CSN5/Jab1 controls multiple events in the mammalian cell cycle |
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| Authors: | Yoshida Akihiro Yoneda-Kato Noriko Panattoni Martina Pardi Ruggero Kato Jun-ya |
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| Institution: | a Graduate School of Biological Sciences, Nara Institute of Science and Technology, Nara, Japan
b Vita-Salute San Raffaele University School of Medicine, 20132 Milano, Italy |
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| Abstract: | The COP9 signalosome (CSN) complex is critical for mammalian cell proliferation and survival, but it is not known how the CSN affects the cell cycle. In this study, MEFs lacking CSN5/Jab1 were generated using a CRE-flox system. MEFs ceased to proliferate upon elimination of CSN5/Jab1. Rescue experiments indicated that the JAMM domain of CSN5/Jab1 was essential. CSN5/Jab1-elimination enhanced the neddylation of cullins 1 and 4 and altered the expression of many factors including cyclin E and p53. CSN5/Jab1-elimination inhibited progression of the cell cycle at multiple points, seemed to initiate p53-independent senescence and increased the ploidy of cells. Thus, CSN5/Jab1 controls different events of the cell cycle, preventing senescence and endocycle as well as the proper progression of the somatic cell cycle.Structured summaryMINT-8046253: Csn1 (uniprotkb:Q99LD4) physically interacts (MI:0914) with Csn5 (uniprotkb:O35864), Csn8 (uniprotkb:Q8VBV7), Csn3 (uniprotkb:O88543), Csn7b (uniprotkb:Q8BV13) and Csn6 (uniprotkb:O88545) by anti bait coimmunoprecipitation (MI:0006) |
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| Keywords: | Cell cycle CSN5/Jab1 Neddylation Cell proliferation COP9 signalosome Senescence Endocycle |
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