The ubiquitylation of IL-1β limits its cleavage by caspase-1 and targets it for proteasomal degradation

Hyperactivation of inflammasome-induced IL-1β can cause immunopathology and is a feature of autoinflammatory diseases. Here, the authors show how ubiquitination of IL-1β limits its activity by targeting it for proteasomal degradation and preventing its cleavage by caspase-1.

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Detalles Bibliográficos
Autores principales: Swarna L. Vijayaraj, Rebecca Feltham, Maryam Rashidi, Daniel Frank, Zhengyang Liu, Daniel S. Simpson, Gregor Ebert, Angelina Vince, Marco J. Herold, Andrew Kueh, Jaclyn S. Pearson, Laura F. Dagley, James M. Murphy, Andrew I. Webb, Kate E. Lawlor, James E. Vince
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2021
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Acceso en línea:https://doaj.org/article/15cc2871bf48403c8f2afd5582cbe869
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Descripción
Sumario:Hyperactivation of inflammasome-induced IL-1β can cause immunopathology and is a feature of autoinflammatory diseases. Here, the authors show how ubiquitination of IL-1β limits its activity by targeting it for proteasomal degradation and preventing its cleavage by caspase-1.