Mode of interaction of TRIP13 AAA-ATPase with the Mad2-binding protein p31comet and with mitotic checkpoint complexes
Copyright policy )Mode of interaction of TRIP13 AAA-ATPase with the Mad2-binding protein p31comet and with mitotic checkpoint complexes
Significance The mitotic checkpoint system is important to ensure accurate segregation of chromosomes in mitosis. It acts by the formation of a mitotic checkpoint complex (MCC), which inhibits the ubiquitin ligase anaphase-promoting complex/cyclosome (APC/C). When the checkpoint is turned off, MCC is disassembled by the joint action of an ATP-utilizing enzyme, thyroid receptor interacting protein 13 (TRIP13), and a Mad2-binding protein, p31comet. It is not well understood how p31comet targets TRIP13 to disassemble MCC. We show here that p31comet and MCC mutually promote the binding of each other to oligomeric TRIP13 and propose a model for the mode of the action of TRIP13 in MCC disassembly. Thus, the results reveal an important molecular mechanism in the inactivation of the mitotic checkpoint.
- Technion – Israel Institute of Technology Israel
- New York University United States
Protein Conformation, Mitosis, Nuclear Proteins, Apoptosis, Cell Cycle Proteins, Spindle Apparatus, Anaphase-Promoting Complex-Cyclosome, Gene Expression Regulation, Enzymologic, Adenosine Triphosphate, Mad2 Proteins, ATPases Associated with Diverse Cellular Activities, Humans, Immunoprecipitation, Carrier Proteins, Adaptor Proteins, Signal Transducing, HeLa Cells, Protein Binding
Protein Conformation, Mitosis, Nuclear Proteins, Apoptosis, Cell Cycle Proteins, Spindle Apparatus, Anaphase-Promoting Complex-Cyclosome, Gene Expression Regulation, Enzymologic, Adenosine Triphosphate, Mad2 Proteins, ATPases Associated with Diverse Cellular Activities, Humans, Immunoprecipitation, Carrier Proteins, Adaptor Proteins, Signal Transducing, HeLa Cells, Protein Binding
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