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PTEN regulates spindle assembly checkpoint timing through MAD1 in interphase

The spindle assembly checkpoint (SAC) restrains anaphase progression to ensure all chromosomes attach properly to the spindle. Although SAC timing has been extensively investigated in mitosis, its mechanism of regulation in interphase is unclear. We report that PTEN functions as a crucial activator...

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Detalles Bibliográficos
Autores principales: Liu, Yu, Du, Xiao, Zhang, Shuting, Liu, Yang, Zhang, Qiaoling, Yin, Qi, McNutt, Michael A., Yin, Yuxin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals LLC 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5716712/
https://www.ncbi.nlm.nih.gov/pubmed/29228672
http://dx.doi.org/10.18632/oncotarget.20532
Descripción
Sumario:The spindle assembly checkpoint (SAC) restrains anaphase progression to ensure all chromosomes attach properly to the spindle. Although SAC timing has been extensively investigated in mitosis, its mechanism of regulation in interphase is unclear. We report that PTEN functions as a crucial activator of SAC timing and protects chromosome segregation under both spindle poison treated and untreated conditions. We show that PTEN physically interacts with MAD1 and promotes its dimerization and localization in the nuclear pore. Consequently, PTEN is important for the formation of the mitotic checkpoint complex (MCC) in interphase. We propose PTEN/MAD1 signaling is essential for maintenance of SAC timing and chromosome integrity.