has been linked to increased genome instability.
30 recombination (HR), and its loss results in genome instability.
31 enously induced DNA damage sites, leading to genome instability.
32 tric chromosomes have been proposed to drive genome instability.
33 genotypes, represents a distinct subtype of genome instability.
34 progression to avoid replication stress and genome instability.
35 ducing the formation of R-loops that lead to genome instability.
36 h would otherwise promote mutagenic NHEJ and genome instability.
37 ivation of post-replication repair (PRR) and genome instability.
38 viral replication, DDR activation, and host genome instability.
39 omatid breaks independent of p53, leading to genome instability.
40 eplicative mechanisms in CNV mutagenesis and genome instability.
41 significance in telomere dysfunction-induced genome instability.
42 aired, DNA double-strand breaks (DSBs) cause genome instability.
43 an inherited cancer disorder associated with genome instability.
44 two processes for protection against general genome instability.
45 be resolved before cell division to prevent genome instability.
46 sincorporated ribonucleotides, in preventing genome instability.
47 ors in driving R-loop-induced DNA damage and genome instability.
48 ase H2 complex as an important suppressor of genome instability.
49 ut checkpoint in Dpb11-depleted cells led to genome instability.
50 event abnormal mitotic spindle formation and genome instability.
51 tood but contributes significantly to B cell genome instability.
52 senchymal transition, stem cell pathways and genome instability.
53 able nature of genomes, which we refer to as genome instability.
54 istargeting represents an important risk for genome instability.
55 ion, which is associated with polyploidy and genome instability.
56 e are associated with replication stress and genome instability.
57 p62 levels, altered NF-kappaB signaling and genome instability.
58 to become deregulated with consequences for genome instability.
59 ibutes to their survival, proliferation, and genome instability.
60 m arrested complexes, potentially triggering genome instability.
61 own about the direct consequences of plastid genome instability.
62 and pathological processes, in particular to genome instability.
63 n shown to block DNA replication and promote genome instability.
64 y linking hormone hypersecretion to SCNA and genome instability.
65 continued proliferation and accumulation of genome instability.
66 defective DNA repair, eventually leading to genome instability.
67 , they can also contribute to DNA damage and genome instability.
68 r-risk first cell cycle that likely promotes genome instability.
69 he spliceosome, including multiple routes to genome instability.
70 ptor diversity but is also a potent cause of genome instability.
71 ive genomic scars associated with pathogenic genome instability.
72 leading to increased error-prone repair and genome instability.
73 hal types of DNA damage and frequently cause genome instability.
74 iciency in DNA ligase are casually linked to genome instability.
75 progression, defects in growth, and nuclear genome instability.
76 DNA at stalled replication forks to prevent genome instability.
77 esses such as transcription, replication and genome instability.
78 t could be a significant cause of lymphocyte genome instability.
79 understanding of mechanisms underlying human genome instability.
80 cumulation causes DNA replication stress and genome instability.
81 ome cases R-loop accumulation, are causes of genome instability.
82 f these phenotypes and also protects against genome instability.
83 olism, and transformation is associated with genome instability.
84 larly in transcription, telomere biology and genome instability.
85 from unscheduled degradation and preventing genome instability.
86 cellular crisis characterized by large-scale genome instability.
87 nd stimulation of micronuclei, a hallmark of genome instability.
88 rrant expression of PRDM9 in oncogenesis and genome instability.
89 rstitial telomeric sequences (ITSs) promotes genome instabilities.
91 ls as a result of cell pathology and trigger genome instability, a hallmark of cancer and a number of
93 cleotides from DNA results in an increase in genome instability, a phenomenon that has been character
95 BS), a rare genetic disease characterized by genome instability, accumulation of micronuclei, suscept
96 reased ZBTB4 expression correlates with high genome instability across many frequent human cancers.
98 DNA (eccDNA) is both a driver of eukaryotic genome instability and a product of programmed genome re
99 promoter CpG islands that presumably lead to genome instability and aberrant expression of tumor supp
100 lts propose a mechanism for progerin-induced genome instability and accelerated replicative senescenc
102 CMV), like many other DNA viruses, can cause genome instability and activate a DNA damage response (D
104 een linked to transcription, replication and genome instability and are implicated in cancer and othe
107 at late-arising RB1 mutations can facilitate genome instability and cancer progression that are beyon
109 man skin from ultraviolet (UV) light-induced genome instability and cancer, as demonstrated by the de
116 ence of androgen receptor signaling inducing genome instability and changing DNA repair capacity in p
118 ch activity might contribute to the observed genome instability and compromised viability in SIRT7 kn
121 ty (MSI) is an important indicator of larger genome instability and has been linked to many genetic d
125 cient miR-31(-/-) rat esophagus displayed no genome instability and limited metabolic activity change
126 ironmental stress conditions lead to general genome instability and mask the Sir2-mediated recombinat
127 Failure to bypass these obstacles results in genome instability and may facilitate errors leading to
132 esis, caspase-3 activation may contribute to genome instability and play a pivotal role in tumor form
133 oss of NORAD or PUM hyperactivity results in genome instability and premature aging in mice (Kopp et
137 aploid cells, but not diploid cells, exhibit genome instability and reduce their ploidy when grown on
140 eplication forks can result in cell death or genome instability and resulting transformation to malig
141 erevisiae, cells lacking RTT107 or SLX4 show genome instability and sensitivity to DNA replication st
143 hase, the critically short telomeres lead to genome instability and telomerase is further up-regulate
146 resulted in delayed DNA repair and increased genome instability and transformation independent of p53
147 DR inactivation in these conditions promotes genome instability and tumor progression, but the underl
148 stabilize DNA replication forks and inhibits genome instability and tumorigenesis induced by oncogene
152 ances diethylnitrosamine-induced DNA damage, genome instability, and further tumorigenesis so that LR
153 ble element activity can lead to detrimental genome instability, and hosts have evolved mechanisms to
154 eal genes under positive selection, sites of genome instability, and repeated loss of a small derived
156 ingle-stranded DNA are potent instigators of genome instability, and RPA and Mre11-Sae2 play importan
157 ges in cellular proliferation and apoptosis, genome instability, angiogenesis and metabolic dysregula
160 The mechanisms responsible for ITS-mediated genome instability are not understood in molecular detai
162 the myriad mechanisms that can give rise to genome instability are still to be fully elucidated.
163 mportant role of ETAA1 in protecting against genome instability arising from incompletely duplicated
167 cations for understanding its involvement in genome instability-associated disorders including cancer
168 replicate across lesions, thereby preventing genome instability at the cost of increased point mutati
170 upport for a function of Top1 in suppressing genome instability at the guanine-run containing sequenc
172 A base damage is an important contributor to genome instability, but how the formation and repair of
175 ements are known to be major contributors to genome instability by generating Alu-mediated copy-numbe
176 surveillance mechanism that protects against genome instability by preventing cell growth after centr
177 nd together define a pathway that suppresses genome instability by recruiting the SMC5/6 cohesion com
180 idea that subtle enhancements of endogenous genome instability can exceed the tolerance of cancer ce
181 The increased mutation load associated with genome instability can lead to neuronal dysfunction and
183 plication is critical for cell division, and genome instability can result if duplication is not rest
184 our-promoting and positively correlates with genome instability, cancer cell invasion, metastasis and
185 ng decreased body mass, telomere elongation, genome instability, carotid artery distension and increa
186 not GIS genes, but suppressed the increased genome instability caused by individual query mutations.
193 ects cell-specific transcription programs in genome instability disorders and even normal cells.
196 Cells from Bloom's syndrome patients display genome instability due to a defective BLM and the downre
198 may arise from telomere crisis, a period of genome instability during tumorigenesis when depletion o
200 inconsistencies and mistakes in the YKOC, or genome instability events that rebalance the effects of
201 function holds promise to maximally exploit genome instability for hereditary and sporadic cancer th
202 l interactions with Saccharomyces cerevisiae genome instability genes, is a druggable target for an i
204 (RNAPII) transcription stress, R-loops, and genome instability have been established, the mechanisms
205 e-strand breaks (DSBs) are a major source of genome instability; however, recent studies from Lee et
206 fied highly transcribed genes as a source of genome instability; however, the degree to which large-s
207 associated with DNA damage accumulation and genome instability; however, the mechanisms underlying R
208 hesis is a prominent source of mitochondrial genome instability; however, the precise molecular deter
209 t cGAS localizes to micronuclei arising from genome instability in a mouse model of monogenic autoinf
211 se, POLIB, act as safeguards against plastid genome instability in Arabidopsis (Arabidopsis thaliana)
217 e mutant of CDC6 promotes re-replication and genome instability in cells lacking the CDT1 inhibitor G
219 ncided with substantially elevated levels of genome instability in Mcm4chaos3/chaos3;Fancc-/- cells,
226 ssion and induces DNA replication stress and genome instability in small cell lung cancer (SCLC) whil
228 ndings identify ZGA as a source of intrinsic genome instability in the germline and suggest that geno
229 ts detrimental effects, and thereby prevents genome instability in the transcribed region of genes.
232 mutations in RAD51 itself may contribute to genome instability in tumor cells, either directly throu
237 at its overexpression suppresses R loops and genome instability induced by depleting five different u
238 gulatory connections may be connected to the genome instability involved in several human diseases, i
242 -1 and ciprofloxacin-treated plants, plastid genome instability is associated with increased reactive
244 tability are crucial to human health because genome instability is considered a hallmark of cancer.
246 GEN1 depletion extend beyond mitosis, since genome instability is observed throughout all phases of
247 As altered Cse4/CENP-A activity leads to genome instability, it is pivotal to understand the mech
248 n of tumor suppressor genes, as well as with genome instability, leading to amplification and aberran
249 ms bone marrow progenitor cells and promotes genome instability, leading to development of chronic my
251 ur data indicate that, upon Sub1-disruption, genome instability linked to co-transcriptionally formed
252 eral oncogenic properties, such as increased genome instability, loss of cell-cell contact inhibition
253 e exhibit DPC-induced replication stress and genome instability, manifesting as premature ageing and
254 charomyces cerevisiae system to characterize genome instability mediated by yeast telomeric (Ytel) re
257 lated PCNA during DNA replication, while the genome instability of an elg1Delta mutant suggests timel
258 clinical rectal tumor samples, likely due to genome instability of precancerous and/or early cancer c
259 nd break repair (DSBR) provides insight into genome instability, oncogenesis and genome engineering,
260 TOP1 is also a major driver of endogenous genome instability, particularly when its catalytic inte
262 s in fruit, we found that Rhizobium causes a genome instability phenotype; we observed abnormally lon
264 e relentless and heterogeneous nature of the genome instability processes, are likely to confound tre
265 yndrome (RJALS), a disorder characterized by genome instability, progeria and early onset hepatocellu
266 ches to develop interventions that attenuate genome instability, reduce disease risk, and increase li
267 uding inflammation, invasion and metastasis, genome instability, resistance to chemo/radiotherapy, an
269 eostasis and suggest a mechanistic basis for genome instability resulting from deregulated DNA replic
272 ngle-base substitutions, LOH, or large-scale genome instability signatures characteristic of BRCA1/2-
273 NA replication involves the inherent risk of genome instability, since replisomes invariably encounte
280 restriction-like therapy for human progeroid genome instability syndromes and possibly neurodegenerat
282 n of DNA damage checkpoint function leads to genome instability that in turn can predispose cellular
283 fy carcinogen susceptibility as an origin of genome instability that is regulated by nuclear architec
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 completely protected cells from ETO-induced genome instability, thereby preserving cellular viabilit
287 t of ORF57 from the KSHV genome led to viral genome instability, thereby reducing viral genome copies
288 double-stranded breaks (DSBs) trigger human genome instability, therefore identifying what factors c
290 To evaluate the contribution of large-scale genome instability to this phenomenon, we analyzed potat
291 s study documents hybrid incompatibility and genome instability triggered by the backcrossing of Brav
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.
295 s role of short telomeres in contributing to genome instability, we propose that telomere shortening
296 results define Top1 as a source of DSBs and genome instability when ribonucleotides incorporated by
297 eir DNA to avoid deleterious consequences of genome instability, which have been linked to human dise
299 ween adults and children are associated with genome instability, which is much more frequent in adult
300 nomes, and when active, are thought to cause genome instability with potential benefit to genome evol