ライフサイエンスコーパス: zebularine

1 r inducers of p16 tumor suppressor gene than zebularine.

2 ucleotide-diphosphate reductase required for zebularine.

3 ssion is reduced shortly after withdrawal of zebularine.

4 mechanism of action of the anti-cancer drug zebularine.

5 he potent cytidine deaminase inhibitor (CDA) zebularine [1-(beta-D-ribofuranosyl)-1, 2-dihydropyrimid

6 Recently, we reported that zebularine [1-(beta-D-ribofuranosyl)-1,2-dihydropyrimidi

7 ar dynamics and free energy simulations that zebularine 3,4-hydrate may in fact be unstable in the en

8 ed that the TSA formed at the active site is zebularine 3,4-hydrate.

9 ation of dZ and the inefficient reduction of zebularine 5'-diphosphate by ribonucleotide-diphosphate

10 Infusions of zebularine (a DNA methyltransferase inhibitor) significa

11 Zebularine, a cytosine analog, elevated all classes.

12 Furthermore, zebularine, a drug that selectively traps and depletes n

13 hypermethylation was significantly abated by Zebularine, a potent demethylating agent, with a consequ

14 Zebularine, an orally administerable DNA methyltransfera

15 Moreover, zebularine and 5-aza-2-deoxycytidine, inhibitors of DNMT

16 ism for coping with the genotoxic effects of zebularine and identify several components of the zebula

17 rimidinone, an analogue often referred to as zebularine and known to give rise to high-affinity compl

18 NitroC), 2-pyrimidinone (P; the free base of zebularine) and 6-methylfuranopyrimidinone (MefP), were

19 g capecitabine, the gene silencing inhibitor zebularine, and the blood vessel inhibitor bevacizumab.

20 Cytidine deaminase (CDA) binds the inhibitor zebularine as its 3,4-hydrate (K(d) ~ 10(-12) M), captur

21 lation inhibitors 5-aza-2'-deoxycytidine and zebularine as well as DNA methyltransferase-specific siR

22 e the greater thermodynamic stability of the zebularine complex.

23 ment with 5-aza-2'-deoxycytidine followed by zebularine hindered the remethylation of the p16 5' regi

24 e of the transition state analogue inhibitor zebularine hydrate (1.2 x 10(-12) M) is very much lower

25 en the deazacytidine, dihydrozebularine, and zebularine--hydrate inhibitor complexes suggest that the

26 ent with the DNA methyltransferase inhibitor Zebularine increases miR-124 expression and retards CC c

27 tors as well as with the demethylating agent zebularine induced a strong apoptotic response.

28 arine and identify several components of the zebularine-induced DNA damage repair pathway.

29 show that the nonmethylable cytidine analog zebularine induces a DNA damage response in Arabidopsis

30 ge in a cell cycle stage-independent manner, zebularine induces damage specifically during strand syn

31 Zebularine is a riboside that must undergo a complex met

32 ate competition assays show that in solution zebularine is released from CDA (k(off) > 0.14 s(-1)) mu

33 xes (other than E(2)Zn(2)) are observed when zebularine is used in place of 5-fluorozebularine.

34 However, when zebularine is withdrawn from the cells, the reestablishm

35 an CDA, but it was 16 times less potent than zebularine (Ki = 38 microM vs Ki(apparent) = 2.3 microM)

36 es and a noncanonical pyrimidine nucleoside (zebularine) phosphate can be formed from the direct coup

37 ic analogues appeared to be more stable than zebularine, replacement of the electronegative CO4' oxyg

38 The DNA methyltransferase inhibitor zebularine reverses the methylation of the p53 promoter,

39 We used the demethylating drug zebularine to induce changes in DNA methylation, then ex

40 Here we show that continuous application of zebularine to T24 cells induces and maintains p16 gene e

41 In addition, continuous zebularine treatment effectively and globally demethylat

42 Even at a non-toxic concentration, Zebularine was effective in suppressing CC cell invasion

43 These three carba-nucleoside versions of zebularine were fashioned to overcome the inherent insta

44 olism of the DNA methytransferase inhibitor, zebularine (Z).

45 Zebularine (ZEB) binds to CDA, and the binding process l

46 ious cell densities with the DNMT1 inhibitor zebularine (ZEB) followed by a 3D culture to identify ce

47 nd liver cancer cell lines were treated with zebularine (ZEB), a potent DNA methyltransferase-1 inhib