Skip to content

Author

Hyun Ho Park

3 papers indexed here

We haven’t gathered this author’s papers yet. Follow them and we’ll fetch their work.

Not the right person? Other researchers publish under this name.

Aug 2026

Bidirectional and regiospecific C21-modification of steroids by a chloramphenicol O-acetyltransferase.

Bidirectional acetylation and deacetylation of small molecules by acetyltransferases (ATs) remain poorly understood. In this study, we present the structural, functional, and computational characterization of a chloramphenicol O-AT from Bacillus sp. PAMC22265 (AT65) that exhibits bidirectional catalytic activity toward the regiospecific C21-acetylation and deacetylation of steroid substrates. The crystal structure of AT65 was determined at 2.40 Å resolution (PDB ID: 24ZY), revealing a trimeric architecture in which the putative active-sites located at the interfaces between adjacent subunits. In vitro kinetic analyses of both acetylation and deacetylation reactions demonstrated substrate-dependent catalytic efficiencies, with comparable activity under the experimental conditions. Molecular docking, 100 ns molecular dynamics simulations, hydrogen-bond analysis, and MM-PBSA free-energy calculations supported stable substrate binding within the active site and suggested that His187 and Asp191 may contribute to substrate recognition and catalysis. Consistent with this observation, substitution of His187 with alanine abolished detectable enzymatic activity, highlighting its functional importance. Whole-cell biotransformation further demonstrated the selective production of C21-acetylated steroid derivatives, some of which exhibited preliminary antiproliferative activity against murine breast cancer cell lines. Collectively, these findings provide structural, biochemical, and computational insights into the bidirectional catalytic properties of AT65 and establish a foundation for further mechanistic studies and the development of selective enzymatic strategies for steroid modification.

Kamal Prasad Regmi, S. Park, Prakash Paudel et al. · 0 citations
Open access Jul 2026

An expanded realm of anti-CRISPR-associated proteins and regulatory mechanisms

Many bacteriophages encode anti-CRISPR (Acr) proteins that inhibit the CRISPR-Cas immune systems. Rapid acr gene expression upon phage entry enables CRISPR-Cas neutralisation, but can impact phage fitness if unregulated. Therefore, Acr production is often controlled by distinct families of co-encoded anti-CRISPR-associated (Aca) proteins, which are usually helix-turn-helix (HTH) regulators that bind DNA within acr–aca operon promoters. Previously, we demonstrated that the Aca2 family additionally represses Acr production translationally by binding structured RNA motifs within the 5′ untranslated regions (UTRs) of the acr–aca mRNA. Here, through systematic bioinformatic analyses, we provide evidence of structured RNA motifs in the 5′ UTRs of operons encoding members of other Aca families, and that Aca1 also specifically binds its cognate RNA motif. Additionally, many Aca proteins are predicted to regulate not only their own but also adjacent operons with potential anti-defence genes. Indeed, we show that Aca14, newly identified in this study, represses two predicted anti-defence operons. Aca14 is a ribbon-helix-helix domain protein, revealing regulatory diversity beyond the canonical HTH Aca family members. Collectively, our findings expand the understanding of acr regulation in mobile genetic elements and reveal novel mechanisms by which phages fine-tune anti-defence gene expression. Graphical abstract

Maximilian Feussner, N. Birkholz, So Yeon Lee et al. · 0 citations
#protein folding Open access Aug 2026

Structural insights into Cas9 inhibition by AcrIIA17 via bridge helix interaction

The crystal structure of AcrIIA17 is presented and its mechanism of Staphylococcus aureus Cas9 (SauCas9) inhibition is elucidated, identifying AcrIIA17 as an Acr protein that targets the Cas9 BH domain and reveal the BH domain as a regulatory checkpoint in Cas9 activation.

G. Kim, Hyo Been Jin, Yong-Jun Kang et al. · 0 citations