ライフサイエンスコーパス: DNA synthesis inhibitor

1 treatment with phosphonoacetic acid (PAA), a DNA synthesis inhibitor.

2 nd checkpoint-defective cells treated with a DNA synthesis inhibitor.

3 esence of another, occur between protein and DNA synthesis inhibitors.

4 ation from latency and was also sensitive to DNA synthesis inhibitors.

5 to the genome after treatment with CHK1 and DNA synthesis inhibitors.

6 o to Top2 inhibitors, alkylating agents, and DNA synthesis inhibitors.

7 of S phase by mild treatments of cells with DNA-synthesis inhibitors.

8 The DNA synthesis inhibitor aphidicolin could block both apo

9 Treatment with the DNA synthesis inhibitor aphidicolin only minimally affec

10 ated HR could proceed in the presence of the DNA synthesis inhibitor aphidicolin.

11 G(2) phase and was completely blocked by the DNA synthesis inhibitor aphidicolin.

12 ls arrested at the beginning of S phase with DNA synthesis inhibitors, but induced low levels of prem

13 irus (HSV) lytic cycle or in the presence of DNA synthesis inhibitors, core viral replication machine

14 , but not phosphonoacetic acid a herpesvirus DNA synthesis inhibitor, could restore the cell surface

15 age T7 RNA polymerase in the presence of the DNA synthesis inhibitor cytosine arabinoside and transfe

16 to differentiate in methylcellulose with the DNA synthesis inhibitor cytosine beta-arabinofuranoside

17 und, sir-2.1 over-expression causes an FUDR (DNA synthesis inhibitor)-dependent reduction in pharynge

18 Time course analysis and viral DNA synthesis inhibitor experiments indicated that p14 w

19 yclines, lincosamides, and chloramphenicol), DNA synthesis inhibitors (fluoroquinolones and quinolone

20 The DNA synthesis inhibitor hydroxyurea (HU) was administere

21 such as UV and ionising radiation and to the DNA synthesis inhibitor hydroxyurea (HU).

22 itivity of S. pombe rad9::ura4+ cells to the DNA synthesis inhibitor hydroxyurea and gamma rays, as w

23 cdc1 mutant cells are supersensitive to the DNA synthesis inhibitor hydroxyurea and to the DNA damag

24 t map to Rpa1N and confer sensitivity to the DNA synthesis inhibitor hydroxyurea, such as rfa1-t11, a

25 cells than in meiotic cells treated with the DNA synthesis inhibitor hydroxyurea.

26 are blocked in S phase by treatment with the DNA synthesis inhibitor hydroxyurea.

27 nto S phase and increased sensitivity to the DNA synthesis inhibitor hydroxyurea.

28 To overcome this, we use DNA synthesis inhibitors (hydroxyurea and 1-beta-d-arabi

29 We show that cell cycle and DNA synthesis inhibitors interfere with TnpA-mediated Sp

30 eatments, using other topoisomerase poisons, DNA synthesis inhibitors, interstrand cross-linking indu

31 The acute effect of RNA and DNA synthesis inhibitors on DNA topoisomerase (topo) I l

32 inhibitor cycloheximide but not by the viral DNA synthesis inhibitor phosphonoacetate, a result which

33 at 6 h postinfection and is sensitive to the DNA synthesis inhibitor phosphonoacetic acid.

34 creased sixfold in the presence of the viral DNA synthesis inhibitor phosphonoacetic acid; thus, UL24

35 t many late transcripts sensitive to a viral DNA synthesis inhibitor (phosphonoacetic acid) were mark

36 is delayed in the presence of hydroxyurea, a DNA synthesis inhibitor, presumably due to the longer ti

37 DNA synthesis inhibitors resulted in a decrease of both

38 DNA synthesis inhibitor studies as well as fractionation

39 When nalidixic acid, a DNA synthesis inhibitor, was added to inhibit cell divis

40 class of nucleotide-based chain-terminating DNA synthesis inhibitors whose base portion consists of