ライフサイエンスコーパス: DNA synthesis inhibitor

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

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

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

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

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

6 esence of another, occur between protein 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 Time course analysis and viral DNA synthesis inhibitor experiments indicated that p14 w

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

19 The DNA synthesis inhibitor hydroxyurea (HU) was administere

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

35 DNA synthesis inhibitors resulted in a decrease of both

36 DNA synthesis inhibitor studies as well as fractionation

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

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

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