Interferon‐stimulated gene 15 enters posttranslational modifications of p53. Issue 5 (14th October 2018)

• Record Type: Journal Article
• Authors: Wang, Yang; Ding, Qi; Lu, Yu‐Chen; Cao, Shi‐Yang; Liu, Qing‐Xue; Zhang, Lei
• Is Part Of: Journal of cellular physiology. Volume 234:Issue 5(2019:May)
• Page Start: 5507
• Page End: 5518
• Publication Date: 2018-10-14
• Subjects: estrogen‐responsive finger protein -- HECT and RLD domain containing E3 ubiquitin protein ligase 5 -- p53 ISGylation -- ubiquitin‐like proteins; Physiology -- Periodicals; Cell physiology -- Periodicals; 571.6
• DOI: 10.1002/jcp.27347
• Languages: English
• ISSNs: 0021-9541

Abstract

Abstract: The tumor suppressor protein p53 is a central governor of various cellular signals. It is well accepted that ubiquitination as well as ubiquitin‐like (UBL) modifications of p53 protein is critical in the control of its activity. Interferon‐stimulated gene 15 (ISG15) is a well‐known UBL protein with pleiotropic functions, serving both as a free intracellular molecule and as a modifier by conjugating to target proteins. Initially, attentions have historically focused on the antiviral effects of ISG15 pathway. Remarkably, a significant role in the processes of autophagy, DNA repair, and protein translation provided considerable insight into the new functions of ISG15 pathway. Despite the deterministic revelation of the relation between ISG15 and p53, the functional consequence of p53 ISGylation appears somewhat confused. More important, more recent studies have hinted p53 ubiquitination or other UBL modifications that might interconnect with its ISGylation. Here, we aim to summarize the current knowledge of p53 ISGylation and the differences in other significant modifications, which would be beneficial for the development of p53‐based cancer therapy.