Stuck in division or passing through: what happens when cells cannot satisfy the spindle assembly checkpoint.

@article{Rieder2004StuckID,
  title={Stuck in division or passing through: what happens when cells cannot satisfy the spindle assembly checkpoint.},
  author={Conly L. Rieder and H{\'e}lder Maiato},
  journal={Developmental cell},
  year={2004},
  volume={7 5},
  pages={
          637-51
        }
}
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666 Citations

The spindle-assembly checkpoint in space and time

Recent molecular analyses have begun to shed light on the complex interaction of the checkpoint proteins with kinetochores — structures that mediate the binding of spindle microtubules to chromosomes in mitosis.

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Adapt or die: how eukaryotic cells respond to prolonged activation of the spindle assembly checkpoint.

Inhibition of factors involved in SAC adaptation could have important therapeutic applications by potentiating the ability of antimitotics to cause cell death.

Cell Size Determines the Strength of the Spindle Assembly Checkpoint during Embryonic Development.

Spindle Architectural Features Must Be Considered Along With Cell Size to Explain the Timing of Mitotic Checkpoint Silencing

The results suggest that spindle size does not always scale with cell size in mammalian cells and cell size is not sufficient to explain the differences in metaphase duration, and it is demonstrated that manipulating spindle geometry can alter mitotic and metaphaseduration.

Reconstituting the spindle assembly checkpoint and the signalling roles of Mad1

This study shows that Mad1 interacts with Bub1 in S. pombe to form a scaffold complex that is essential for SAC function, and provides evidence in support of the hypothesis that the C-terminus of Mad1 has additional roles in SAC signalling aside from Mad2 kinetochore recruitment.

Microtubules do not promote mitotic slippage when the spindle assembly checkpoint cannot be satisfied

Compared with cells lacking MTs, exit from mitosis is accelerated over a range of spindle poison concentrations that allow MT assembly because the SAC becomes satisfied on abnormal spindles and not because slippage is accelerated.

Sustaining the spindle assembly checkpoint to improve cancer therapy

It is found that the FCP1 phosphatase and its downstream target WEE1 kinase oppose the SAC, promoting mitosis exit despite malformed spindles, and it is shown that targeting this pathway might be useful for cancer therapy.

Mitosis and apoptosis: how is the balance set?

Prolonged Prometaphase Blocks Daughter Cell Proliferation Despite Normal Completion of Mitosis

...

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