Publications by authors named "K B Shur"

Drug resistance (DR) in is the main problem in fighting tuberculosis (TB). This pathogenic bacterium has several types of DR implementation: acquired and intrinsic DR. Recent studies have shown that exposure to various antibiotics activates multiple genes, including genes responsible for intrinsic DR.

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The emergence and spread of drug-resistant strains (including MDR, XDR, and TDR) force scientists worldwide to search for new anti-tuberculosis drugs. We have previously reported a number of imidazo[1,2-][1,2,4,5]tetrazines - putative inhibitors of mycobacterial eukaryotic-type serine-threonine protein-kinases, active against . Whole genomic sequences of spontaneous drug-resistant mutants revealed four genes possibly involved in imidazo[1,2-][1,2,4,5]tetrazines resistance; however, the exact mechanism of resistance remain unknown.

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Article Synopsis
  • The study presents draft genome sequences for 15 isolates from the Beijing-B0/W-148 sublineage of bacteria.
  • These isolates have a specific 7-base pair insertion in a gene that produces a fusion protein called Pks15/1.
  • Pks15/1 plays a role in synthesizing phenolglycolipids and forming biofilms, which may increase the virulence and drug resistance of this bacterial lineage.
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We report the draft genome sequences of three isolates belonging to the B0/N-90 sublineage, EKB34, EKB53, and EKB79. The B0/N-90 sublineage belongs to the prevalent (in Russia) and highly virulent Beijing-B0/W148 sublineage. Isolates EKB34 and EKB79 were obtained from people with immune deficiency.

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Tuberculosis (TB) has recently become the leading killer among infectious diseases. Multidrug and extensively drug-resistant Mycobacterium tuberculosis strains urge the need to develop anti-TB drugs with a novel mechanism of action. We describe synthesis of 22 novel imidazo[1,2-b][1,2,4,5]tetrazine derivatives with different substituents at C(3) and C(6) positions, and their antimycobacterial activity in vitro.

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