ArticleMolecular and cellular biochemistry2009
De-ubiquitylation is the most critical step in the ubiquitin-mediated homeostatic control of the NF-kappaB/IKK basal activity.
Article in Molecular and cellular biochemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 4 citations in OpenAlex.
- A negative feedback mechanism links UBC gene expression to ubiquitin levels by affecting RNA splicing rather than transcription.Scientific reports · 2019Article
- Deleted in Breast Cancer 1 Suppresses B Cell Activation through RelB and Is Regulated by IKKα Phosphorylation.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Dexamethasone restrains ongoing expression of interleukin-23p19 in peripheral blood-derived human macrophages.BMC pharmacology · 2011Article
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4 authors at 1 institution in 1 country.
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Abstract
The role of ubiquitylation in signal-induced activation of nuclear factor -kappaB (NF-kappaB) has been well established, while its involvement in maintaining NF-kappaB basal activity is less certain. Recent evidences demonstrate that in unstimulated cells, NF-kappaB homeostasis is actually the result of opposing forces: pro-activating activity of the IkappaB Kinase (IKK) and inhibitory activity of the Inhibitor of -kappaB (IkappaB) proteins. It is well known that endogenous de-ubiquitylating mechanisms are less effective on Ub motifs containing UbG76A. Here, we show that overexpression of a ubiquitin (Ub) G76A mutant leads to persistent activation of the IKK/NF-kappaB pathway in the absence of extra-cellular stimuli. In contrast, no effects on NF-kappaB activation were observed upon expression of UbK48R and UbK63R mutants, which are known to impair elongation of Lys(48)- and Lys(63)-linked poly-ubiquitin chains, respectively. Overall, these findings indicate that under basal conditions, the rate of de-ubiquitylation, rather than that of substrate ubiquitylation, is critical for the maintenance of appropriate levels of IKK/NF-kappaB activity.
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