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1 ytidine > beta-d-2'-deoxycytidine >/= beta-d-arabinofuranosylcytosine.
2 iation, cisplatin, doxorubicin, and 1-beta-D-arabinofuranosylcytosine.
3 of apoptosis by the antimetabolite, 1-beta-d-arabinofuranosylcytosine.
4 henylethyl) phosphoramidate (8a), and 1-beta-arabinofuranosylcytosine 5'-N-(1-carbomethoxy-2-indolyle
5 -2-indolylethyl)phosphoramidate (5b), 1-beta-arabinofuranosylcytosine 5'-N-(1-carbomethoxy-2-phenylet
6 ytosine (ara-C) and generate higher 1-beta-D-arabinofuranosylcytosine 5'-triphosphate (ara-CTP) than
8 utants were all able to add araCTP (1-beta-D-arabinofuranosylcytosine-5'-triphosphate) to a primer bu
10 strate that treatment of cells with 1-beta-D-arabinofuranosylcytosine and other genotoxic agents indu
11 evealed a striking correlation with 1-beta-D-arabinofuranosylcytosine (Ara-C) and 2,2'-O-cyclocytidin
12 ficantly more sensitive in vitro to 1-beta-D-arabinofuranosylcytosine (ara-C) and generate higher 1-b
13 ling systems in the cytotoxicity of 1-beta-D-arabinofuranosylcytosine (ara-C) and modulation of ara-C
14 nes display enhanced sensitivity to 1-beta-D-arabinofuranosylcytosine (Ara-C) and other deoxycytidine
15 cleaved during apoptosis induced by 1-beta-d-arabinofuranosylcytosine (ara-C) and other genotoxic age
16 in kinase (SAPK) in the response to 1-beta-D-arabinofuranosylcytosine (ara-C) and other genotoxic age
17 nt of cells with the antimetabolite 1-beta-D-arabinofuranosylcytosine (ara-C) and other genotoxic age
18 ed sensitivity of DS myeloblasts to 1-beta-D-arabinofuranosylcytosine (ara-C) and the enhanced metabo
19 id leukemia cells to treatment with 1-beta-D-arabinofuranosylcytosine (ara-C) includes activation of
20 loid leukemia cells to treatment with 1-beta-arabinofuranosylcytosine (ara-C) includes the induction
21 demonstrate that the antimetabolite 1-beta-D-arabinofuranosylcytosine (ara-C) induces binding of c-Ab
24 f human myeloid leukemia cells with 1-beta-D-arabinofuranosylcytosine (ara-C) is associated with indu
25 that treatment of U-937 cells with 1-beta-D-arabinofuranosylcytosine (ara-C) is associated with tyro
27 7 human myeloid leukemia cells with 1-beta-D-arabinofuranosylcytosine (ara-C) was associated with ind
30 red with respect to potentiation of 1-beta-D-arabinofuranosylcytosine (ara-C)-induced apoptosis in hu
33 old increase in drug sensitivity to 1-beta-D-arabinofuranosylcytosine (AraC) and 2-chloro-2'-deoxyade
34 se (SAPK/JNK) in cells treated with 1-beta-d-arabinofuranosylcytosine (araC) and other genotoxic agen
35 deoxycytidine (dFdC; gemcitabine) and beta-D-arabinofuranosylcytosine (AraC), both of which are D-con
36 e analogues, gemcitabine (dFdC) and 1-beta-d-arabinofuranosylcytosine (AraC), show significant therap
37 fter treatment with cisplatinum and 1-beta-D-arabinofuranosylcytosine but not after exposure to UV an
38 s exhibited enhanced sensitivity to 1-beta-D-arabinofuranosylcytosine, but only on exposure for an ex
39 es cell killing by chemotherapeutic agents 5-arabinofuranosylcytosine, cisplatin, and camptothecin.
40 dine, 2'-deoxy-5-fluorouridine, and 1-beta-D-arabinofuranosylcytosine compared with WT (wild-type) ES
42 rations of the nucleoside analogues 1-beta-d-arabinofuranosylcytosine (cytarabine; ara-C), gemcitabin
43 ce in sensitivity to colchicine and 1-beta-D-arabinofuranosylcytosine existed between the cell lines.
46 5-fluorodeoxyuridine monophosphate, 1-beta-D-arabinofuranosylcytosine monophosphate, and gemcitabine
47 ntaining the nonnatural nucleosides 1-beta-D-arabinofuranosylcytosine or 5-fluoro-2'-deoxyuridine.
48 AAG, which induced hsp70, inhibited 1-beta-D-arabinofuranosylcytosine or etoposide-induced apoptosis
50 a ribonucleotide, the chemotherapeutic drug arabinofuranosylcytosine triphosphate is efficiently ins
51 y the dCK+ cell line phosphorylated 1-beta-D-arabinofuranosylcytosine (used as a substrate for dCK) i
52 amaging agents such as cisplatinum, 1-beta-D-arabinofuranosylcytosine, UV light, ionizing radiation,
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