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1 ceptibility to the iron-dependent antibiotic streptonigrin.
2 ensitivity to the iron-activated antibiotic, streptonigrin.
3 hat SodA plays a protective role against the streptonigrin.
4 we show that B. burgdorferi is resistant to streptonigrin, a metal-dependent redox cycling compound
6 o-hydroxyphenylacetic acid) and resistant to streptonigrin, an antibiotic whose lethal effect require
7 uptake, the mtsR mutant is hypersensitive to streptonigrin and hydrogen peroxide, and (55)Fe uptake a
8 polar mutation in shr was more resistant to streptonigrin and hydrogen peroxide, suggesting decrease
9 p53-mutant fibroblasts are more sensitive to streptonigrin and paraquat when deleted for Ku80 as comp
11 sensitivity to the iron-dependent antibiotic streptonigrin, and a strain containing disrupted copies
12 sensitivity to the iron-dependent antibiotic streptonigrin, and impaired virulence in a mouse model o
14 y sensitive to the iron-dependent antibiotic streptonigrin as the wild-type strain, suggesting that A
16 ynthesis of the potent antitumor agent (+/-)-streptonigrin has been achieved in 14 linear steps and 1
17 eration approach ultimately furnishing (+/-)-streptonigrin in 14 linear steps and 11% overall yield f
18 led enantioenriched (up to 42% ee) synthetic streptonigrin intermediates to be prepared for the first
22 ghput screening, a specific RAD54 inhibitor, streptonigrin (SN), and used it to investigate the mecha
23 on of (55)Fe accumulation and sensitivity to streptonigrin suggested that equibactin is secreted by S
24 B mutant was also 2.5 logs more resistant to streptonigrin than wild-type 130b, confirming its decrea
25 transformed bacteria were more sensitive to streptonigrin, which suggested that fit transports iron
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