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Related Experiment Video

Updated: Jun 13, 2026

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis

Published on: February 16, 2015

Caspase-9-dependent decrease of nuclear pore channel hydrophobicity is accompanied by nuclear envelope leakiness.

Armin Kramer¹, Ivan Liashkovich, Hans Oberleithner

¹Institute of Physiology II, University of Münster, Münster, Germany.

Nanomedicine : Nanotechnology, Biology, and Medicine

|May 18, 2010

Summary

This summary is machine-generated.

Caspase-9 activation during apoptosis disrupts the nuclear pore complex (NPC) hydrophobicity, causing nuclear envelope (NE) leakiness. This finding advances nanomedicine and gene therapy by explaining NE permeability during early apoptosis.

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Last Updated: Jun 13, 2026

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis

Published on: February 16, 2015

Area of Science:

Cell biology
Nanomedicine
Biophysics

Background:

Apoptosis involves increased nuclear envelope (NE) permeability, hindering nanoparticle delivery for gene therapy.
Understanding NE barrier breakdown during apoptosis is crucial for nanomedicine advancements.

Purpose of the Study:

To elucidate the mechanism of NE leakiness during apoptosis.
To investigate the role of caspases in nuclear pore complex (NPC) dysfunction.

Main Methods:

Induction of apoptosis in isolated cell nuclei.
Fluorescence techniques to monitor NE permeability.
Atomic force microscopy (AFM) with hydrophobic nanosensors to probe NPC hydrophobicity.

Main Results:

Caspase-9 activation was identified as a trigger for NE leakiness to macromolecules.
Importin-β mutant pretreatment prevented NE leakiness by obstructing NPCs.
AFM detected a significant decrease in hydrophobic binding sites within the apoptotic NPC channel.

Conclusions:

Caspase-9 perturbs the hydrophobicity-based barrier within the NPC channel, leading to NE leakiness.
This mechanism explains the increased passive NE permeability observed in early apoptosis.
Findings provide insights for developing targeted gene therapy delivery systems.