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1 aks, and pronounced susceptibility to single-strand breakage.
2  detectable levels or caused significant DNA strand breakage.
3 hat regulates apoptotic cell death after DNA strand breakage.
4  major specific effect on the rate of double-strand breakage.
5 excision, which generates an abasic site for strand breakage.
6        SIN-1 but not SNAP induced DNA single-strand breakage.
7 he phosphoryl transfer reaction that induces strand breakage.
8  to 48 hours and resulted in significant DNA strand breakage.
9 the DNA-methylating agent MMS and to the DNA strand breakage agent phleomycin, with conjugational rec
10 mbilical vein endothelial cells (HUVEC), DNA strand breakage (alkaline unwinding assay), PARS activat
11 r Ca(2+) chelators also inhibited DNA single-strand breakage and activation of poly(ADP-ribose) synth
12 oposed the importance of oxidant-induced DNA strand breakage and activation of the nuclear enzyme pol
13                                   DNA single strand breakage and activation of the nuclear enzyme pol
14 participates in multiple steps of DNA single-strand breakage and base excision repair.
15 on of mitochondrial respiration, induced DNA strand breakage and caused an activation of PARS.
16 roducts with several abasic sites, producing strand breakage and duplex melting, respectively.
17  anticancer drug cisplatin, which causes DNA strand breakage and is highly recombinogenic in some mod
18 ecombinase in three different reactions: DNA strand breakage and joining, and two types of RNA cleava
19 ar and molecular processes, including double strand breakage and modifications of sugar moieties and
20 l replication making DNA more susceptible to strand breakage and mutations.
21 t that inflammatory cell injury involved DNA strand breakage and PARS, triggering an energy-consuming
22                                          DNA strand breakage and perturbation of cell-cycle progressi
23    A cytotoxic cycle triggered by DNA single-strand breakage and poly (ADP-ribose) synthetase activat
24 nomic rearrangements that result from double-strand breakage and rejoining in cells of the skin in wh
25 led DNA through a concerted mechanism of DNA strand breakage and religation.
26 lthough more complex models involving double-strand breakage and repair could produce reciprocal exch
27                  We show here that an active strand breakage and reunion activity is required for for
28 in cells exposed to ONOO- is mediated by DNA strand breakage and the subsequent activation of the DNA
29              LEDGF protected DNA from single-strand breakage and upregulated the expression of Hsp27.
30  increase in peroxynitrite formation and DNA strand breakage, and a decrease in intracellular NAD+ co
31 ating in oxidative DNA adduct formation, DNA strand breakage, and cell death.
32  mtDNA in older animals along with increased strand breakage, and that this results in its selective
33               To investigate the role of DNA strand breakage as the molecular lesion responsible for
34 se deficiencies may perpetually generate DNA strand breakage as we have found chromosomal abnormaliti
35 d hyphal DNA fragmentation, primarily single-strand breakage, as shown by increased electrophoretic m
36 romatin domains flanking sites of DNA double-strand breakage associated with gamma-irradiation, meiot
37 f oligonucleotide fragment sizes produced by strand breakage at the damaged sites.
38 sociated AP lyase activity also catalyze DNA strand breakage at the resulting or preexisting AP site
39 reakage data, extracting the rates of single-strand breakage at two dye staining ratios and measuring
40 [V(D)J recombination] begins with DNA double-strand breakage by the RAG1 and RAG2 proteins, acting at
41                             Finally, the DNA strand breakage elongation assay showed that Tpo inhibit
42 e rapid activation of PARP-1 at sites of DNA strand breakage facilitates DNA repair by recruiting the
43 ts could be explained by drug-induced double-strand breakage followed by trimming, templated patching
44 used by reduced susceptibility to DNA double-strand breakage for IR makes double-strand breaks (DSBs)
45  of mitochondrial respiration and DNA single strand breakage in response to peroxynitrite.
46 d by AP endonuclease 1, introducing a single-strand breakage in the hairpin loop.
47      Within 2 h, etoposide caused marked DNA strand breakage in xenograft tumor-derived endothelial c
48  dUTP-biotin nick end labeling of DNA double-strand breakage, indicative of late stages of apoptosis,
49 sterol oxidation and supercoiled plasmid DNA strand breakage inhibition induced by both peroxyl and h
50                    Therefore accumulation of strand breakages is avoided.
51  increased phosphorylation of the DNA double-strand breakage marker H2AX and augmentation of clonogen
52 may be explained by a lesion-specific double-strand breakage mechanism involving the RAG complex acti
53 a C1'-oxidized abasic site implicated in DNA strand breakage, mutagenesis, and formation of covalent
54 TTAGGG)81 human telomere insert, 7-fold more strand breakage occurred in the restriction fragment wit
55                                       Double-strand breakage occurs only when these proteins are boun
56 ur-containing amino acid that can induce DNA strand breakage, oxidative stress and apoptosis.
57 cemia, intravascular oxidant production, DNA strand breakage, PARP activation and a selective loss of
58                 These data indicate that DNA strand breakage per se does not necessarily lead to chro
59 ralleled by a dose-dependent increase in DNA strand breakage, reaching its maximum at 20-30 min after
60 arkers of cell cycle activity and DNA double-strand breakage, respectively, associated with neuron de
61     Activation of PARS by ONOO--mediated DNA strand breakage resulted in a significant decrease in in
62 NA by a conserved mechanism of transient DNA strand breakage, rotation, and religation.
63 lso led to a replication blockade and double-strand breakage using an SV40 in vitro replication assay
64             Neither histone staining nor DNA strand breakage was observed in freshly isolated PBTs; h
65 ent of (N7 guanine)-DNA adducts leads to DNA strand breakage, we were able to determine the site of a
66 itric oxide (NO) and superoxide, induces DNA strand breakage, which activates the nuclear enzyme poly
67 ve oxygen species are potent triggers of DNA strand breakage, with subsequent activation of the nucle
68 s of 4.5 to 18 x 10(9) W m(-2), to determine strand breakage yields and the frequency and pattern of

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