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PMID: 11459826 Published · ppublish English Journal Article

MAD2B is an inhibitor of the anaphase-promoting complex.

Genes & development ·Vol. 15 ·No. 14 ·2001-07-15 ·Pages 1765-70

Chen J, Fang G

Abstract

Anaphase-promoting complex (APC), a ubiquitin ligase, controls both sister chromatid separation and mitotic exit. The APC is activated in mitosis and G1 by CDC20 and CDH1, and inhibited by the checkpoint protein MAD2, a specific inhibitor of CDC20. We show here that a MAD2 homolog MAD2B also inhibits APC. In contrast to MAD2, MAD2B inhibits both CDH1-APC and CDC20-APC. This inhibition is targeted to CDH1 and CDC20, but not directly to APC. Unlike MAD2, whose interaction with MAD1 is required for mitotic checkpoint control, MAD2B does not interact with MAD1, suggesting that MAD2B may relay a different cellular signal to APC.

MeSH Terms
Anaphase-Promoting Complex-Cyclosome Animals Cdc20 Proteins Cell Cycle Proteins/metabolism Chromatids/physiology Cloning, Molecular Cyclin B/metabolism Humans Ligases/antagonists & inhibitors Mad2 Proteins Mitosis/physiology Nuclear Proteins Phosphoproteins/metabolism Proteins/genetics,metabolism Repressor Proteins/metabolism Saccharomyces cerevisiae Proteins Subcellular Fractions/metabolism Ubiquitin-Protein Ligase Complexes Ubiquitin-Protein Ligases Xenopus
Chemicals
CDC20 protein, S cerevisiae Cdc20 Proteins Cell Cycle Proteins Cyclin B MAD1 protein, S cerevisiae MAD1L1 protein, human MAD2L2 protein, human Mad2 Proteins Nuclear Proteins Phosphoproteins Proteins Repressor Proteins Saccharomyces cerevisiae Proteins Ubiquitin-Protein Ligase Complexes Anaphase-Promoting Complex-Cyclosome Ubiquitin-Protein Ligases Ligases
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Chen J
Department of Biological Sciences, Stanford University, Stanford, California 94305-5020, USA.
Fang G
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Article Info
Journal
Genes & development
Abbr.
Genes Dev
ISSN
0890-9369
Published
2001-07-15
Pages
1765-70
Language
English
Region
United States
NLM ID
8711660
PMCID
PMC312737
Subset
IM
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