ライフサイエンスコーパス: bizelesin

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1 ith hypercytotoxicity of an anticancer drug, bizelesin.

2 extremely lethal AT-specific drugs, such as bizelesin.

3 an lesions by an unrelated AT-specific drug, bizelesin.

4 Bizelesin, a bifunctional DNA minor groove alkylating ag

5 be approximately 18 times more sensitive to Bizelesin, a DNA alkylating drug compared to WT parasite

6 Within 1 h of bizelesin addition to infected cells, a similar rapid de

7 Actual bizelesin adducts clustered within the model AT island n

8 level, are less lethal than region-specific bizelesin adducts.

9 lesin is likely to affect similar regions as bizelesin, adozelesin's more promiscuous binding probabl

10 rich DNA sequences with a bent conformation; bizelesin also reacts with the minor groove of AT-rich s

11 quences but is selective for a conformation; bizelesin also reacts with the minor groove of AT-rich s

12 ed the sequence- and region-specificity of a bizelesin analogue, U-78779, designed to interact with m

13 Bizelesin and adozelesin are DNA-reactive antitumor drug

14 DNA-reactive antitumor agents: (+)-CC-1065, bizelesin, and pluramycin.

15 The distribution of bizelesin binding motifs in several regions analyzed "in

16 lly low motif density, clusters of potential bizelesin binding sites were found in the matrix-associa

17 ong MARs) correlate with the total number of bizelesin binding sites.

18 dant in CEM cells that are hypersensitive to bizelesin compared to normal WI-38 cells.

19 pause sites may result from the formation of bizelesin covalent bonds on replicating SV40 molecules.

20 fect was not dependent upon the formation of bizelesin covalent bonds with the template DNA.

21 dozelesin exceeded by severalfold lesions by bizelesin in four selected regions (within the c-myc and

22 rrelated cytotoxic activities of U-78779 and bizelesin in several cell lines further imply that both

23 Accordingly, lesions induced by bizelesin in these domains (2.13 and 7.06 lesions kbp(-1

24 Bizelesin inhibition of SV40 DNA replication was analyze

25 Bizelesin is the first anticancer drug capable of damagi

26 to as "AT islands." Experimentally detected bizelesin lesions agree with these in silico predictions

27 eplication origin, it did not interfere with bizelesin modification of the same sequence.

28 In cancer cells, bizelesin produced high levels of lesions (approximately

29 In contrast, findings for bizelesin provide for the first time a proof of principl

30 es corresponded to pure AT motifs similar to bizelesin sites.

31 in the same long islands of AT-rich DNA that bizelesin targets.

32 observed with the bisfunctional CPI analogue bizelesin, this is the first time that such an observati

33 experiments, using extracts from control and bizelesin-treated cells, indicated that reduced DNA repl

34 SV40 DNA also was reduced when extracts from bizelesin-treated HeLa cells were used.

35 However, prolonged bizelesin treatment (>/=2 h) was associated with a reduc

36 e motifs 5'-T(A/T)(4)A-3' motifs targeted by bizelesin, while also infrequent, cluster in defined AT-

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