ArticleACS omega2019
Dynamic Basis for Auranofin Drug Recognition by Thiol-Reductases of Human Pathogens and Intermediate Coordinated Adduct Formation with Catalytic Cysteine Residues.
Article in ACS omega, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Article
- Auranofin targets UBA1 and enhances UBA1 activity by facilitating ubiquitin trans-thioesterification to E2 ubiquitin-conjugating enzymes.Nature communications · 2023Article
- Article
- Review
- Auranofin Targeting the NDM-1 Beta-Lactamase: Computational Insights into the Electronic Configuration and Quasi-Tetrahedral Coordination of Gold Ions.Pharmaceutics · 2023Article
- Gold(I) Phosphine Derivatives with Improved Selectivity as Topically Active Drug Leads to Overcome 5-Nitroheterocyclic Drug Resistance inJournal of medicinal chemistry · 2021Article
- New Amides Containing Selenium as Potent Leishmanicidal Agents Targeting Trypanothione Reductase.Antimicrobial agents and chemotherapy · 2020Article
- Combined computational and experimental studies on cysteine-sulfadiazine adduct formation.Turkish journal of chemistry · 2020Article
- Mechanistic Insights Into the Anticancer Properties of the Auranofin Analog Au(PEtFrontiers in chemistry · 2020Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In all the living systems, reactive oxygen species (ROS) metabolism provides resistance against internal and external oxidative stresses. Auranofin (AF), an FDA-approved gold [Au(I)]-conjugated drug, is known to selectively target thiol-reductases, key enzymes involved in ROS metabolism. AF has been successfully tested for its inhibitory activity through biochemical studies, both in vitro and in vivo, against a diverse range of pathogens including protozoa, nematodes, bacteria, and so forth. Cocrystal structures of thiol-reductases complexed with AF revealed that Au(I) was coordinately linked to catalytic cysteines, but the mechanism of transfer of Au(I) from AF to catalytic cysteines still remains unknown. In this study, we have employed computational approaches to understand the interaction of AF with thiol-reductases of selected human pathogens. A similar network of interactions of AF was observed in all the studied enzymes. Also, we have shown that tailor-made analogues of AF can be designed against selective thiol-reductases for targeted inhibition. Molecular dynamics studies show that the AF-intermediates, tetraacetylthioglucose (TAG)-gold, and triethylphosphine (TP)-gold, coordinately linked to one of catalytic cysteines, remain stable in the binding pocket of thiol-reductases for
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Registered trials
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.