Metal Preference Hierarchy in the HDAC8 Active Site: A DFT Study

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Authors: Nikolay Toshev, Diana Cheshmedzhieva, Yordanka I. Uzunova, Kristiyan Velichkov, Todor Dudev
Cited by: 1
References: 51

Abstract

HDAC8 is a histone deacetylase enzyme that plays a key role in the development of various diseases in humans, including cancers, neurodegenerative diseases, and alcohol use disorder. Although HDAC8 is classified as a Zn2+-dependent metalloenzyme, available data regarding the affinity of other biologically relevant ions, such as Fe2+, Ni2+, Co2+, and Mg2+, for the HDAC8 enzyme active site remain unclear and contradictory. The mechanism by which these ions compete with Zn2+ for the HDAC8 active site is not well understood. In this study, we performed density functional theory (DFT) calculations at the B3LYP/6-31+G(d) level of theory, combined with polarizable continuum model computations (PCM) in water (ε = 78) and methanol (ε = 32). The results show that Zn2+ remains the thermodynamically preferred cofactor across all modeled reactions. Although Fe2+ and Co2+ gain partial stabilization upon increasing coordination number, the associated entropic and desolvation penalties prevent them from outcompeting Zn2+ under physiologically relevant conditions. Only a limited number of substitution reactions for Fe2+ and Co2+ yield ∆G values near thermodynamic neutrality, and only in specific coordination states. In contrast, all modeled Ni2+ substitution reactions are unfavorable, and Mg2+ is strongly excluded from the HDAC8 active site in all reactions. The resulting metal preference hierarchy—Zn2+ > Co2+ ≈ Fe2+ > Ni2+ > Mg2+—supports experimental observations and clarifies the intrinsic selectivity of the HDAC8 enzyme towards Zn2+. These insights provide a molecular basis for understanding HDAC8 metallo-regulation and may guide the rational design of novel, isoform-specific HDACi with improved binding properties.

Fields of Study & Subjects

Histone Deacetylase Inhibitors Research Peptidase Inhibition and Analysis Signaling Pathways in Disease

Publication details

Journal / source
Molecules
Publisher
MDPI AG
Volume
31
Issue
2
Pages
306–306
Publication date
15 January 2026
Language
EN