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1                                              DSBR proteins including Mre11, Rad50, Rad51, Rad54, and
2 on of C-NHEJ factors significantly abrogates DSBR in transcribed but not in non-transcribed genes.
3  products involved in checkpoint control and DSBR have been studied in great detail in yeast.
4 e requisite for both V(D)J recombination and DSBR, the DNA-dependent protein kinase.
5 obile group II intron-encoded RT has a basal DSBR activity that uses conserved structural features of
6 A-PKcs kinase activity is essential for both DSBR and V(D)J recombination.
7 h p53-Exo1(null) mice, whose defects in both DSBR and mismatch repair also compromised survival.
8 cts are difficult to rationalize strictly by DSBR, these properties are most readily consistent with
9 ses a topoisomerase to resolve the canonical DSBR intermediate, are supported by these data.
10 ss of tetrads not predicted by the canonical DSBR model was identified.
11                              The "canonical" DSBR model, in which only 5' ends are degraded and resol
12 e data suggest that E4orf6 disrupts cellular DSBR signaling by inhibiting PP2A, leading to prolonged
13                  We recently described a CHO DSBR mutant belonging to the XRCC7 complementation group
14 uclease and monitored temporally constrained DSBR at a specific chromosomal site in bloodstream form
15 sion and presumably occurs by a conventional DSBR recombination mechanism initiated by cleavage of th
16 t deficiency and reliance upon ATM-dependent DSBR renders TP53 mutant GBMs hypersensitive to TMZ/AZD1
17 , I-SceI and Cas9 induced markedly different DSBR profiles.
18  interactions promote engagement of distinct DSBR pathways.
19 of late-onset tumors due to its roles in DNA DSBR as well as in DNA MMR.
20  required as for cells without induced DSBs: DSBR proteins, DinB-error-prone polymerase, and the RpoS
21                                       During DSBR involving nonhomologous ends, Msh2p localized stron
22 e joint-molecule intermediate arising during DSBR usually leads to crossing over); (2) cutting only o
23 ssess coordination of the broken ends during DSBR in bacteriophage T4.
24  role in clustering DNA breaks to facilitate DSBR by homologous recombination (HR).
25 reen clinically relevant small molecules for DSBR inhibition with the aim of identifying improved GBM
26 CA1 functions differ from those required for DSBR.
27 tic insights into C-NHEJ-mediated error-free DSBR of the transcribed genome.
28 ctivity of Pol eta is required in error-free DSBR.
29  missing sequences, thus allowing error-free DSBR.
30  solution to the long-standing puzzle of how DSBR pathway 'choice' is regulated through the cell cycl
31 rved 'conditional' haploinsufficiency for HR-DSBR in BRCA1(mut/+) cells in the face of replication st
32 s formation, reflecting a defect in Palb2 HR-DSBR function, a strongly suspected contributor to Brca1
33 bination-type double strand break repair (HR-DSBR) through physical interactions with BRCA1, BRCA2, a
34 ination- type double-strand break repair (HR-DSBR), checkpoint functions, centrosome number control,
35 o disrupt PALB2 binding and disable BRCA2 HR/DSBR function.
36 ity and allosteric control of ABC-ATPases in DSBR, membrane transport, and chromosome condensation by
37 suggests that SPR-5 may function directly in DSBR.
38 Msh3p associates with intermediates early in DSBR to participate in the rejection of homeologous pair
39 mes may have inherent ability to function in DSBR in a wide range of organisms.
40 ions that optimized its cellular function in DSBR.
41 de that the Ku70 gene product is involved in DSBR and V(D)J recombination and confirm that the Ku70 g
42 unction of the four mammalian DNA ligases in DSBR, V(D)J recombination and other reactions.
43 f DNA-PK-mediated protein phosphorylation in DSBR and V(D)J recombination, we assessed the effects of
44 s for investigating cell cycle variations in DSBR.
45 f intrachromosomal end joining in individual DSBR survivors exclusively revealed MMEJ-based deletions
46 r in U251 human glioblastoma cells, inhibits DSBR and induces significant radiosensitization in the a
47                                Research into DSBR exploits rare-cutting endonucleases to cleave exoge
48 ow no transcriptional misregulation of known DSBR involved genes.
49 ssays that can efficiently measure the major DSBR pathways of homologous recombination (HR), classica
50                       In addition, mammalian DSBR proteins and their activities are discussed.
51 NA molecules, supporting a homology-mediated DSBR mechanism.
52 e lacZ locus causes a second RecBCD-mediated DSBR event to occur in the terminus region of the chromo
53 ction and the relationships between multiple DSBR pathways at a single endogenous disease gene.
54 54l and Rad54b, genes important for multiple DSBR pathways.
55 proach for simultaneously measuring multiple DSBR pathways in treatment selection and oncology resear
56 olled switch from high-fidelity to mutagenic DSBR under stress.
57 se data implicate reduced rates of SSBR, not DSBR, as the source of both neurodevelopmental and neuro
58                     Quantitative analysis of DSBR pathways employed indicated that inter-chromosomal
59  by both DSB ends may be a common feature of DSBR that increases repair efficiency but also the likel
60 pansion involves an NHEJ-independent form of DSBR.
61  human tumor cells through the inhibition of DSBR, notably in the absence of E1B-55K.
62 n serve as tools to dissect the interplay of DSBR pathway networks in cells and will have broad impli
63 indings are consistent with the ECR model of DSBR.
64 onsistent with several coordinated models of DSBR, including a modified version of the ECR model.
65 eral phenotypes indicating a perturbation of DSBR, including increased p53-dependent germ cell apopto
66 presses radiation-induced phosphorylation of DSBR proteins, blocks DSB end resection, and enhances th
67 ults in germline-specific down-regulation of DSBR genes, thereby impairing maintenance of genomic int
68 e true forward-mutation sequence spectrum of DSBR-associated stress-induced mutagenesis, for which pr
69  will have broad implications for studies of DSBR mechanisms in basic research and drug discovery.
70                          Several variants of DSBR reporters are available, however these are often li
71 tent with the inhibitory effect of E4orf6 on DSBR, expression of wild-type but not mutant E4orf6 redu
72                   In contrast, several other DSBR models propose that the two ends of a break are rep
73 ase active form of DNA-PKcs can reconstitute DSBR and V(D)J recombination in a DNA-PKcs-deficient cel
74                               E4orf6 reduced DSBR capacity in transfected and infected cells, as meas
75 ts endo- and exonuclease activities regulate DSBR by nonhomologous end-joining (NHEJ) versus homologo
76 ), a form of DNA double-strand break repair (DSBR) active in mammalian V(D)J recombination.
77  involved in DNA double-strand break repair (DSBR) and DNA damage-induced checkpoint activation.
78 , error-free DNA double-strand break repair (DSBR) and intra-S phase DNA damage checkpoint control.
79 ized in both DNA double-strand break repair (DSBR) and V(D)J recombination, but the mechanism by whic
80 -over during DNA double-strand-break repair (DSBR) by disassembling double-Holliday junctions (dHJs)
81 ajor pathway for double-strand break repair (DSBR) in mammalian cells, protects against expansion in
82 otic bimolecular double-strand break repair (DSBR) intermediate.
83 ith the accepted double-strand-break repair (DSBR) model for intron inheritance, and implicate additi
84 edictions of the double-strand break repair (DSBR) model for meiotic recombination by examining the s
85              The double-strand break repair (DSBR) model of recombination predicts that heteroduplexe
86 variation of the double-strand-break repair (DSBR) model that has the following features: (1) Hollida
87 fficiency of double-strand DNA break repair (DSBR) of the BRCA1-/- human breast cancer line, HCC1937.
88 ing is the major double-strand break repair (DSBR) pathway in mammals.
89 ance between DNA double strand break repair (DSBR) pathways is essential for understanding treatment
90 ption of meiotic double-strand break repair (DSBR) progression.
91 n (ECR) model of double-strand-break repair (DSBR) proposes that each end of a double-strand break (D
92 teracts with the double-strand break repair (DSBR) protein DNA-dependent protein kinase and cooperate
93              DNA double-strand break repair (DSBR) proteins and the SOS and RpoS stress responses are
94  inactivated DNA double-strand break repair (DSBR) proteins, DNA Ligase IV (Lig4), Xrcc2, and Brca2,
95  on cellular DNA double strand break repair (DSBR) proteins.
96 s of chromosomal double-strand break repair (DSBR) provides insight into genome instability, oncogene
97 and completed by double-strand break repair (DSBR) recombination with the donor allele.
98              DNA double strand break repair (DSBR) represents a fundamental process required to maint
99 se including DNA double-strand break repair (DSBR) through DNA end resection, chromosomal stability,
100 teins act during double-strand break repair (DSBR) to correct mismatches in heteroduplex DNA, to supp
101 d to function in double-strand break repair (DSBR) via microhomology-mediated end-joining (MMEJ) and
102 NA synthesis and double-strand break repair (DSBR) via microhomology-mediated end-joining (MMEJ).
103 plex acts in DNA double-strand break repair (DSBR), detection, and signaling; yet, how its endo- and
104 inks between DNA double-strand break repair (DSBR), illegitimate recombination and plasmid DNA integr
105  of Rad50 in DNA double-strand break repair (DSBR), we biochemically and structurally characterized A
106  involved in DNA double-strand break repair (DSBR).
107 rchestrating DNA double-strand break repair (DSBR).
108 reak (SSBR), and double-strand break repair (DSBR).
109 tion and for DNA double-strand break repair (DSBR).
110 ir (BER) and low double strand break repair (DSBR).
111 is important for double-strand break repair (DSBR).
112  a defect in DNA double-strand break repair (DSBR).
113 5 in meiotic DNA double-strand break repair (DSBR).
114 aling (SDSA) and double-strand break repair (DSBR).
115  error-prone DNA double-strand break repair (DSBR).
116 neral process of double strand break repair (DSBR).
117  through mitotic double-strand break-repair (DSBR), typically involving homologous recombination (HR)
118 nd titratable assays of cellular DSB repair (DSBR) are important to functionally interrogate the inte
119 HEJ) is the dominant pathway for DSB repair (DSBR) in adult mammalian cells.
120 t detect a significant defect in DSB repair (DSBR) in primary fibroblasts from PNKP patients spanning
121    In these protozoan parasites, DSB repair (DSBR) is dominated by homologous recombination (HR) and
122 s of action of MDC1 and 53BP1 in DSB repair (DSBR).
123 al reverse transcriptase that facilitates RT-DSBR.
124        Altogether, our findings highlight RT-DSBR as an alternative pathway for repairing DSBs in tra
125 letions - a distinct genomic signature of RT-DSBR that occurs when spliced mRNA guides repair.
126 rs that promote RNA-templated DSB repair (RT-DSBR).
127  that is not absolutely required for XRCC4's DSBR function.
128              Here we report that during such DSBR, mammalian C-NHEJ proteins form a multiprotein comp
129  for the Bloom RecQ DNA helicase (BLM) in TC-DSBR in human cells.
130 athway, Transcription-Coupled DSB Repair (TC-DSBR), that entails R-loop accumulation and dissolution.
131  Our genomic analysis has also revealed that DSBR at the lacZ locus causes a second RecBCD-mediated D
132 l transducers, cell cycle regulators and the DSBR pathways is illustrated.
133 ated protein 53 (Trp53)-null background, the DSBR defect caused by the E109K mutation altered the tum
134 germ cell apoptosis, increased levels of the DSBR marker RAD-51, and sensitivity toward DSB-inducing
135 hotspot are consistent with a variant of the DSBR model in which the extent of heteroduplex on one si
136                     Modified versions of the DSBR model, including one that uses a topoisomerase to r
137                                        These DSBR pathways available to T. brucei likely underlie pat
138                  Moreover, we show that this DSBR defect is also observed in a subset of patients wit
139 we monitor the relative utilization of three DSBR pathways following cleavage by I-SceI or CRISPR/Cas
140 ved in the theta-mediated end joining (TMEJ) DSBR pathway, has been proposed to play a role in repeat
141 terface that localizes G2L4 RT homodimers to DSBR sites with both monomers positioned for MMEJ.
142 PH1 mutations may be caused by an underlying DSBR defect.
143 tructs have been developed to detect various DSBR pathways.
144 gulates its distinct role in BER/SSBR versus DSBR.
145       Moreover, purified Pol eta, along with DSBR proteins PNKP, XRCC4, and Ligase IV can fully repai
146 tes only with BER/SSBR, and AcK226 PNKP with DSBR proteins.

 
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