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2 ment of MALME-3M cells with 10 microM N1,N11-diethylnorspermine caused an increase in hypophosphoryla
5 netic parameters of i.v.-administered N1,N11-diethylnorspermine (DENSPM) are evaluated in Cebus apell
6 clinically relevant polyamine analog N1,N11-diethylnorspermine (DENSPM) causes rapid apoptosis in hu
7 Treatment with the polyamine analogue N1,N11-diethylnorspermine (DENSPM) increased SSAT activity in t
8 cally relevant polyamine analogue N(1),N(11)-diethylnorspermine (DENSPM) inhibits cell growth by down
11 leukemia cell growth than either N(1),N(11)-diethylnorspermine (DENSPM) or (2R,10R)-N(1),N(11)-dieth
12 lly target polyamine metabolism, i.e. N1,N11-diethylnorspermine (DENSPM) or alpha-difluoromethylornit
13 tor of ornithine decarboxylase 1 (ODC1), and diethylnorspermine (DENSpm), an activator of spermidine/
14 n the presence of the spermine analog N1,N11-diethylnorspermine (DENSPM), cell proliferation ceased;
15 most potently induces SSAT activity, N1, N11-diethylnorspermine (DENSPM), increases SSAT mRNA in MALM
16 e impact of four polyamine analogues, N1,N11-diethylnorspermine (DENSPM), N1,N14-diethylhomospermine
17 e to the growth inhibitory effects of N1,N11-diethylnorspermine (DENSPM)-a polyamine analogue also un
18 unhydroxylated parent drug (e.g., N(1),N(11)-diethylnorspermine [DENSPM]) at 1 microM; however, S-ade
19 eprivation before treatment with N(1), N(11)-diethylnorspermine markedly increased analog induction o
20 inear molecules include norspermine, N1, N11-diethylnorspermine, N1,N12-bis(2,2,2-trifluoroethyl)sper
21 servation, we examined the effects of N1,N11-diethylnorspermine on cell cycle regulatory proteins ass
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