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1 sensitive to cycloheximide and resistant to phosphonoacetic acid.
2 is sensitive to the DNA synthesis inhibitor phosphonoacetic acid.
3 n of both EBV and KSHV DNAs was inhibited by phosphonoacetic acid.
4 netics, and their expression is inhibited by phosphonoacetic acid.
5 umulates in larger amounts in the absence of phosphonoacetic acid.
6 ophosphate and with the pyrophosphate analog phosphonoacetic acid.
7 steps of virus replication were inhibited by phosphonoacetic acid.
8 iated acylation of electron-rich arenes with phosphonoacetic acids.
9 imide a protein synthesis inhibitor, but not phosphonoacetic acid a herpesvirus DNA synthesis inhibit
10 hibitors of the viral DNA polymerase such as phosphonoacetic acid, although the reporters lack a euka
11 late gene whose expression was abolished by Phosphonoacetic acid, an inhibitor of KSHV DNA replicati
12 d K8.1 induced by KSHV Rta was eliminated by phosphonoacetic acid, an inhibitor of viral DNA polymera
13 umulates to higher levels in the presence of phosphonoacetic acid, an inhibitor of viral DNA synthesi
14 ed in infected cells even in the presence of phosphonoacetic acid, an inhibitor of viral late gene ex
17 ctions performed in the presence of the drug phosphonoacetic acid confirmed that the process of viral
18 lotting) only at 48 h p.i. in the absence of phosphonoacetic acid, consistent with late gene expressi
19 te that inhibition of DNA replication, using phosphonoacetic acid, did not affect HHV-6A/B integratio
20 n to the nucleus occurred in the presence of phosphonoacetic acid, indicating that viral DNA and true
22 nhibitor (K(i) = 5.1 +/- 1.6 microM) whereas phosphonoacetic acid (K(i) = 380 +/- 45 microM) and acet
23 with an automated DNA synthesizer to prepare phosphonoacetic acid modified internucleotide linkages o
24 and plaques was inhibited in the presence of phosphonoacetic acid or gangciclovir, but these antiherp
27 es in the presence of cycloheximide (CHX) or phosphonoacetic acid (PAA) also permitted identification
28 f BrdU were both abolished by treatment with phosphonoacetic acid (PAA) and by omission of any one of
29 cked by viral polymerase inhibitors, such as phosphonoacetic acid (PAA) or acyclovir (ACV), UL29 (ICP
31 this increase is sensitive to treatment with phosphonoacetic acid (PAA), a DNA synthesis inhibitor.
32 al cells) are TPA induced in the presence of phosphonoacetic acid (PAA), an inhibitor of herpesvirus
33 sitive to a viral DNA replication inhibitor, phosphonoacetic acid (PAA), suggesting that DDB2 affects
34 was added at the time of release from a 12-h phosphonoacetic acid (PAA)-induced block in viral DNA sy
36 modeoxyuridine, and their formation was both phosphonoacetic acid sensitive and oriLyt dependent.
37 dium containing inhibitory concentrations of phosphonoacetic acid, suggesting that it is regulated as
38 PERK is blocked by cycloheximide but not by phosphonoacetic acid, suggesting that the accumulation o
39 resence of the viral DNA synthesis inhibitor phosphonoacetic acid; thus, UL24 was expressed with leak
42 ensitive to a viral DNA synthesis inhibitor (phosphonoacetic acid) were markedly reduced by pM79 muta
43 arison, the treatment of infected cells with phosphonoacetic acid, which interferes with viral late p