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. 2024 Aug 13;44(10):429–442. doi: 10.1080/10985549.2024.2382445

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Figure 6. — Proposed model depicting how β-TrCP depletion contributes to CIN. (A) β-TrCP being a substrate specifying factor for SCF E3 ubiquitin ligase recognizes Mis18β for ubiquitination and targets it for proteasomal degradation. The remaining physiological levels of Mis18β along with the other subunits of Mis18 complex helps in centromeric localization of CENP-A which ensures accurate chromosome segregation. (B) The steady state levels of Mis18β is increased in two ways, first with β-TrCP depletion and second with Mis18β overexpression. Such increased steady state levels of Mis18β contributes to noncentromeric localization of CENP-A and hence causes chromosomal instability.