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Int. J. Mol. Sci. 2017, 18(7), 1476;

Ubiquitination in Periodontal Disease: A Review

Division of Clinical Mass Spectrometry, Chiba University Hospital, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan
Division of Laboratory Medicine, Clinical Genetics and Proteomics, Chiba University Hospital, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan
Author to whom correspondence should be addressed.
Received: 27 April 2017 / Revised: 4 July 2017 / Accepted: 5 July 2017 / Published: 10 July 2017
(This article belongs to the Special Issue Ubiquitin System)
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Periodontal disease (periodontitis) is a chronic inflammatory condition initiated by microbial infection that leads to gingival tissue destruction and alveolar bone resorption. The periodontal tissue’s response to dental plaque is characterized by the accumulation of polymorphonuclear leukocytes, macrophages, and lymphocytes, all of which release inflammatory mediators and cytokines to orchestrate the immunopathogenesis of periodontal disease. Ubiquitination is achieved by a mechanism that involves a number of factors, including an ubiquitin-activating enzyme, ubiquitin-conjugating enzyme, and ubiquitin–protein ligase. Ubiquitination is a post-translational modification restricted to eukaryotes that are involved in essential host processes. The ubiquitin system has been implicated in the immune response, development, and programmed cell death. Increasing numbers of recent reports have provided evidence that many approaches are delivering promising reports for discovering the relationship between ubiquitination and periodontal disease. The scope of this review was to investigate recent progress in the discovery of ubiquitinated protein in diseased periodontium and to discuss the ubiquitination process in periodontal diseases. View Full-Text
Keywords: ubiquitination; proteasome; periodontal diseases ubiquitination; proteasome; periodontal diseases

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Tsuchida, S.; Satoh, M.; Takiwaki, M.; Nomura, F. Ubiquitination in Periodontal Disease: A Review. Int. J. Mol. Sci. 2017, 18, 1476.

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