The spindle assembly checkpoint (SAC) is a surveillance mechanism that prevents mitotic
exit at the metaphase-to-anaphase transition until all chromosomes have established correct bipolar
attachment to spindle microtubules. Activation of SAC relies on the assembly of the mitotic
checkpoint complex (MCC), which requires conformational change from inactive open Mad2 (OMad2)
to the active closed Mad2 (C-Mad2) at unattached kinetochores. The Mad2-binding protein
p31comet plays a key role in controlling timely mitotic exit by promoting SAC silencing, through preventing
Mad2 activation and promoting MCC disassembly. Besides, increasing evidences highlight
the p31comet potential as target for cancer therapy. Here, we provide an updated overview of the functional
significance of p31comet in mitotic progression, and discuss the potential of deregulated expression
of p31comet in cancer and in therapeutic strategies.
Keywords: p31comet, mitosis, Mad2, spindle assembly checkpoint, mitotic checkpoint complex, cancer, therapeutic target.
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