NDLI: Targeted disruption of Skp2 results in accumulation of cyclin E and p27Kip1, polyploidy and centrosome overduplication

Content Provider	PubMed Central
Author	Nakayama, Keiko Nagahama, Hiroyasu Minamishima, Yohji A. Matsumoto, Masaki Nakamichi, Ikuo Kitagawa, Kyoko Shirane, Michiko Tsunematsu, Ryosuke Tsukiyama, Tadasuke Ishida, Noriko Kitagawa, Masatoshi Nakayama, Kei-ichi Hatakeyama, Shigetsugu
Copyright Year	2000
Abstract	The ubiquitin–proteasome pathway plays an important role in control of the abundance of cell cycle regulators. Mice lacking Skp2, an F-box protein and substrate recognition component of an Skp1–Cullin–F-box protein (SCF) ubiquitin ligase, were generated. Although Skp2 –/– animals are viable, cells in the mutant mice contain markedly enlarged nuclei with polyploidy and multiple centrosomes, and show a reduced growth rate and increased apoptosis. Skp2 –/– cells also exhibit increased accumulation of both cyclin E and p27Kip1. The elimination of cyclin E during S and G2 phases is impaired in Skp2 –/– cells, resulting in loss of cyclin E periodicity. Biochemical studies showed that Skp2 interacts specifically with cyclin E and thereby promotes its ubiquitylation and degradation both in vivo and in vitro. These results suggest that specific degradation of cyclin E and p27Kip1 is mediated by the SCFSkp2 ubiquitin ligase complex, and that Skp2 may control chromosome replication and centrosome duplication by determining the abundance of cell cycle regulators.
Related Links	http://dx.doi.org/10.1093/emboj/19.9.2069
Ending Page	2081
Page Count	13
Starting Page	2069
File Format	PDF
ISSN	14602075
e-ISSN	14602075
Journal	The EMBO Journal
Issue Number	9
Volume Number	19
Language	English
Publisher	Oxford University Press
Publisher Date	2000-05-02
Access Restriction	Open
Rights Holder	Oxford University Press
Subject Keyword	Biochemistry, Genetics and Molecular Biology(all) Immunology and Microbiology(all) Neuroscience(all) Molecular Biology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Neuroscience Immunology and Microbiology Medicine Molecular Biology

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