SCFβ-TRCP promotes cell growth by targeting PR-Set7/Set8 for degradation

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SCFβ-TRCP promotes cell growth by targeting PR-Set7/Set8 for degradation

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Title: SCFβ-TRCP promotes cell growth by targeting PR-Set7/Set8 for degradation
Author: Wang, Zhiwei; Dai, Xiangpeng; Zhong, Jiateng; Inuzuka, Hiroyuki; Wan, Lixin; Li, Xiaoning; Wang, Lixia; Ye, Xiantao; Sun, Liankun; Gao, Daming; Zou, Lee; Wei, Wenyi

Note: Order does not necessarily reflect citation order of authors.

Citation: Wang, Z., X. Dai, J. Zhong, H. Inuzuka, L. Wan, X. Li, L. Wang, et al. 2015. “SCFβ-TRCP promotes cell growth by targeting PR-Set7/Set8 for degradation.” Nature Communications 6 (1): 10185. doi:10.1038/ncomms10185. http://dx.doi.org/10.1038/ncomms10185.
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Abstract: The Set8/PR-Set7/KMT5a methyltransferase plays critical roles in governing transcriptional regulation, cell cycle progression and tumorigenesis. Although CRL4Cdt2 was reported to regulate Set8 stability, deleting the PIP motif only led to partial resistance to ultraviolet-induced degradation of Set8, indicating the existence of additional E3 ligase(s) controlling Set8 stability. Furthermore, it remains largely undefined how DNA damage-induced kinase cascades trigger the timely destruction of Set8 to govern tumorigenesis. Here, we report that SCFβ-TRCP earmarks Set8 for ubiquitination and degradation in a casein kinase I-dependent manner, which is activated by DNA-damaging agents. Biologically, both CRL4Cdt2 and SCFβ-TRCP-mediated pathways contribute to ultraviolet-induced Set8 degradation to control cell cycle progression, governing the onset of DNA damage-induced checkpoints. Therefore, like many critical cell cycle regulators including p21 and Cdt1, we uncover a tight regulatory network to accurately control Set8 abundance. Our studies further suggest that aberrancies in this delicate degradation pathway might contribute to aberrant elevation of Set8 in human tumours.
Published Version: doi:10.1038/ncomms10185
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4682171/pdf/
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:23993465
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