Functional disruption of HypB, a GTPase of Helicobacter pylori, by bismuth

Bismuth (Bi3+) binds equal molar amounts of HypB from Helicobacter pylori at the conserved metal site with a dissociation constant of 0.94 (0.25)x10(-17) uM, and concomitantly induces the protein dimerization similarly to Ni2+. Excess Bi3+ causes HypB further oligomerization, leading to HypB GTPase dysfunction. The results extend our understanding on the inhibitory mechanism of bismuth drugs against the pathogen