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Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis
Published on: February 16, 2015
Survivin withdrawal by nuclear export failure as a physiological switch to commit cells to apoptosis
K-S Chan1, C-H Wong, Y-F Huang
1Division of Molecular and Cell Biology, School of Biological Sciences, College of Science, Nanyang Technological University, Singapore, Singapore.
Cell Death & Disease
|March 3, 2011
Summary
The prosurvival protein Survivin acts as a physiological switch, moving to the nucleus during apoptosis. This nuclear shift, driven by cellular stress, commits cells to programmed cell death by blocking Survivin's protective functions.
Area of Science:
- Cell Biology
- Molecular Biology
- Biochemistry
Background:
- Apoptosis is a critical cellular process, yet the precise mechanisms governing cell fate decisions remain unclear.
- The protein Survivin is known for its prosurvival role, but its function during apoptosis is not fully elucidated.
Purpose of the Study:
- To investigate the role and regulation of Survivin during apoptotic stress.
- To identify the molecular events that lead to Survivin's altered localization and function in dying cells.
Main Methods:
- Analysis of Survivin protein localization and dynamics under apoptotic conditions.
- Investigation of the RanGTP-CRM1 export complex assembly and function.
- Assessment of Survivin ubiquitination and degradation pathways.
Main Results:
- Survivin redistributes from the cytoplasm to the nucleus upon apoptotic stress, acting as a commitment switch.
- Nuclear relocalization is caused by the collapse of the RanGTP gradient, impairing the Survivin export complex.
- Survivin ubiquitination in the nucleus prevents its return to the cytoplasm and targets it for degradation, abolishing its prosurvival function.
Conclusions:
- Survivin withdrawal is an active physiological mechanism that promotes apoptosis progression.
- The spatial and functional regulation of Survivin is a novel regulatory pathway controlling cell death.
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