The RAS GTPase RIT1 compromises mitotic fidelity through spindle assembly checkpoint suppression.

ABSTRACT: The spindle assembly checkpoint (SAC) functions as a sensor of unattached kinetochores that delays mitotic progression into anaphase until proper chromosome segregation is guaranteed.^1,2 Disruptions to this safety mechanism lead to genomic instability and aneuploidy, which serve as the genetic cause of embryonic demise, congenital birth defects, intellectual disability, and cancer.^3,4 However, despite the understanding of the fundamental mechanisms that control the SAC, it remains unknown how signaling pathways directly interact with and regulate the mitotic checkpoint activity. In response to extracellular stimuli, a diverse network of signaling pathways involved in cell growth, survival, and differentiation are activated,

SUBMITTER: Cuevas-Navarro A 

PROVIDER: S-EPMC8440430 | biostudies-literature | 2021 Sep

REPOSITORIES: biostudies-literature