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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 expression in maltreated dams normalized by zebularine.
5 mechanism of action of the anti-cancer drug zebularine.
6 epair of DPCs induced by the cytidine analog zebularine.
7 he potent cytidine deaminase inhibitor (CDA) zebularine [1-(beta-D-ribofuranosyl)-1, 2-dihydropyrimid
9 2% sodium alginate containing high loads of zebularine (240 mg/ml) and retinoic acid (0.8 mg/ml) pro
10 ar dynamics and free energy simulations that zebularine 3,4-hydrate may in fact be unstable in the en
12 ation of dZ and the inefficient reduction of zebularine 5'-diphosphate by ribonucleotide-diphosphate
18 hypermethylation was significantly abated by Zebularine, a potent demethylating agent, with a consequ
20 In syngeneic tumor models, administration of zebularine alone reduced tumor burden and extended mice
21 oligonucleotides with a single incorporated zebularine also did not disrupt editing in vitro, sugges
24 ism for coping with the genotoxic effects of zebularine and identify several components of the zebula
25 rimidinone, an analogue often referred to as zebularine and known to give rise to high-affinity compl
26 on of two putative transition-state analogs, zebularine and tetrahydrouridine, failed to disrupt RNA-
27 NitroC), 2-pyrimidinone (P; the free base of zebularine) and 6-methylfuranopyrimidinone (MefP), were
28 g capecitabine, the gene silencing inhibitor zebularine, and the blood vessel inhibitor bevacizumab.
29 Cytidine deaminase (CDA) binds the inhibitor zebularine as its 3,4-hydrate (K(d) ~ 10(-12) M), captur
30 lation inhibitors 5-aza-2'-deoxycytidine and zebularine as well as DNA methyltransferase-specific siR
31 In vitro studies showed rapid discharge of zebularine but not retinoic acid from the alginate formu
33 es have shown that ssDNA containing 2'-deoxy-zebularine (dZ-ssDNA) is an inhibitor of A3s such as A3A
34 d, we show that maltreated-dams treated with zebularine exhibit lower levels of adverse care toward t
35 ment with 5-aza-2'-deoxycytidine followed by zebularine hindered the remethylation of the p16 5' regi
36 e of the transition state analogue inhibitor zebularine hydrate (1.2 x 10(-12) M) is very much lower
37 en the deazacytidine, dihydrozebularine, and zebularine--hydrate inhibitor complexes suggest that the
40 ent with the DNA methyltransferase inhibitor Zebularine increases miR-124 expression and retards CC c
44 show that the nonmethylable cytidine analog zebularine induces a DNA damage response in Arabidopsis
45 ge in a cell cycle stage-independent manner, zebularine induces damage specifically during strand syn
48 ate competition assays show that in solution zebularine is released from CDA (k(off) > 0.14 s(-1)) mu
51 an CDA, but it was 16 times less potent than zebularine (Ki = 38 microM vs Ki(apparent) = 2.3 microM)
54 es and a noncanonical pyrimidine nucleoside (zebularine) phosphate can be formed from the direct coup
56 ic analogues appeared to be more stable than zebularine, replacement of the electronegative CO4' oxyg
57 DNA hypomethylating agents (azacitidine and zebularine) restored Kupffer cell autophagy, M1/M2 polar
60 Here we show that continuous application of zebularine to T24 cells induces and maintains p16 gene e
64 These three carba-nucleoside versions of zebularine were fashioned to overcome the inherent insta
66 therapy that combines a demethylating agent, zebularine, with retinoic acid, acting as a transcriptio
69 ious cell densities with the DNMT1 inhibitor zebularine (ZEB) followed by a 3D culture to identify ce
70 nd liver cancer cell lines were treated with zebularine (ZEB), a potent DNA methyltransferase-1 inhib