Implications of protein post-translational modifications in IBD

Authors

  • Stefan F. Ehrentraut SE, MD,

    Corresponding author
    1. Department of Medicine and the Mucosal Inflammation Program, University of Colorado School of Medicine, Aurora, Colorado
    • University of Colorado School of Medicine, 12700 East 19th Ave., MS B-146, Aurora, CO 80045
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  • Sean P. Colgan SC, PhD

    1. Department of Medicine and the Mucosal Inflammation Program, University of Colorado School of Medicine, Aurora, Colorado
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  • Supported by a German Research Foundation (DFG) grant (EH 371/1-1) to S.E. and by National Institutes of Health Grants DK50189, HL60569, and by funding from the Crohn's and Colitis Foundation of America.

  • The authors are not aware of any affiliations, memberships, funding, or financial holdings that might be perceived as influencing the objectivity of this review.

Abstract

Abstract: In recent years our understanding of the pathogenesis of inflammatory bowel disease (IBD) has greatly increased. Hallmarks of IBD include loss of intestinal barrier function, increased cytokine production, and failed resolution of tissue damage. Lasting treatments are still lacking and, therefore, a better understanding of the underlying molecular mechanisms is necessary to design novel therapeutic approaches. Apart from transcriptional and posttranscriptional regulation of relevant genes, mammals have evolved a complex and efficient series of mechanisms to rapidly modify newly made proteins for the purposes of signaling and adaptation. These posttranslational protein modifications include, among others, phosphorylation, hydroxylation, neddylation, and cytokine cleavage by the inflammasome. This review focuses on our current understanding of posttranslational protein modifications with a particular focus on their relevance to IBD pathogenesis. (Inflamm Bowel Dis 2012;)

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