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. 2020 Feb 3;48(5):2199–2208. doi: 10.1093/nar/gkaa056

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© The Author(s) 2020. Published by Oxford University Press on behalf of Nucleic Acids Research.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 5. — Functional model of repressor and non-repressor forms of Zur unbinding behaviors in E. coli upon encountering zinc sufficiency or deficiency. When zinc is sufficient, unbinding of the repressor form from operator site is facilitated (A) while that of the non-repressor form from storage site is impeded (B) due to higher cellular protein concentration. Upon zinc deficiency, the facilitated unbinding of the repressor form is attenuated (C) while the unbinding of the non-repressor form is less impeded (D) due to lower cellular protein concentration. Released non-repressors into cytosol could facilitate the repressor to unbind (E), helping transition to de-repression of zinc uptake.