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. Author manuscript; available in PMC: 2012 Feb 25.
Published in final edited form as: Chem Biol. 2011 Feb 25;18(2):210–221. doi: 10.1016/j.chembiol.2010.12.010

Figure 6. Myricetin blocked DnaJ-mediated enhancement of DnaK’s binding to substrate and interfered with the DnaK-DnaJ interaction.

Figure 6

(A) Myricetin inhibited the DnaJ-mediated stimulation of DnaK binding to partially-digested firefly luciferase. Each data point is the average of triplicates and the error bars represent the standard error of the mean. (B) Labeled DnaJ was titrated into fluorescent DnaK and the apparent binding affinity (Kapp) measured by FRET. Myricetin, but not the control compound (catechin), partially blocked binding. The results are the average of triplicate and the error bars represent standard error of the mean. Further results are shown in Figure S5. (C) Model for the allosteric mechanism of myricetin. By impacting the clam-like motions of the subdomains, myricetin might impact DnaJ binding at a distal site. The hydrophobic cleft between subdomains IA and IIA is shown in green.