Journal
GENES & DEVELOPMENT
Volume 22, Issue 21, Pages 2926-2931Publisher
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/gad.1677208
Keywords
Mad1; Mad2; mitotic spindle checkpoint; Tpr
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Funding
- National Center for Research Resources [NIH NCRR RR015804, NIH NCRR RR001614, NIH NCRR RR012961]
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The mitotic arrest-deficient protein Mad1 forms a complex with Mad2, which is required for imposing mitotic arrest on cells in which the spindle assembly is perturbed. By mass spectrometry of affinity-purified Mad2-associated factors, we identified the translocated promoter region (Tpr), a component of the nuclear pore complex (NPC), as a novel Mad2-interacting protein. Tpr directly binds to Mad1 and Mad2. Depletion of Tpr in HeLa cells disrupts the NPC localization of Mad1 and Mad2 during interphase and decreases the levels of Mad1-bound Mad2. Furthermore, depletion of Tpr decreases the levels of Mad1 at kinetochores during prometaphase, correlating with the inability of Mad1 to activate Mad2, which is required for inhibiting APC(Cdc20). These findings reveal an important role for Tpr in which Mad1-Mad2 proteins are regulated during the cell cycle and mitotic spindle checkpoint signaling.
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