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