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• W2896753632 abstract "Faithful chromosome segregation relies on the ability of the spindle assembly checkpoint (SAC) to delay anaphase onset until chromosomes are attached to the mitotic spindle via their kinetochores. MPS1 kinase is recruited to kinetochores to initiate SAC signaling and is removed from kinetochores once stable microtubule attachments have been formed to allow normal mitotic progression. Here, we show that a helical fragment within the kinetochore-targeting N-terminal extension (NTE) module of MPS1 is required for interactions with kinetochores and forms intramolecular interactions with its adjacent tetratricopeptide repeat (TPR) domain. Bypassing this NTE-TPR interaction results in high MPS1 levels at kinetochores due to loss of regulatory input into MPS1 localization, inefficient MPS1 delocalization upon microtubule attachment, and SAC silencing defects. These results show that SAC responsiveness to attachments relies on regulated intramolecular interactions in MPS1 and highlight the sensitivity of mitosis to perturbations in the dynamics of the MPS1-NDC80-C interactions." @default.
• W2896753632 created "2018-10-26" @default.
• W2896753632 creator A5011542881 @default.
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• W2896753632 creator A5045168589 @default.
• W2896753632 creator A5051958551 @default.
• W2896753632 creator A5056545178 @default.
• W2896753632 date "2019-02-01" @default.
• W2896753632 modified "2023-10-04" @default.
• W2896753632 title "Interactions between N-terminal Modules in MPS1 Enable Spindle Checkpoint Silencing" @default.
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• W2896753632 doi "https://doi.org/10.1016/j.celrep.2019.01.017" @default.
• W2896753632 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30784592" @default.
• W2896753632 hasPublicationYear "2019" @default.
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