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Related Experiment Video

Updated: Mar 19, 2026

Detection of Mitochondria Membrane Potential to Study CLIC4 Knockdown-induced HN4 Cell Apoptosis In Vitro

Detection of Mitochondria Membrane Potential to Study CLIC4 Knockdown-induced HN4 Cell Apoptosis In Vitro

Published on: July 17, 2018

Cl^- channels in apoptosis.

Podchanart Wanitchakool¹, Jiraporn Ousingsawat¹, Lalida Sirianant¹

¹Institut für Physiologie, Universität Regensburg, Universitätsstraße 31, 93053, Regensburg, Germany.

European Biophysics Journal : EBJ

|June 9, 2016

Summary

This summary is machine-generated.

Cell shrinkage during apoptosis involves ion channels releasing substances to drive water out. This study examines chloride channels LRRC8, TMEM16/anoctamin, and CFTR in apoptosis, revealing their roles in cell volume regulation and cell death.

Keywords:

Anoctamin Apoptosis CFTR Ca2+-activated chloride channels Cell death Chloride channel LRRC8A RVD TMEM16A TMEM16F TMEM16J TMEM16K Volume regulation

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Published on: July 17, 2018

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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
Ion Channel Physiology
Apoptosis Research

Background:

Apoptosis involves massive cell shrinkage driven by ion and osmolyte release through ion channels.
Chloride (Cl-) channels are critical for regulating cell volume during apoptosis.

Purpose of the Study:

To investigate the roles of LRRC8, TMEM16/anoctamin, and CFTR chloride channels in cellular apoptosis.
To elucidate the functional relationships between these chloride channels during apoptotic volume decrease.

Main Methods:

Analysis of literature and existing data on LRRC8, TMEM16/anoctamin, and CFTR.
Review of studies on regulatory and apoptotic volume decrease (RVD, AVD).
Examination of the impact of these channels on cellular sensitivity to drugs like cisplatin.

Main Results:

LRRC8 channels are essential for RVD and AVD in cell lines and influence drug sensitivity.
Anoctamins (ANO6, 9, 10) enhance apoptotic Cl- currents and AVD, potentially interacting with LRRC8.
CFTR activation by cell swelling may contribute to AVD via ROS accumulation and subsequent activation of channels like ANO6.

Conclusions:

LRRC8, TMEM16/anoctamin, and CFTR play significant roles in the ion flux and volume changes characteristic of apoptosis.
Further research is needed to clarify the precise mechanisms and interactions between these channels, particularly ANO6's role in CFTR-mediated apoptosis.