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Rifamycins do not function by allosteric modulation of binding of Mg~(2+) to the RNA polymerase active center

机译:利福霉素不能通过变构调节Mg〜(2+)与RNA聚合酶活性中心的结合而起作用

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摘要

Rifamycin antibacterial agents inhibit bacterial RNA polymerase (RNAP) by binding to a site adjacent to the RNAP active center and preventing synthesis of RNA products >2-3 nt in length. Recently, Artsimovitch et al. [(2005) Cell 122:351-363] proposed that rifamycins function by allosteric modulation of binding of Mg~(2+) to the RNAP active center and presented three lines of biochemical evidence consistent with this proposal. Here, we show that rifamycins do not affect the affinity of binding of Mg~(2+) to the RNAP active center, and we reassess the three lines of biochemical evidence, obtaining results not supportive of the proposal. We conclude that rifamycins do not function by allosteric modulation of binding of Mg~(2+) to the RNAP active center.
机译:利福霉素抗菌剂通过与邻近RNAP活性中心的位点结合并阻止合成长度> 2-3 nt的RNA产物来抑制细菌RNA聚合酶(RNAP)。最近,Artsimovitch等。 [(2005)Cell 122:351-363]提出利福霉素通过变构调节Mg 2+与RNAP活性中心的结合而起作用,并提出了与该提议相一致的三行生化证据。在这里,我们表明利福霉素不影响Mg〜(2+)与RNAP活性中心结合的亲和力,并且我们重新评估了三行生化证据,得出的结果不支持该提议。我们得出的结论是,利福霉素不能通过Mg〜(2+)与RNAP活性中心结合的变构调节而起作用。

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