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1 blocked by inhibition of HIF-1 signaling via echinomycin.
2 sed to examine the conformational effects of echinomycin, a DNA bis-intercalating antibiotic, on line
5 mplexes containing different drugs including echinomycin, actinomycin-D, ethidium bromide, Hoechst 33
6 tranded DNA is not inhibited indicating that echinomycin acts by interacting with the DNA and not the
8 ts that direct molecular recognition between echinomycin and DNA, mediated by hydrogen bonding and va
9 respectively, L1210 cell line) comparable to echinomycin and one analogue, which bears the luzopeptin
10 us choshinensis conferred resistance against echinomycin and other quinomycin antibiotics, including
12 of anticancer depsipeptides thiocoraline and echinomycin, and by mutants of these domains, for which
13 mportantly, in mice with complete remission, echinomycin appeared to completely eliminate LICs becaus
14 portantly, in X.laevis embryos injected with echinomycin at the two-cell stage the drug specifically
15 which the 2-amino group that is crucial for echinomycin binding has been added or removed, respectiv
16 The structural perturbations induced when echinomycin binds to closed circular duplex pBR322 DNA w
17 available among the different DNA fragments; echinomycin binds to TpD sites much more tightly than to
19 insertion domain allows Ecm16 to distinguish echinomycin-bound DNA from normal DNA and link substrate
20 high-affinity bisintercalation analogous to echinomycin, but with little or no perceptible sequence
21 poxia-inducible factor (HIF)1alpha inhibitor echinomycin can be used to treat relapsed AML without af
26 at a combination of actinomycin D (ActD) and echinomycin (Echi), can interact in novel ways with nati
27 d patient-derived AML cells, we tested a new echinomycin formulation with longer half-life and signif
28 , we tested efficacy of HIF-1alpha inhibitor echinomycin in TP53-mutated AML samples in vitro and in
34 One of the most potent compounds identified, echinomycin (NSC-13502), a small-molecule known to bind
37 duplexes complexed with the DNA binding drug echinomycin result in increased occupancy of the (w)cWH
39 t in a mouse model of relapsed AML, low-dose echinomycin selectively targets LICs and spares normal h
40 rcalating antibiotics (e.g., triostine A and echinomycin), the detailed interactions between those tw
41 ve examined the binding of actinomycin D and echinomycin to artificial DNA molecules asymmetrically s
46 lex, free and in complex with the antibiotic echinomycin, which features two central adenine-thymine