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1 hat SodA plays a protective role against the streptonigrin.
2 ceptibility to the iron-dependent antibiotic streptonigrin.
3 ensitivity to the iron-activated antibiotic, streptonigrin.
4  highly stereoselective total synthesis of P-streptonigrin.
5  we show that B. burgdorferi is resistant to streptonigrin, a metal-dependent redox cycling compound
6                 The total synthesis of (+/-)-streptonigrin, a potent tetracyclic aminoquinoline-5,8-d
7 o-hydroxyphenylacetic acid) and resistant to streptonigrin, an antibiotic whose lethal effect require
8 uptake, the mtsR mutant is hypersensitive to streptonigrin and hydrogen peroxide, and (55)Fe uptake a
9  polar mutation in shr was more resistant to streptonigrin and hydrogen peroxide, suggesting decrease
10 p53-mutant fibroblasts are more sensitive to streptonigrin and paraquat when deleted for Ku80 as comp
11 cient medium, a high degree of resistance to streptonigrin, and a reduced rate of iron uptake.
12 sensitivity to the iron-dependent antibiotic streptonigrin, and a strain containing disrupted copies
13 sensitivity to the iron-dependent antibiotic streptonigrin, and impaired virulence in a mouse model o
14 ient conditions had a similar sensitivity to streptonigrin as the aconitase mutant.
15 y sensitive to the iron-dependent antibiotic streptonigrin as the wild-type strain, suggesting that A
16                                We infer that streptonigrin can reduce bound oxygen directly to a ferr
17  isolated following chemical mutagenesis and streptonigrin enrichment.
18 ynthesis of the potent antitumor agent (+/-)-streptonigrin has been achieved in 14 linear steps and 1
19 eration approach ultimately furnishing (+/-)-streptonigrin in 14 linear steps and 11% overall yield f
20                                              Streptonigrin, in contrast, was poorer at redox cycling
21 n line with a previous report, we found that streptonigrin inhibits STAT3 phosphorylation, raising th
22 led enantioenriched (up to 42% ee) synthetic streptonigrin intermediates to be prepared for the first
23 results suggest that, at low concentrations, streptonigrin may primarily enhance heterochromatin form
24                                              Streptonigrin methylesterase A (StnA) is one of the tail
25                           Among these drugs, streptonigrin most prominently caused an increase in Hoe
26        Comparison of the susceptibilities to streptonigrin of the individual pit, piu, and pia mutant
27 AT function may contribute to the effects of streptonigrin on heterochromatin.
28                 Interestingly, we found that streptonigrin promotes heterochromatin at a concentratio
29 d following an enrichment procedure based on streptonigrin resistance.
30 ghput screening, a specific RAD54 inhibitor, streptonigrin (SN), and used it to investigate the mecha
31 on of (55)Fe accumulation and sensitivity to streptonigrin suggested that equibactin is secreted by S
32 B mutant was also 2.5 logs more resistant to streptonigrin than wild-type 130b, confirming its decrea
33                           This scheme allows streptonigrin to kill a bacterial cell without interfere
34                         We further show that streptonigrin treated cells exhibit compacted DNA foci i
35 tionally, in vitro experiments revealed that streptonigrin was able to damage DNA without inhibition
36  transformed bacteria were more sensitive to streptonigrin, which suggested that fit transports iron
37              ES936 abrogates the toxicity of streptonigrin, with greater effects seen in cell lines e