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1 otency of geldanamycin, but did not affect L-alanosine.
2 and other MTAP-deficient malignancies with L-alanosine.
3 led the early steps in the biosynthesis of l-alanosine.
4       Thus, our results support the use of L-alanosine alone or in combination with a salvage agent a
5 is bound to carbamyl phosphate (CP) and to L-alanosine (an analogue of aspartate).
6                                              Alanosine, an inhibitor of AMP synthesis, inhibited the
7 ells are more sensitive to the toxicity of L-alanosine, an inhibitor of de novo AMP synthesis, than a
8  cells, allows for selective therapy using L-alanosine, an inhibitor of de novo AMP synthesis.
9 trexate, 5,10-dideazatetrahydrofolate, and L-alanosine and by methionine depletion.
10 rve as a predictor of cellular response to L-alanosine and glutathione-mediated resistance to geldana
11 rian SK-OV-3 cells, reduced the potency of L-alanosine and lowered intracellular glutathione levels.
12 e correlations, e.g., amino acid analogue, L-alanosine, and 296 with negative correlations, e.g., gel
13 e that SLC7A11 mediates cellular uptake of L-alanosine but confers resistance to geldanamycin by supp
14                   The therapeutic index of L-alanosine can be increased by the use of a MTAP substrat
15 t strongly supports the kinetic results that alanosine did not inhibit the carbamylation of aspartate
16                                            l-Alanosine is a diazeniumdiolate (N-nitrosohydroxylamine)
17                                Moreover, the alanosine position in this T-state is somewhat displaced
18 cinate pathway genes found in the original l-alanosine producer.
19  we used genome mining to discover two new l-alanosine-producing strains that lack the aspartate-nitr
20 ctive agent for salvaging MTAP+ cells from L-alanosine toxicity and is superior to MTA due to lower c
21 ls obtained at relapse are as sensitive to L-alanosine toxicity as diagnosis samples.
22 electively rescued MTAP+ MOLT-4 cells from L-alanosine toxicity at 25 microM with negligible toxicity
23 TAP+ primary T-ALL cells were rescued from L-alanosine toxicity by the MTAP substrate 5'-deoxyadenosi
24 rinsically MTAP+, would be protected from L.-alanosine toxicity, whereas MTAP-tumor cells would be ki
25 P+ T-ALL cells and normal lymphocytes from L-alanosine toxicity.
26 MTAP(+) cells but not the MTAP(-) cells from alanosine toxicity.
27  MTAP-primary T-ALL cells was inhibited by L-alanosine with a mean IC50 of 4.8+/-5.3 ILM (range, 0.3-