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1 horylation, and subsequent resolution of the DNA damage foci.
2 repair enzyme, RAD51, to replication-induced DNA damage foci.
3 ment of RAD51 to stalled replication-induced DNA damage foci.
4 bility to resolve ionizing radiation-induced DNA damage foci.
5 turn facilitating the recruitment of MDC1 to DNA damage foci.
6 oint 1) and 53BP1 (p53 binding protein 1) to DNA damage foci.
7 tes, repair of DNA breaks, and resolution of DNA damage foci.
8 itate DNA repair, but also maintain BRCA1 in DNA damage foci.
9 r proteins, forming DSB-protein complexes at DNA damage foci.
10 h the colocalization of L1CAM and persistent DNA damage foci.
11 ion and nuclear translocation and persistent DNA damage foci.
12 ruit Rap80 and the entire Brca1 A complex to DNA-damage foci.
13  resulted in G(2) arrest and accumulation of DNA damage foci, a finding suggestive of an essential ro
14 hortening with age, which is associated with DNA damage foci and cellular senescence.
15 1 depletion results in increased spontaneous DNA damage foci and elevated levels of H2AK15ub and impa
16 ies, including formation of telomere-induced DNA damage foci and loss or duplication of telomeric seq
17 a-H2AX coimmunoprecipitate and colocalize in DNA damage foci and PP2A dephosphorylates gamma-H2AX in
18 Rather, loss of MYSM1 resulted in persistent DNA damage foci and prolonged DDR signaling.
19  contributes to the persistence of gammaH2AX DNA damage foci and promotes the DNA damage response lea
20 t telomeres can take place in the absence of DNA damage foci and underscore the functional compartmen
21   Akt prevents the translocation of BRCA1 to DNA damage foci and, thereby, inhibiting the activation
22 d-type RPA2, was competent to associate with DNA damage foci as determined by colocalization with gam
23          The frequency of DN thymocytes with DNA damage foci at multiple TCR loci simultaneously is i
24       ALT tumor cells often contain abundant DNA damage foci at telomeres and rely on the alternative
25 sion of Rrm3p suppressed the accumulation of DNA damage foci but not the hydroxyurea sensitivity of c
26 BP1 (also known as TRP53BP1), a component of DNA damage foci, changes the dynamic behaviour of chroma
27  with etoposide with a significant number of DNA damage foci colocalizing with telomeres in cytologic
28                                              DNA damage foci consistent with collapsed replication fo
29 e in ATM activation and RAD51 recruitment to DNA damage foci during the response to genotoxic stresse
30  of spontaneous recombination, mutation, and DNA damage foci formation arising during DNA replication
31 ruited to heterochromatic gammaH2AX-labelled DNA damage foci in an ATM- and ATR-dependent manner.
32 feration resulted in a marked enhancement of DNA damage foci in Brca1(-/-) mouse mammary.
33                                 Formation of DNA damage foci in neurons and gliosis were confirmed in
34 iently translocated to telomerically located DNA damage foci in response to the synthesis of aberrant
35 test ends colocalize with gammaH2AX-positive DNA damage foci in senescent cells.
36 d the colocalization of short telomeres with DNA damage foci in senescent interphase cells suggests t
37 bridization and ChIP, that up to half of the DNA damage foci in stress-induced senescence are located
38 antioxidant prevented the development of the DNA damage foci in WRN-depleted cells, whereas acute oxi
39 d replicative senescence and accumulation of DNA-damage foci in cultured cells, as well as increased
40 ction results in delayed CtIP clearance from DNA damage foci, increased DNA-end resection, and reduce
41 l output and reduced the number of gammaH2AX DNA damage foci, indicating that dietary restriction pre
42 008H rescued the tardy exchange of ATM-KD at DNA damage foci, indicating that PRD coordinates ATM act
43                The recruitment of PP2A(C) to DNA damage foci is H2AX dependent.
44 The functional significance of the resulting DNA damage foci is poorly understood.
45         Therefore, gamma-H2AX elimination at DNA damage foci is required for DNA damage repair, but a
46        Consistent with its role in promoting DNA damage foci, MDC1 knockdown affected the formation o
47 eaction, microsteatosis, pleomorphic nuclei, DNA damage, foci of altered hepatocytes, focal lobular a
48  damage resulted in localization of Pfh1p to DNA damage foci, suggesting that nuclear Pfh1p also func
49                                        These DNA damage foci tended to colocalize with telomeres, whi
50 rradiation induces translocation of RAP80 to DNA damage foci that colocalize with gamma-H2AX.
51 epair proteins at ionizing radiation-induced DNA damage foci that Wwox expression suppresses DSB repa
52 y targeting BRCA1/BRCA2 tumor suppressors to DNA damage foci through multivalent binding of Lys-63-li
53 t of active ataxia telangiectasia mutated to DNA damage foci, thus affecting the formation of gamma-H
54 ohesin subunit Rad21 caused telomere-induced DNA damage foci (TIF) formation, and destabilized TRF1 a
55 ngth assay, and telomere-dysfunction-induced DNA damage foci (TIF) in placentas and CAMs between 18-w
56 analysis allowed microbeams to be traced and DNA damage foci to be quantified in valleys between beam
57 tion facilitates recruitment of Rad51 to the DNA damage foci to initiate DNA repair through homologou
58 stream signaling proteins 53bp1 and Brca1 to DNA damage foci was completely abolished.
59                  Intense nuclear staining of DNA damage foci was observed in nuclei within the centra
60 he formation of telomere dysfunction-induced DNA damage foci was reduced in both cre-infected Mre11(A
61 tion of 53BP1, as well as its recruitment to DNA damage foci, was strongly suppressed by proteasome i
62                                      Nuclear DNA damage foci were detected in the endothelium of ex v
63 fibrosis and the colocalization of L1CAM and DNA damage foci, while Ab417 attenuates these effects.
64 ere, we use a telomere-based system to track DNA damage foci with high resolution in living cells.
65 hagy, and significantly delays resolution of DNA damage foci with little reduction of overall protein
66 rolonged retention of DDB2 at the subnuclear DNA damage foci within micropore irradiated cells.
67  biological damage can be assessed measuring DNA damage foci yields, only provided that artefacts rel