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1 within the repeats, facilitating slippage or sister chromatid exchange.
2 r maximal induction of replication-dependent sister chromatid exchange.
3 chromosomal aberrations and 3-fold elevated sister chromatid exchange.
4 acilitate FA pathway activation and suppress sister chromatid exchange.
5 to an increase in the incidence of telomere sister chromatid exchange.
6 unctional BLM show 10-fold elevated rates of sister chromatid exchange.
7 synthesis and caused a 3-4-fold increase in sister chromatid exchange.
8 relatively normal XRCC1 levels but elevated sister chromatid exchange.
9 erence in HeLa cells leads to an increase in sister chromatid exchange.
10 gene conversion but maintain proficiency in sister chromatid exchange.
11 recombination with a concomitant increase in sister chromatid exchange.
12 rmal replication intermediates and increased sister chromatid exchange.
13 toxicant as well as an effective inducer of sister-chromatid exchange.
14 t functions in a protein complex to suppress sister-chromatid exchange.
15 ative capacity and an increased frequency of sister chromatid exchanges.
16 itro induced enhanced chromosomal breaks and sister chromatid exchanges.
17 This leads to an increase in sister chromatid exchanges.
18 A damage, and displayed elevated spontaneous sister chromatid exchanges.
19 Bloom's syndrome is an elevated frequency of sister chromatid exchanges.
20 the potential for loss of heterozygosity and sister-chromatid exchanges.
21 on in response to DNA damage, and suppresses sister-chromatid exchanges.
22 e of genome stability and the suppression of sister-chromatid exchanges.
25 recombination repair, we observed extensive sister chromatid exchanges after treatment with tirapaza
26 e fibroblasts displayed an increased rate of sister chromatid exchange and a high frequency of sponta
27 n cells results in an increased frequency of sister chromatid exchange and DNA damage sensitivity aft
30 ing membrane signaling, and the induction of sister chromatid exchange and HPRT mutations by very low
31 ely to be intact as basal and damage induced sister chromatid exchange and immunoglobulin gene conver
32 hyper-recombination manifested as excessive sister chromatid exchange and loss of heterozygosity.
33 re partially defective in the suppression of sister chromatid exchange and resistance to camptothecin
35 We conclude that ORD activity suppresses sister chromatid exchange and stimulates inter-homologue
36 n relieved the cells with the suppression of sister chromatid exchange and therefore led to a hyper-r
37 ase activity to suppress spontaneous unequal sister chromatid exchanges and DNA double-strand break-i
38 c mitotic recombination, a high frequency of sister chromatid exchanges and double strand DNA breaks,
39 telomeres, manifested as increased telomere sister chromatid exchanges and formation of telomere cir
40 ous recombination (HR), exhibiting decreased sister chromatid exchanges and HR-dependent repair as de
41 notype manifests as an elevated frequency of sister chromatid exchanges and interhomologue recombinat
42 ected into BS cells reduces the frequency of sister chromatid exchanges and restores BLM in the nucle
43 ary Pml(C62A/C65A) cells exhibited increased sister-chromatid exchange and chromosome abnormalities.
44 types of Bloom syndrome cells as assessed by sister-chromatid exchange and micronuclei formation assa
45 d telomere shortening, elevation of telomere sister-chromatid exchanges and increased aphidicolin-ind
46 integrated recombination substrate, unequal sister-chromatid exchanges and repair of collapsed repli
47 omycin C (MMC), as measured by cell killing, sister chromatid exchange, and chromosome aberrations.
48 51-mediated D-loop formation, suppression of sister chromatid exchange, and resistance to camptotheci
49 ases karyotype abnormalities and spontaneous sister chromatid exchange, and slows down cell prolifera
50 tability, as quantified by chromatid breaks, sister chromatid exchanges, and H2AX phosphorylation.
51 quency of recombination, gene amplification, sister chromatid exchanges, and micronuclei formation in
52 come hypermutable, exhibit high frequency of sister chromatid exchanges, and show increased micronucl
53 lts may explain why cytologically observable sister chromatid exchanges are induced only weakly by DN
54 fects, including specific gene mutations and sister chromatid exchanges, are induced in neighboring,
55 we examined these cell types for evidence of sister chromatid exchange at telomeres, and observed an
56 centromeric CO-FISH patterns consistent with sister chromatid exchange at the frequency of 5% in prim
59 BLM, telomeric circle formation and telomere sister chromatid exchange, both arising out of nucleolyt
60 n resistance and increased cisplatin-induced sister chromatid exchange, both of which were reversed b
61 s expressing BLM-S144A show normal levels of sister chromatid exchange but fail to maintain the mitot
62 We previously found that the induction of sister chromatid exchanges by UV irradiation was greatly
63 nomic instability and increased frequency of sister chromatid exchange characteristic of Bloom's synd
64 ly 7-methylguanine), can specifically induce sister chromatid exchange, chromatid and chromosome gaps
66 relation between chromosomal instability and sister chromatid exchange, delayed mutation, and mismatc
69 eletion of mRtel1 increased the frequency of sister chromatid exchange events and suppressed gene rep
70 ally, evidence of gene conversion or unequal sister chromatid exchange events in T. quasimodo and T.
73 heir integrity, it also permits rare unequal sister chromatid-exchange events within palindromes that
75 e not affected by the absence of Rad51d, but sister chromatid exchange frequencies did fail to be ind
79 d points such as chromosome destabilization, sister chromatid exchanges, gene mutation and amplificat
80 on can be induced display elevated levels of sister chromatid exchange, gross chromosomal aberrations
81 s can occur by replication slippage, unequal sister chromatid exchange, homologous recombination, and
82 the elevated level of gene targeting and of sister chromatid exchanges, implying that Blm primarily
86 fic biomarkers (DNA and albumin adducts) and sister chromatid exchanges in the blood of 48 reinforced
89 ents are the probable consequence of unequal sister chromatid exchanges involving chromosome 2, as we
90 e show that gene conversion, and not unequal sister chromatid exchange, is the predominant recombinat
91 hey suggest that gene conversion rather than sister chromatid exchange may be the primary recombinati
93 BS cells, chromosomal abnormalities such as sister chromatid exchanges occur at highly elevated rate
94 orce in the evolution of the rRNA genes with sister chromatid exchange occurring more often than exch
96 with RAD18 deficiency, reverses the elevated sister chromatid exchange of the rad18 mutant, and reduc
98 ut R1 and R2 retrotransposition the frequent sister chromatid exchanges postulated from various empir
99 nce of chromosomal gaps and breaks, elevated sister chromatid exchange, quadriradial formations, and
100 re unstable genetically and exhibit frequent sister chromatid exchanges, reflective of homologous rec
101 cause in its absence cells display increased sister chromatid exchanges, replication origin firing an
103 , called Strand-seq, that can be used to map sister chromatid exchange (SCE) events genome-wide in si
104 This activity suppresses potentially harmful sister chromatid exchange (SCE) events in wild-type cell
105 ay be responsible for the elevated levels of sister chromatid exchange (SCE) found in BLM(-/-) cells.
107 d human aging, we analyzed the dependence of sister chromatid exchange (SCE) frequencies on location
109 p53 further enhanced the rate of spontaneous sister chromatid exchange (SCE) in Bloom syndrome (BS) c
112 likely to be accommodated by adjustments in sister chromatid exchange (SCE) rate, rather than by dir
113 mportance of G2 arrest in DNA damage-induced sister chromatid exchange (SCE) was evident by a 10-fold
114 recombination visualized cytogenetically as sister chromatid exchange (SCE), and that this rate is d
116 the simultaneous high-resolution mapping of sister chromatid exchange (SCE), facilitating the study
117 , 10- and 30-fold higher rate of spontaneous sister chromatid exchange (SCE), heteroallelic recombina
119 n a significant increase in the frequency of sister chromatid exchange (SCE), whereas deleting both B
120 DT40 cells results in an increased level of sister chromatid exchange (SCE)--the hallmark feature of
125 mic instability epitomized by high levels of sister-chromatid exchange (SCE) and cancer predispositio
126 ctures in vivo, increase spontaneous unequal sister-chromatid exchange (SCE) in vegetatively growing
128 der characterized cellularly by increases in sister chromatid exchanges (SCEs) and numbers of micronu
129 defective for BLM exhibit elevated levels of sister chromatid exchanges (SCEs) and patients with Bloo
131 x2(null) cells exhibited reduced spontaneous sister chromatid exchanges (SCEs) but this was not due t
132 itization with caffeine and the induction of sister chromatid exchanges (SCEs) by UV irradiation are
133 somal instability, characterized by elevated sister chromatid exchanges (SCEs), as well as chromosoma
134 isiae RAD51 in DNA damage-associated unequal sister chromatid exchanges (SCEs), translocations, and i
135 repair of mitomycin C (MMC)-induced DSBs and sister chromatid exchanges (SCEs), two RAD51-dependent p
137 eted of BLAP75 display an increased level of sister-chromatid exchange, similar to cells depleted of
138 telomeres may be maintained through telomere sister chromatid exchange (T-SCE) in murine telomere rev
139 elicase-deficient mutant, abolished telomere sister chromatid exchange (T-SCE), indicating that WRN n
141 of BS and FA cells-an elevated frequency of sister chromatid exchanges-was due to a loss of interact
144 subjects, albumin and DNA adducts as well as sister chromatid exchanges were significantly correlated
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