ReferenceID 534
Cardiac glycosides are potent inhibitors of interferon-β gene expression
Nat Chem Biol
Here we report that bufalin and other cardiac glycoside inhibitors of the sodium-potassium ATPase (sodium pump) potently inhibit the induction of the interferon-β (IFNβ) gene by virus, double-stranded RNA or double-stran
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Record Fields
Scalar fields from the final reference record.
- Reference Id
- 534
- Evidence Id
- 17124
- Core Evidence Id
- 17124
- Source Reference Id
- 1034
- Herb2 Reference Id
- HBREF001760
- Subject Paper Key
- HBIN018981_21076398
- Pubmed Id
- 21076398
- Doi
- 10.1038/nchembio.476
- Paper Title
- Cardiac glycosides are potent inhibitors of interferon-β gene expression
- Paper Abstract
- Here we report that bufalin and other cardiac glycoside inhibitors of the sodium-potassium ATPase (sodium pump) potently inhibit the induction of the interferon-β (IFNβ) gene by virus, double-stranded RNA or double-stranded DNA. Cardiac glycosides increase the intracellular sodium concentration, which appears to inhibit the ATPase activity of the RNA sensor RIG-I, an essential and early component in the IFNβ activation pathway. This, in turn, prevents the activation of the critical transcription factors IRF3 and NFκB. Bufalin inhibition can be overcome by expressing a drug-resistant variant of the sodium pump and knocking down the pump by short hairpin RNA inhibits IFNβ expression. Thus, bufalin acts exclusively through the sodium pump. We also show that bufalin inhibits tumor necrosis factor (TNF) signaling, at least in part by interfering with the nuclear translocation of NFκB. These findings suggest that bufalin could be used to treat inflammatory and autoimmune diseases in which IFN or TNF are hyperactivated.
- Journal
- Nat Chem Biol
- Publish Year
- 2011
- Experiment Subject
- Experiment Type
- Others
- Phenotype Related
- Autoimmune Diseases
- Paper Title Cn
- Paper Title En
- Cardiac glycosides are potent inhibitors of interferon-β gene expression
- Bilingual Status
- semi_complete