Evidence map›Paper›PMID 39738057›Full record

ArticleNature communications2024

Structure-function analysis of carrier protein-dependent 2-sulfamoylacetyl transferase in the biosynthesis of altemicidin.

Yuhao Zhu, Takahiro Mori, Masayuki Karasawa, Kohei Shirai, Wenjiao Cheng, Tohru Terada, Takayoshi Awakawa, Ikuro Abe

Abstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Yuhao ZhuGraduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan.
Takahiro MoriGraduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan. tmori@mol.f.u-tokyo.ac.jp.ORCID 0000-0002-2754-5858
Masayuki KarasawaGraduate School of Agricultural and Life Sciences, The University of Tokyo, Tokyo, Japan.
Kohei ShiraiGraduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan.
Wenjiao ChengGraduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan.
Tohru TeradaGraduate School of Agricultural and Life Sciences, The University of Tokyo, Tokyo, Japan.ORCID 0000-0002-7091-0646
Takayoshi AwakawaGraduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan. takayoshi.awakawa@riken.jp.ORCID 0000-0003-2575-3175
Ikuro AbeGraduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan. abei@mol.f.u-tokyo.ac.jp.ORCID 0000-0002-3640-888X

Funding

Japan Agency for Medical Research and Development (AMED) JP21ak0101164MEXT | Japan Society for the Promotion of Science (JSPS) 23H00393New Energy and Industrial Technology Development Organization (NEDO) JPNP20011
6 · The paper itself

Abstract

The general control non-repressible 5 (GCN5)-related N-acetyltransferase (GNAT) SbzI, in the biosynthesis of the sulfonamide antibiotic altemicidin, catalyzes the transfer of the 2-sulfamoylacetyl (2-SA) moiety onto 6-azatetrahydroindane dinucleotide. While most GNAT superfamily utilize acyl-coenzyme A (acyl-CoA) as substrates, SbzI recognizes a carrier-protein (CP)-tethered 2-SA substrate. Moreover, SbzI is the only naturally occurring enzyme that catalyzes the direct incorporation of sulfonamide, a valuable pharmacophore in medicinal chemistry. Here, we present the structure-function analysis and structure-based engineering of SbzI. The crystal structure of SbzI in complex with the CP SbzG, along with cross-linking and isothermal titration calorimetry analyses of their variants, revealed the structural basis for CP recognition by the GNAT SbzI. Furthermore, docking simulation, molecular dynamics simulation, and mutagenesis studies indicated the intimate structural details of the unique reaction mechanism of SbzI, which does not utilize a general base residue in contrast to other typical GNATs. These findings facilitated rational engineering of the enzyme to expand the substrate range and to generate azaindane dinucleotide derivatives.

Indexed as

Molecular Dynamics SimulationAcetyltransferasesAnti-Bacterial AgentsBacterial ProteinsCarrier ProteinsCrystallography, X-RayMolecular Docking SimulationStructure-Activity RelationshipSubstrate SpecificitySulfonamidesAcetyltransferasesAnti-Bacterial AgentsBacterial ProteinsCarrier ProteinsSulfonamides

Identifiers

PMID39738057
PMCPMC11685415

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.