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Eukaryotic elongation factor 2 controls TNF-α translation in LPS-induced hepatitis

AuthorsManieri, Elisa; Verdugo, Ángeles; González-Rodríguez, Águeda; Valverde, Ángela M.; Sabio, Guadalupe
Issue Date2013
PublisherAmerican Society for Clinical Investigation
CitationJournal of Clinical Investigation 123(1): 164-178 (2013)
AbstractBacterial LPS (endotoxin) has been implicated in the pathogenesis of acute liver disease through its induction of the proinflammatory cytokine TNF-α. TNF-α is a key determinant of the outcome in a well-established mouse model of acute liver failure during septic shock. One possible mechanism for regulating TNF-α expression is through the control of protein elongation during translation, which would allow rapid cell adaptation to physiological changes. However, the regulation of translational elongation is poorly understood. We found that expression of p38γ/δMAPK proteins is required for the elongation of nascent TNF-α protein in macrophages. The MKK3/6-p38γ/δpathway mediated an inhibitory phosphorylation of eukaryotic elongation factor 2 (eEF2) kinase, which in turn promoted eEF2 activation (dephosphorylation) and subsequent TNF-α elongation. These results identify a new signaling pathway that regulates TNF-α production in LPS-induced liver damage and suggest potential cell-specific therapeutic targets for liver diseases in which TNF-α production is involved.
Description15 páginas, 7 figuras.-- et al.
Publisher version (URL)http://dx.doi.org/10.1172/JCI65124
Identifiersdoi: 10.1172/JCI65124
issn: 0021-9738
e-issn: 1558-8238
Appears in Collections:(CNB) Artículos
(IIBM) Artículos
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