Ivan Gusarov

TL;DR: It is demonstrated that the feedback regulation of riboflavin and thiamin genes relies on a novel transcription attenuation mechanism that involves the formation of specific complexes between a conserved leader region of the cognate RNA and FMN or TPP.

TL;DR: It is demonstrated that the hairpin inactivates and then destabilizes TEC by weakening interactions in the RNA-DNA hybrid-binding site and the RNA, DNA, and an RNA polymerase that hold TEC together.

TL;DR: It is shown that NO generated by bNOS increases the resistance of bacteria to a broad spectrum of antibiotics, enabling the bacteria to survive and share habitats with antibiotic-producing microorganisms, and suggests that the inhibition of NOS activity may increase the effectiveness of antimicrobial therapy.

TL;DR: It is shown that NO immediately protects bacterial cells from reactive oxygen species by two independent mechanisms, revealing a critical role for bacterial NO-synthase in adaptation to oxidative stress associated with fast metabolic changes, and suggesting a possible role in defending pathogens against immune oxidative attack.

TL;DR: It is demonstrated that pathogenic bacteria use their own NO as a key defense against the immune oxidative burst, thereby establishing bNOS as an essential virulence factor and representing an attractive antimicrobial target for treatment of anthrax and other infectious diseases.