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J Cell Biol. 2004 Aug 16;166(4):507-16. Epub 2004 Aug 9.

Chfr acts with the p38 stress kinases to block entry to mitosis in mammalian cells.

Author information

1
Wellcome/Cancer Research UK Gurdon Institute, and Department of Zoology, Tennis Court Rd., University of Cambridge, Cambridge CB2 1QR, England, UK.

Abstract

Entry into mitosis in vertebrate cells is guarded by a checkpoint that can be activated by a variety of insults, including chromosomal damage and disrupting microtubules. This checkpoint acts at the end of interphase to delay cells from entering mitosis, causing cells in prophase to decondense their chromosomes and return to G2 phase. Here, we show that in response to microtubule poisons this "antephase" checkpoint is primarily mediated by the p38 stress kinases and requires the Chfr protein that is absent or inactive in several transformed cell lines and lung tumors. Furthermore, in contrast to previous reports, we find that the checkpoint requires ubiquitylation but not proteasome activity, which is in agreement with the recent demonstration that Chfr conjugates ubiquitin through lysine 63 and not lysine 48.

PMID:
15302856
PMCID:
PMC2172205
DOI:
10.1083/jcb.200401139
[Indexed for MEDLINE]
Free PMC Article
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