Signal-induced ubiquitination of p57(Kip2) is independent of the C-terminal consensus Cdk phosphorylation site

FEBS Letters
Marie Pierre LeibovitchSerge Alexandre Leibovitch

Abstract

The cyclin-dependent kinase inhibitor p57(Kip2) is required for normal mouse embryonic development. p57(Kip2) consists of four structurally distinct domains in which the conserved C-terminal nuclear targeting domain contains a putative Cdk phosphorylation site (Thr(342)) that shares a great similitude in the adjacent sequences with p27(Kip1) but not with p21(Cip1). Phosphorylation on Thr(187) has been shown to promote degradation of p27(Kip1). Although there is sequence homology between the C-terminal part of p27(Kip1) and p57(Kip2), we show that the ubiquitination and degradation of p57(Kip2) are independent of Thr(342). In contrast a destabilizing element located in the N-terminal is implicated in p57(Kip2) destabilization.

References

Apr 16, 1996·Proceedings of the National Academy of Sciences of the United States of America·M H LeeJ Massagué
Feb 1, 1996·Current Opinion in Genetics & Development·J W Harper, S J Elledge
Jan 30, 1999·Genes & Development·P ZhangS J Elledge
Oct 19, 1999·Molecular and Cellular Biology·E G ReynaudS A Leibovitch
Nov 13, 1999·Nature Cell Biology·A C CarranoM Pagano
Nov 13, 1999·Nature Cell Biology·H SutterlütyW Krek
Apr 15, 2000·The Journal of Biological Chemistry·E G ReynaudS A Leibovitch
Jul 26, 2002·Nature·Yukiko YoshidaTadashi Tai

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Citations

Jan 13, 2006·Journal of Molecular Biology·Giovanna VaccarelloRossella Maione
Apr 19, 2006·Acta Oto-laryngologica·Guo-Kang FanShigeharu Fujieda
Aug 6, 2004·The Journal of Immunology : Official Journal of the American Association of Immunologists·Guiming LiErwin W Gelfand
Aug 6, 2011·Molecular Cancer Research : MCR·Adriana BorrielloFulvio Della Ragione

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