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Related Experiment Video

Updated: Feb 11, 2026

Mitochondrial Ca2+ Retention Capacity Assay and Ca2+-triggered Mitochondrial Swelling Assay

Mitochondrial Ca2+ Retention Capacity Assay and Ca2+-triggered Mitochondrial Swelling Assay

Published on: May 1, 2018

A novel function of BCL-2 overexpression in regulatory volume decrease. Enhancing swelling-activated Ca(2+) entry and

Meng-Ru Shen¹, Tzi-Peng Yang, Ming-Jer Tang

¹Department of Obstetrics and Gynecology, National Cheng Kung University Medical College, Tainan 701, Taiwan, Republic of China.

The Journal of Biological Chemistry

|February 28, 2002

Summary

This summary is machine-generated.

The oncogene BCL-2 enhances cell volume regulation by improving regulatory volume decrease (RVD) under hypotonic stress. BCL-2 overexpression up-regulates calcium signaling and chloride channels crucial for RVD.

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Examining BCL-2 Family Function with Large Unilamellar Vesicles

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Published on: October 5, 2012

Area of Science:

Cell Biology
Oncology
Physiology

Background:

The precise cellular role of the oncogene BCL-2, a known apoptosis regulator, remains under investigation.
Understanding BCL-2's function in cell volume homeostasis is crucial for its broader implications in cancer biology.

Purpose of the Study:

To investigate the link between BCL-2 overexpression and cellular volume regulation.
To elucidate the mechanisms by which BCL-2 influences ion transport and signaling pathways involved in cell volume control.

Main Methods:

Utilized Madin-Darby canine kidney (MDCK) cells with stable and inducible BCL-2 expression.
Assessed regulatory volume decrease (RVD) under hypotonic stress.
Measured outwardly rectified chloride currents and calcium transients using electrophysiological and imaging techniques.
Employed antibody neutralization in HT-3 cervical cancer cells.

Main Results:

BCL-2 overexpression significantly enhanced RVD capacity in MDCK cells.
Hypotonic stress-induced chloride currents were upregulated by BCL-2.
BCL-2 overexpression potentiated swelling-activated calcium transients and capacitative calcium entry.
Antibody-mediated BCL-2 neutralization impaired RVD and chloride channel activation in HT-3 cells.

Conclusions:

BCL-2 plays a novel role in regulating cell volume and ion flux.
Overexpression of BCL-2 enhances the cellular defense mechanism against hypotonic stress via modulation of chloride channels and calcium signaling.
These findings offer new perspectives on BCL-2's function beyond apoptosis regulation.