ライフサイエンスコーパス: DSBR

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 A-PKcs kinase activity is essential for both DSBR and V(D)J recombination.

6 h p53-Exo1(null) mice, whose defects in both DSBR and mismatch repair also compromised survival.

7 cts are difficult to rationalize strictly by DSBR, these properties are most readily consistent with

8 ses a topoisomerase to resolve the canonical DSBR intermediate, are supported by these data.

9 ss of tetrads not predicted by the canonical DSBR model was identified.

10 The "canonical" DSBR model, in which only 5' ends are degraded and resol

11 e data suggest that E4orf6 disrupts cellular DSBR signaling by inhibiting PP2A, leading to prolonged

12 We recently described a CHO DSBR mutant belonging to the XRCC7 complementation group

13 uclease and monitored temporally constrained DSBR at a specific chromosomal site in bloodstream form

14 sion and presumably occurs by a conventional DSBR recombination mechanism initiated by cleavage of th

15 , I-SceI and Cas9 induced markedly different DSBR profiles.

16 interactions promote engagement of distinct DSBR pathways.

17 of late-onset tumors due to its roles in DNA DSBR as well as in DNA MMR.

18 required as for cells without induced DSBs: DSBR proteins, DinB-error-prone polymerase, and the RpoS

19 During DSBR involving nonhomologous ends, Msh2p localized stron

20 e joint-molecule intermediate arising during DSBR usually leads to crossing over); (2) cutting only o

21 ssess coordination of the broken ends during DSBR in bacteriophage T4.

22 CA1 functions differ from those required for DSBR.

23 tic insights into C-NHEJ-mediated error-free DSBR of the transcribed genome.

24 missing sequences, thus allowing error-free DSBR.

25 solution to the long-standing puzzle of how DSBR pathway 'choice' is regulated through the cell cycl

26 rved 'conditional' haploinsufficiency for HR-DSBR in BRCA1(mut/+) cells in the face of replication st

27 s formation, reflecting a defect in Palb2 HR-DSBR function, a strongly suspected contributor to Brca1

28 bination-type double strand break repair (HR-DSBR) through physical interactions with BRCA1, BRCA2, a

29 ination- type double-strand break repair (HR-DSBR), checkpoint functions, centrosome number control,

30 o disrupt PALB2 binding and disable BRCA2 HR/DSBR function.

31 ity and allosteric control of ABC-ATPases in DSBR, membrane transport, and chromosome condensation by

32 suggests that SPR-5 may function directly in DSBR.

33 Msh3p associates with intermediates early in DSBR to participate in the rejection of homeologous pair

34 de that the Ku70 gene product is involved in DSBR and V(D)J recombination and confirm that the Ku70 g

35 unction of the four mammalian DNA ligases in DSBR, V(D)J recombination and other reactions.

36 f DNA-PK-mediated protein phosphorylation in DSBR and V(D)J recombination, we assessed the effects of

37 s for investigating cell cycle variations in DSBR.

38 f intrachromosomal end joining in individual DSBR survivors exclusively revealed MMEJ-based deletions

39 r in U251 human glioblastoma cells, inhibits DSBR and induces significant radiosensitization in the a

40 Research into DSBR exploits rare-cutting endonucleases to cleave exoge

41 ow no transcriptional misregulation of known DSBR involved genes.

42 In addition, mammalian DSBR proteins and their activities are discussed.

43 NA molecules, supporting a homology-mediated DSBR mechanism.

44 e lacZ locus causes a second RecBCD-mediated DSBR event to occur in the terminus region of the chromo

45 ction and the relationships between multiple DSBR pathways at a single endogenous disease gene.

46 olled switch from high-fidelity to mutagenic DSBR under stress.

47 Quantitative analysis of DSBR pathways employed indicated that inter-chromosomal

48 by both DSB ends may be a common feature of DSBR that increases repair efficiency but also the likel

49 human tumor cells through the inhibition of DSBR, notably in the absence of E1B-55K.

50 indings are consistent with the ECR model of DSBR.

51 onsistent with several coordinated models of DSBR, including a modified version of the ECR model.

52 eral phenotypes indicating a perturbation of DSBR, including increased p53-dependent germ cell apopto

53 ults in germline-specific down-regulation of DSBR genes, thereby impairing maintenance of genomic int

54 e true forward-mutation sequence spectrum of DSBR-associated stress-induced mutagenesis, for which pr

55 tent with the inhibitory effect of E4orf6 on DSBR, expression of wild-type but not mutant E4orf6 redu

56 In contrast, several other DSBR models propose that the two ends of a break are rep

57 ase active form of DNA-PKcs can reconstitute DSBR and V(D)J recombination in a DNA-PKcs-deficient cel

58 E4orf6 reduced DSBR capacity in transfected and infected cells, as meas

59 ts endo- and exonuclease activities regulate DSBR by nonhomologous end-joining (NHEJ) versus homologo

60 ), a form of DNA double-strand break repair (DSBR) active in mammalian V(D)J recombination.

61 involved in DNA double-strand break repair (DSBR) and DNA damage-induced checkpoint activation.

62 , error-free DNA double-strand break repair (DSBR) and intra-S phase DNA damage checkpoint control.

63 ized in both DNA double-strand break repair (DSBR) and V(D)J recombination, but the mechanism by whic

64 -over during DNA double-strand-break repair (DSBR) by disassembling double-Holliday junctions (dHJs)

65 otic bimolecular double-strand break repair (DSBR) intermediate.

66 ith the accepted double-strand-break repair (DSBR) model for intron inheritance, and implicate additi

67 edictions of the double-strand break repair (DSBR) model for meiotic recombination by examining the s

68 The double-strand break repair (DSBR) model of recombination predicts that heteroduplexe

69 variation of the double-strand-break repair (DSBR) model that has the following features: (1) Hollida

70 fficiency of double-strand DNA break repair (DSBR) of the BRCA1-/- human breast cancer line, HCC1937.

71 ption of meiotic double-strand break repair (DSBR) progression.

72 n (ECR) model of double-strand-break repair (DSBR) proposes that each end of a double-strand break (D

73 teracts with the double-strand break repair (DSBR) protein DNA-dependent protein kinase and cooperate

74 DNA double-strand break repair (DSBR) proteins and the SOS and RpoS stress responses are

75 inactivated DNA double-strand break repair (DSBR) proteins, DNA Ligase IV (Lig4), Xrcc2, and Brca2,

76 on cellular DNA double strand break repair (DSBR) proteins.

77 s of chromosomal double-strand break repair (DSBR) provides insight into genome instability, oncogene

78 and completed by double-strand break repair (DSBR) recombination with the donor allele.

79 se including DNA double-strand break repair (DSBR) through DNA end resection, chromosomal stability,

80 teins act during double-strand break repair (DSBR) to correct mismatches in heteroduplex DNA, to supp

81 plex acts in DNA double-strand break repair (DSBR), detection, and signaling; yet, how its endo- and

82 inks between DNA double-strand break repair (DSBR), illegitimate recombination and plasmid DNA integr

83 of Rad50 in DNA double-strand break repair (DSBR), we biochemically and structurally characterized A

84 tion and for DNA double-strand break repair (DSBR).

85 a defect in DNA double-strand break repair (DSBR).

86 5 in meiotic DNA double-strand break repair (DSBR).

87 aling (SDSA) and double-strand break repair (DSBR).

88 error-prone DNA double-strand break repair (DSBR).

89 neral process of double strand break repair (DSBR).

90 involved in DNA double-strand break repair (DSBR).

91 through mitotic double-strand break-repair (DSBR), typically involving homologous recombination (HR)

92 HEJ) is the dominant pathway for DSB repair (DSBR) in adult mammalian cells.

93 In these protozoan parasites, DSB repair (DSBR) is dominated by homologous recombination (HR) and

94 s of action of MDC1 and 53BP1 in DSB repair (DSBR).

95 that is not absolutely required for XRCC4's DSBR function.

96 Here we report that during such DSBR, mammalian C-NHEJ proteins form a multiprotein comp

97 Our genomic analysis has also revealed that DSBR at the lacZ locus causes a second RecBCD-mediated D

98 l transducers, cell cycle regulators and the DSBR pathways is illustrated.

99 ated protein 53 (Trp53)-null background, the DSBR defect caused by the E109K mutation altered the tum

100 germ cell apoptosis, increased levels of the DSBR marker RAD-51, and sensitivity toward DSB-inducing

101 hotspot are consistent with a variant of the DSBR model in which the extent of heteroduplex on one si

102 Modified versions of the DSBR model, including one that uses a topoisomerase to r

103 These DSBR pathways available to T. brucei likely underlie pat

104 we monitor the relative utilization of three DSBR pathways following cleavage by I-SceI or CRISPR/Cas

105 tructs have been developed to detect various DSBR pathways.