ライフサイエンスコーパス: aminopterin

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1 nitiate DNA replication following removal of aminopterin.

2 owed by ester hydrolysis afforded the target aminopterins.

3 ction, we used methionine in the presence of aminopterin, a folate antagonist, co-administered with h

4 creases growth inhibitory potency of MTX and aminopterin against CCRF-CEM cells when both AICAr and a

5 eviously reported values 4.4 +/- 0.10 nM for aminopterin (AMT) and 1.5 +/- 0.39 nM for PT523.

6 Heretofore unknown analogues of aminopterin (AMT) and methotrexate (MTX) in which free r

7 Aminopterin (AMT) is a potent folate analog that is no l

8 t of 3 (0.35 pM), 11-fold lower than that of aminopterin (AMT, 1), and 15-fold lower than that of met

9 activity of this novel non-polyglutamatable aminopterin analogue.

10 deaza- and 5,10-dideazaaminopterin series of aminopterin analogues were evaluated for antiarthritic a

11 For example, while aminopterin and methotrexate both form binary complexes,

12 tance to 10(-4) M hypoxanthine, 4 x 10(-7) M aminopterin, and 1.6 x 10(-5) M thymidine (HAT) + G418;

13 alent antifolates, pemetrexed (also Alimta), aminopterin, and methotrexate.

14 The Ki for antifolates, methotrexate, aminopterin, and trimetrexate are more dramatically affe

15 t of the antifolate analogs methotrexate and aminopterin, as evidenced by their ability to greatly in

16 tation, the binding of all three substrates (aminopterin, ATP, and glutamic acid) was affected.

17 d resistance to the toxic peptide derivative aminopterin; however, only mutants lacking oppA1 display

18 on of cell killing occurred after removal of aminopterin in both wild-type and apn1 mutant cells.

19 ive permeants, such as the unsubstituted N1O aminopterin or C1O analogues.

20 inhibitors of dihydrofolate-reductase (MTX, aminopterin, PT523) and thymidylate synthase (ZD1694, ZD

21 of Hcy to methionine by the anitifolate drug aminopterin results in greatly enhanced synthesis of Hcy

22 e group of abnormalities referred to as the "aminopterin syndrome." Although weekly low-dose MTX has

23 mutants displayed a profound sensitivity to aminopterin that was relieved in an apn1 ung1 double mut

24 An optimum of 173 +/- 70 hypoxanthine aminopterin thymidine (HAT)-selected clones of the hybri

25 poor growth in media containing hypoxanthine-aminopterin-thymidine (HAT) and low incorporation of [(3

26 egained the ability to clone in hypoxanthine-aminopterin-thymidine medium and reexpressed virus tk mR

27 nies that survived selection in hypoxanthine-aminopterin-thymidine medium.

28 The generation of hypoxanthine-aminopterin-thymidine-resistant colonies after one cycle

29 vels of DNA damage and S-phase arrest during aminopterin treatment.

30 midine deprivation induced by the antifolate aminopterin was measured in a series of mutant Saccharom

31 although the Ki values for methotrexate and aminopterin were increased 88- and 118-fold, respectivel

32 Methotrexate and the chemically similar drug aminopterin were independently identified as strong inhi

33 -synthase gene and/or by an antifolate drug, aminopterin (which prevents remethylation of homocystein

34 Thus, values for influx Km for aminopterin, which were 1-1.2 microM in each cell type,

35 layed modest changes in their sensitivity to aminopterin, with the exception of cells lacking the aba

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