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@ARTICLE{Kling:220438,
      author       = {Kling, A. and Lukat, P. and Almeida, D. V. and Bauer, A.
                      and Fontaine, E. and Sordello, S. and Zaburannyi, N. and
                      Herrmann, J. and Wenzel, S. C. and Konig, C. and Ammerman,
                      N. C. and Barrio, M. B. and Borchers, K. and Bordon-Pallier,
                      F. and Bronstrup, M. and Courtemanche, G. and Gerlitz, M.
                      and Geslin, M. and Hammann, P. and Heinz, D. W. and
                      Hoffmann, H. and Klieber, S. and Kohlmann, M. and Kurz, M.
                      and Lair, C. and Matter, H. and Nuermberger, E. and Tyagi,
                      S. and Fraisse, L. and Grosset, J. H. and Lagrange, S. and
                      Muller, R.},
      title        = {{T}argeting {D}na{N} for tuberculosis therapy using novel
                      griselimycins},
      journal      = {Science},
      volume       = {348},
      number       = {6239},
      issn         = {1095-9203},
      address      = {Washington, DC [u.a.]},
      publisher    = {American Association for the Advancement of Science16205},
      reportid     = {PUBDB-2015-02248},
      pages        = {1106 - 1112},
      year         = {2015},
      note         = {(c) AAAS. Post referee full text in progress. Embargo for
                      full text 6 months from 06.06.15.},
      abstract     = {The discovery of Streptomyces-produced streptomycin founded
                      the age of tuberculosis therapy. Despite the subsequent
                      development of a curative regimen for this disease,
                      tuberculosis remains a worldwide problem, and the emergence
                      of multidrug-resistant Mycobacterium tuberculosis has
                      prioritized the need for new drugs. Here we show that new
                      optimized derivatives from Streptomyces-derived griselimycin
                      are highly active against M. tuberculosis, both in vitro and
                      in vivo, by inhibiting the DNA polymerase sliding clamp
                      DnaN. We discovered that resistance to griselimycins,
                      occurring at very low frequency, is associated with
                      amplification of a chromosomal segment containing dnaN, as
                      well as the ori site. Our results demonstrate that
                      griselimycins have high translational potential for
                      tuberculosis treatment, validate DnaN as an antimicrobial
                      target, and capture the process of antibiotic
                      pressure-induced gene amplification.},
      cin          = {DOOR},
      ddc          = {500},
      cid          = {I:(DE-H253)HAS-User-20120731},
      pnm          = {6G3 - PETRA III (POF3-622)},
      pid          = {G:(DE-HGF)POF3-6G3},
      experiment   = {EXP:(DE-H253)P-P11-20150101},
      typ          = {PUB:(DE-HGF)16},
      UT           = {WOS:000355590500040},
      pubmed       = {pmid:26045430},
      doi          = {10.1126/science.aaa4690},
      url          = {https://bib-pubdb1.desy.de/record/220438},
}