ライフサイエンスコーパス: radiomimetic

1 pe generated by ionizing radiation and other radiomimetics.

2 utations confer only weak sensitivity to the radiomimetic agent methyl methane sulfonate (MMS) but co

3 after DNA damage by gamma irradiation or the radiomimetic agent neocarzinostatin.

4 /M phases is inhibited by treatment with the radiomimetic agent, adriamycin.

5 also analyzed the PCNA complex induced by a radiomimetic agent, Bleomycin (BLM), which produces pred

6 cells, and rendered cells sensitive toward a radiomimetic agent, neocarzinostatin.

7 erlying the cellular response to this unique radiomimetic agent.

8 following exposure to ionizing radiation or radiomimetic agents.

9 ntrinsic apoptosis induced by UV mimetic and radiomimetic agents.

10 phosphorylation at Ser1981, yet unlike other radiomimetics and IR, DNA breaks induced by C-1027 resul

11 hese proteins was required for resistance to radiomimetics, and many were required for resistance to

12 ontrasted cell responses to IR and C-1027, a radiomimetic antibiotic that induces DNA strand breaks.

13 lication stress inducer, hydroxyurea, or the radiomimetic antibiotic, neocarzinostatin.

14 are formed in DNA by ionising radiation and radiomimetic anticancer agents and are thought to be bio

15 que characteristic of ionizing radiation and radiomimetic anticancer drugs is the induction of cluste

16 etylated state and experience treatment with radiomimetic anticancer drugs.

17 The ability of the radiomimetic anticancer enediyne C-1027 to induce ataxia

18 are formed in cells by ionizing radiation or radiomimetic antitumor drugs.

19 Unique among radiomimetics, ataxia-telangiectasia mutated (ATM) is di

20 such as ionizing radiation and conventional radiomimetics because their mechanisms require oxygen to

21 eatments with cobalt-60 gamma irradiation or radiomimetic bleomycin, except after high bleomycin dose

22 Like ionizing radiation (IR) and other radiomimetics, breaks induced by C-1027 efficiently acti

23 Like other radiomimetics, C-1027 induced DNA breaks to a lesser ext

24 itivity to DNA-damaging agents, particularly radiomimetic chemicals inducing DNA double-strand breaks

25 e of the transgenic cells to UV light or the radiomimetic chemicals methyl methanesulfonate and mitom

26 uction of DSBs utilize ionizing radiation or radiomimetic chemicals, such as neocarzinostatin (NCS),

27 oma cells to UV-, ribotoxic (anisomycin) and radiomimetic chemicals-induced programmed cell death in

28 the UV mimetic compound oxaliplatin and the radiomimetic compound doxorubicin promoted apoptosis by

29 After treatment of HCT116 cells with a radiomimetic compound neocarzinostatin, active Chk2 exis

30 cell cycle after treatment with radiation or radiomimetic compounds.

31 nt at bypassing subtle terminal mispairs and radiomimetic damage by direct ligation.

32 ase Chinese hamster ovary CHO cells with the radiomimetic DNA double-strand cleaving agent neocarzino

33 smid DNA containing DNA DSBs produced by the radiomimetic drug bleomycin.

34 mal human cells to gamma-irradiation and the radiomimetic drug neocarzinostatin had no effect on ATM

35 d with actinomycin D, anisomycin or with the radiomimetic drug neocarzinostatin.

36 in cells treated with gamma-radiation or the radiomimetic drug neocarzinostatin.

37 rtemis-deficient ES cells are sensitive to a radiomimetic drug, but less sensitive to ionizing radiat

38 slocations induced by ionizing radiation and radiomimetic drugs are thought to arise by incorrect joi

39 osure of cells to ionizing radiation (IR) or radiomimetic drugs induces Chk2 phosphorylation by ATM,

40 agents, such as ionizing radiation (IR) and radiomimetic drugs is crucial in maintaining genomic int

41 Delta cells are hypersensitive to a range of radiomimetic drugs that share the feature of creating le

42 recombination, sensitivity to radiation and radiomimetic drugs, and failure to repair a subset of DN

43 are usually caused by ionizing radiation and radiomimetic drugs, but can also occur under normal phys

44 reaks are produced by ionizing radiation and radiomimetic drugs, but it was not known whether they ca

45 t uniquely induced by ionizing radiation and radiomimetic drugs, but their level of production by UVB

46 o DSBs induced by ionizing radiation (IR) or radiomimetic drugs, including bleomycin, in living cells

47 pecially in patients previously treated with radiomimetic drugs, may not be feasible.

48 e that is activated by ionizing radiation or radiomimetic drugs, whereas p95/nbs1 is part of a protei

49 ced in DNA by ionizing radiation and by some radiomimetic drugs.

50 itive to DNA replication inhibitors, but not radiomimetic drugs.

51 (DSBs) caused by ionizing radiation (IR) and radiomimetic drugs.

52 ers treated with ionizing radiation (IR) and radiomimetic drugs.

53 olon carcinoma HCT116 cells by the antitumor radiomimetic enediyne antibiotic C-1027.

54 The radiomimetic enediyne C-1027 induces almost exclusively

55 response to DNA strand breaks induced by the radiomimetic enediyne C-1027.

56 For example, the conventional radiomimetic enediyne neocarzinostatin is 4-fold less cy

57 CF7 induced apoptosis, which was enhanced by radiomimetic neocarcinostatin treatment.

58 ound maintains the characteristic ability of radiomimetics to cleave DNA in cell-free systems, varyin