βTrCP-dependent degradation of CDC25B phosphatase at the metaphase-anaphase transition is a pre-requisite for correct mitotic exit

p53 and p16INK4A independent induction of senescence by chromatin-dependent alteration of S-phase progression

“…Interestingly, Cdc25B is degraded by the ubiquitin-proteasome pathway and depends on the F-box protein β-TrCp. Thomas and colleagues established a stabilized mutant of Cdc25B, which can not interact with βTrCP, increasing the halflife of the protein 41 . It might be interesting to overexpress this stabilized mutant to see whether it could impair the G2/M cell cycle arrest induced by p300 inhibition.…”

Synaptotagmin1 is required for spindle stability and metaphase-to-anaphase transition in mouse oocytes

“…Its complete degradation is βTrCP-dependent and required for the metaphase-anaphase transition, and this biological process is pre-requisite for correct mitotic exit. 38 What's more, their interaction was confirmed in the heterologous system of Xenopus laevis eggs. 39 The relationship between Syt1 and CDC25B or the function mechanism with βTrCP could be the next step for Syt1 function in mouse oocyte meiosis.…”

Phosphorylation Mediated Regulation of Cdc25 Activity, Localization and Stability

“…[117] Cdc25B binds β-TrCP strongly and contains the residues DAG rather than the DSG degron motif. [202,204] In contrast, Cdc25B accumulates following G2 DNA damage checkpoint arrest induced by a variety of agents. [205] This is reminiscent of the "stockpiling" phenomena noted earlier in S. pombe.…”

“…[70] β-TrCP interaction with Cdc25B may also be required for mitotic exit. [204] A Cdc25B-DDA degron mutant which cannot bind β-TrCP accelerates mitotic entry slightly, but has a significant delay completing mitosis and progressing to G1. This mitotic delay is due to an extended metaphase in which Cdc25B-DDA shows a high proportion of lagging, misaligned and bridged chromosomes as well as mis-oriented spindles.…”

“…This mitotic delay is due to an extended metaphase in which Cdc25B-DDA shows a high proportion of lagging, misaligned and bridged chromosomes as well as mis-oriented spindles. [204] Figure 3. Multi-step phosphorylation cascades involved in targeting human Cdc25A for degradation by the β-TrCP SCF complex following DNA damage in S-phase and G2.…”