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1 the link between chromatin assembly and DNA replication control.
2 /6 inhibition had no effect on cell cycle or replication control.
3 d be unambiguously linked to its role in DNA replication control.
4 imers can bind to iterons, a new paradigm in replication control.
5 y partially due to alterations in centrosome replication control.
6 upon prolonged growth suggesting a defect in replication control.
7 OB1 bypass activity and other aspects of DNA replication control.
8 ation origin, thus elucidating a key step of replication control.
9 recG mutant that shows defects in repair and replication control.
10 ssing DnaBS371P are consistent with aberrant replication control.
11 plex picture emerging for papillomavirus DNA replication control.
12 that were proposed to play distinct roles in replication control.
13 e I elements, the only known determinant for replication control.
14 h is believed to be the major determinant of replication control.
15 sults is discussed in the context of plasmid replication control.
16 iral ISG expression, which results in better replication control.
17 evidence in support of the coupling model of replication control.
18 an extended time owing to methylation-based replication control.
19 critical role for architectural proteins in replication control.
20 for treating malignancies with defective DNA replication control.
21 hase, illustrating the dynamic nature of DNA replication controls.
22 ells participate with T cells to restore CMV replication control, although their relative contributio
23 Cdks may inhibit ORC function as part of re-replication control and show that DmORC activity may be
24 tion between facultative heterochromatin and replication control and show that heterochromatin machin
25 oth inhibitory and facilitating roles in DNA replication control and that the sole essential function
26 ight be associated with its function in cell replication control, and that p53-independent mechanisms
27 of the F plasmid as a model system to study replication control, and these investigations led to the
30 tivators; (3) high-copy plasmids with sloppy replication control arise because intracellular selectio
31 1 degradation plays an essential role in DNA replication control, as overexpression of Cdt1 leads to
33 s of data support the hypothesis of negative replication control by pi binding to the non-iteron site
35 within the Rif1 sequence, it is likely that replication control by Rif1 through PP1 is a conserved m
37 Ad-sPSA-E1, an adenoviral vector with viral replication controlled by a strong super prostate-specif
40 that compounds that do not bind to this RNA replication control element fail to induce plasmid loss
41 boundaries and the necessity of these "early replication control elements" (ERCEs) was validated by d
46 to determine if viral reprogramming of host replication controls had an impact on host DNA replicati
47 aster host, we have tracked the evolution of replication control in both somatic and reproductive tis
48 , E2f2, Dp, and Rbf1 genes all contribute to replication control in ovarian follicle cells, which bec
50 romosome generally match in copy number, the replication control is apparently lost over several mega
52 ticular it is hypothesized that: (1) tighter replication control is more vulnerable to selfishness; (
55 firming the involvement of the host cellular replication control mechanism, and prevented rereplicati
57 Escherichia coli mutant highly perturbed for replication control, obgE::Tn5-EZ seqADelta, we isolated
59 ar processes such as cell cycle control, DNA replication, control of gene expression, tumor suppresso
60 ich are known to be directly involved in DNA replication, control of viral and cellular transcription
61 s to be a well-conserved and central mode of replication control, optimal replication might require a
62 mbers; or (ii) require multiple plasmids for replication control; or (iii) are restricted to speciali
63 PLpromoter of phage lambda; (iv) and (v) the replication control promoters PRNAIand PRNAIIof plasmid
64 hypothesis that the N-terminal region of the replication control protein Cdc6 acts as an inhibitor of
65 d identified three up-regulated genes: a DNA replication control protein, a basic helix-loop-helix tr
66 nalysis of the DNA fragment representing the replication control region of the rodent mitochondrial g
68 after DNA damage, it relocalizes to selected replication control sites and suppresses abnormal, postd
69 of neuromuscular disease, exhibited at mtDNA replication control sites in muscle an accumulation of t
70 To assess the role of conserved sequences in replication control, structural and functional studies w
71 binding to ORC provides an origin-localized replication control switch that specifically prevents re
73 have very different chromosome copy numbers, replication control systems and even employ distinct mac
74 we demonstrate a novel role for p16ink4a in replication control that is distinct from that of RB.
75 ndent kinases (Cdks) are critical for the re-replication controls that inhibit the activities of comp
77 iple stages of viral infection including DNA replication, controlling the cell cycle, and virion matu
78 nin knockdown 4pX-1 cell line used as DNA re-replication control, the Cdt1/geminin ratio is greater i
80 ta correlate the pppGpp/ppGpp ratio with DNA replication control under bacterial starvation condition
81 s were dependent on T cell degranulation for replication control with only a minor additional contrib