期刊
FRONTIERS IN ONCOLOGY
卷 11, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fonc.2021.659049
关键词
HECT E3 ubiquitin ligases; WWP1; HERC2; HECW1; SMURF1; p53; DNA damage response
类别
资金
- National Institutes of Health [R15GM126432]
- Arthur E. Martell and Thomas T. Sugihara Summer Undergraduate Scholarship from Clark University
Cellular homeostasis is regulated by gene expression controlling protein translation, localization, and termination. Mutations caused by environmental and biological factors can lead to protein malfunction and malignant transformations. The tumor suppressor protein p53 undergoes numerous posttranslational modifications and plays a role in apoptosis, transcription, and DNA damage response. Irregular interactions between HECT E3 ubiquitin ligases and p53 can induce tumorigenesis.
Cellular homeostasis is governed by the precise expression of genes that control the translation, localization, and termination of proteins. Oftentimes, environmental and biological factors can introduce mutations into the genetic framework of cells during their growth and division, and these genetic abnormalities can result in malignant transformations caused by protein malfunction. For example, p53 is a prominent tumor suppressor protein that is capable of undergoing more than 300 posttranslational modifications (PTMs) and is involved with controlling apoptotic signaling, transcription, and the DNA damage response (DDR). In this review, we focus on the molecular mechanisms and interactions that occur between p53, the HECT E3 ubiquitin ligases WWP1, SMURF1, HECW1 and HERC2, and other oncogenic proteins in the cell to explore how irregular HECT-p53 interactions can induce tumorigenesis.
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