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1 repair enzyme, RAD51, to replication-induced DNA damage foci.
2 ment of RAD51 to stalled replication-induced DNA damage foci.
3 turn facilitating the recruitment of MDC1 to DNA damage foci.
4 oint 1) and 53BP1 (p53 binding protein 1) to DNA damage foci.
5 tes, repair of DNA breaks, and resolution of DNA damage foci.
6 itate DNA repair, but also maintain BRCA1 in DNA damage foci.
7 r proteins, forming DSB-protein complexes at DNA damage foci.
8 horylation, and subsequent resolution of the DNA damage foci.
9 ruit Rap80 and the entire Brca1 A complex to DNA-damage foci.
10 resulted in G(2) arrest and accumulation of DNA damage foci, a finding suggestive of an essential ro
11 1 depletion results in increased spontaneous DNA damage foci and elevated levels of H2AK15ub and impa
12 ies, including formation of telomere-induced DNA damage foci and loss or duplication of telomeric seq
13 a-H2AX coimmunoprecipitate and colocalize in DNA damage foci and PP2A dephosphorylates gamma-H2AX in
14 contributes to the persistence of gammaH2AX DNA damage foci and promotes the DNA damage response lea
15 t telomeres can take place in the absence of DNA damage foci and underscore the functional compartmen
16 Akt prevents the translocation of BRCA1 to DNA damage foci and, thereby, inhibiting the activation
17 d-type RPA2, was competent to associate with DNA damage foci as determined by colocalization with gam
19 sion of Rrm3p suppressed the accumulation of DNA damage foci but not the hydroxyurea sensitivity of c
20 BP1 (also known as TRP53BP1), a component of DNA damage foci, changes the dynamic behaviour of chroma
21 with etoposide with a significant number of DNA damage foci colocalizing with telomeres in cytologic
22 e in ATM activation and RAD51 recruitment to DNA damage foci during the response to genotoxic stresse
23 of spontaneous recombination, mutation, and DNA damage foci formation arising during DNA replication
24 ruited to heterochromatic gammaH2AX-labelled DNA damage foci in an ATM- and ATR-dependent manner.
26 iently translocated to telomerically located DNA damage foci in response to the synthesis of aberrant
28 d the colocalization of short telomeres with DNA damage foci in senescent interphase cells suggests t
29 bridization and ChIP, that up to half of the DNA damage foci in stress-induced senescence are located
30 antioxidant prevented the development of the DNA damage foci in WRN-depleted cells, whereas acute oxi
31 d replicative senescence and accumulation of DNA-damage foci in cultured cells, as well as increased
32 ction results in delayed CtIP clearance from DNA damage foci, increased DNA-end resection, and reduce
33 l output and reduced the number of gammaH2AX DNA damage foci, indicating that dietary restriction pre
38 damage resulted in localization of Pfh1p to DNA damage foci, suggesting that nuclear Pfh1p also func
41 epair proteins at ionizing radiation-induced DNA damage foci that Wwox expression suppresses DSB repa
42 y targeting BRCA1/BRCA2 tumor suppressors to DNA damage foci through multivalent binding of Lys-63-li
43 t of active ataxia telangiectasia mutated to DNA damage foci, thus affecting the formation of gamma-H
44 ohesin subunit Rad21 caused telomere-induced DNA damage foci (TIF) formation, and destabilized TRF1 a
45 analysis allowed microbeams to be traced and DNA damage foci to be quantified in valleys between beam
46 tion facilitates recruitment of Rad51 to the DNA damage foci to initiate DNA repair through homologou
49 he formation of telomere dysfunction-induced DNA damage foci was reduced in both cre-infected Mre11(A
50 tion of 53BP1, as well as its recruitment to DNA damage foci, was strongly suppressed by proteasome i
52 ere, we use a telomere-based system to track DNA damage foci with high resolution in living cells.
53 hagy, and significantly delays resolution of DNA damage foci with little reduction of overall protein
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