ライフサイエンスコーパス: araC

1 16 familial AD patients tested had abnormal araC and caffeine tests, as did XP-A cells.

2 ne that has been integrated with an adjacent araC-P(BAD) control element into the bacterial chromosom

3 opose that Ad12 infection, actinomycin D and araC all induce a similar or identical global damage arr

4 % lethal doses (LD(50)s) of the Deltacrp and araC P(BAD) crp mutants were approximately 1,000,000-fol

5 spase activation after treatment with MP and araC.

6 ated with 1-beta-d-arabinofuranosylcytosine (araC) and other genotoxic agents.

7 tiviral agents such as cytosine arabinoside (araC) and gemcitabine.

8 Cytosine arabinoside (araC) is an important drug used for the treatment of hum

9 eated with either beta-cytosine arabinoside (araC) or caffeine, and chromatid breaks were quantified.

10 s with 5-fluorouracil, cytosine arabinoside (araC), and mercaptopurine (MP) demonstrated that Hmgb1(-

11 rs that treatment with cytosine arabinoside (araC), but not aphidicolin, can also phenocopy Ad12 infe

12 ted with pro-apoptotic cytosine arabinoside (araC), PP1alpha protein increased twofold and PP1 activi

13 ated on both the plasmid and the chromosome (araC P(BAD) c2).

14 Parallels with the Escherichia coli araC-araBAD regulatory region are discussed.

15 vo have increased sensitivity to cytarabine (araC) and daunorubicin, suggesting that optimizing drug

16 sine-1-beta-D-arabinofuranoside (cytarabine, araC).

17 Beta-D-arabinofuranosylcytosine (cytarabine, araC) and 2',2'-difluoro-2'-deoxycytidine (gemcitabine,

18 h d(pGpC) of the isomorphous Z-DNA hexamer d(araC-dG)3 without the 2'-OH group of arabinose, was used

19 th the tightly regulated arabinose-dependent araC P(BAD) promoter so that rfaH expression was depende

20 High-dose araC (HD-araC) was used in the second induction cycle in

21 The gadX gene and a second downstream araC-like transcription factor gene, gadW, were mutated

22 In order to exert its cytotoxic effects, araC must be incorporated into chromosomal DNA.

23 lated and delayed shutoff of crp expression (araC P(BAD) crp) and replacement of the msbB gene with t

24 nt regulated delayed-shutoff crp expression (araC P(BAD) crp), were constructed, characterized in vit

25 High-dose araC (HD-araC) was used in the second induction cycle instead of

26 Our results indicated that earlier use of HD-araC led to better EFS and OS in AAML0431 than in past C

27 Therefore, the effects of incorporated araC residues on the DNA cleavage/religation equilibrium

28 ts show that BER is capable of incorporating araC and dFdC into the genome.

29 o reduced drug resistance, as shown for MMC, araC and cisplatinum.

30 tumefaciens requires a plasmid-borne copy of araC, and is not affected by endogenous regulators.

31 may mediate some of the cellular effects of araC.

32 poration of the 5'-triphosphorylated form of araC, dFdC, 2'-fluoro-2'-deoxycytidine (FdC), and cytidi

33 (araCTP) levels in the liver than levels of araC in the plasma and >12-fold higher araCTP levels in

34 oduction of inhibitor-2 delayed the onset of araC-induced apoptosis, whereas concomitant introduction

35 NA cleavage were observed in the presence of araC lesions and etoposide.

36 However, the positional specificity of araC residues differed from that previously reported for

37 1-deficient cells after treatment with MP or araC, consistent with reduced transcriptional activity o

38 and >28-fold improvement, respectively, over araC administration.

39 lacI, expressed from the arabinose-regulated araC PBAD promoter.

40 d on the substitution of a tightly regulated araC P(BAD) cassette for the promoters of the fur, crp,

41 3 Delta asdA16 Delta araBAD23 Delta relA198::araC P(BAD) lacI TT [TT is the T4ipIII transcription ter

42 Similarly, araC-resistant cells, normally unable to die in response

43 of the arabinose operon of E. coli, and the araC gene, which is both a positive and negative regulat

44 xpression was very tightly controlled by the araC-P(araBAD) promoter/regulator system.

45 t-range (BHR) cloning vectors that carry the araC-PBAD controlled expression cassette from Escherichi

46 Mice vaccinated with 3.0 x 10(4) CFU of the araC P(BAD) crp mutant also developed high anti-Y. pesti

47 e, achieves good liver targeting compared to araC, generating >19-fold higher cytarabine triphosphate

48 cells, normally unable to die in response to araC, initiated apoptosis when electroporated with activ

49 amsbB868::P(msbB) msbB(EC) DeltaP(crp21)::TT araC P(BAD) crp] for use with a balanced-lethal Asd-posi

50 e expression and improving chemotherapy with araC and gemcitabine.

51 l) by replacing the psl promoter region with araC-p(BAD), so that expression of psl could be controll