ArticleOncotarget2017
Isoliquiritigenin suppresses human T Lymphocyte activation via covalently binding cysteine 46 of IκB kinase.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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Who cites it
4 citing papers in PubMed, 13 citations in OpenAlex.
- IκB kinase β (IKKβ): Structure, transduction mechanism, biological function, and discovery of its inhibitors.International journal of biological sciences · 2023Review
- Perspectives on the Role of Isoliquiritigenin in Cancer.Cancers · 2021Review
- Isoliquiritigenin inhibits the proliferation, migration and metastasis of Hep3B cells via suppressing cyclin D1 and PI3K/AKT pathway.Bioscience reports · 2020Article
- Isoliquiritigenin attenuates spinal tuberculosis through inhibiting immune response in a New Zealand white rabbit model.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2018Article
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The efficacious practice of precision personalized medicine requires a more exact understanding of the molecular mechanisms of drug, hence then it is necessary to identify the binding site of the drugs derived from natural sources. In the study, we investigated the suppressive effect and underlying mechanism of isoliquiritigenin (2',4',4-trihydroxychalcone; ILG), a phyto-flavonoid, on human T lymphocyte activation in vitro and in vivo. The results showed that ILG dose-dependently suppressed human T cell activation via suppressing IκBα phosphorylation and degradation, NF-κB nuclear translocation and IKKβ activity. Molecular docking results predicted that cysteine 46 (Cys-46) is probably the binding site of ILG on IKKβ, and this prediction has been validated by competition assay and kinase assay. To further verify the binding site of this compound in vivo, IKKβC46A transgenic (IKKβC46A) mice were generated. We found that ILG had a less potent immune-suppressive effect in homozygous IKKβC46A mice than IKKβ wild type (IKKβ wt) littermates with the delay-type hypersensitivity (DTH), suggesting that ILG cannot significantly suppress the inflammation due to the mutation of Cys-46 in the transgenic mice. Collectively, our findings indicate that the ILG inhibited T cell activation in vivo and in vitro via directly binding to IKKβ Cys46.
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