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Related Experiment Video

Updated: Jun 19, 2026

Examining BCL-2 Family Function with Large Unilamellar Vesicles

Examining BCL-2 Family Function with Large Unilamellar Vesicles

Published on: October 5, 2012

Membrane promotes tBID interaction with BCL(XL).

Ana J García-Sáez¹, Jonas Ries, Mar Orzáez

¹Biophysics Group, BIOTEC, TU Dresden, Dresden, Germany. ana.garcia@biotec.tu-dresden.de

Nature Structural & Molecular Biology

|October 13, 2009

Summary

The BCL2 protein BCL(XL) inhibits apoptosis by binding to BID. Membrane presence enhances this interaction, suggesting a key role for lipid bilayers in regulating BCL2 protein activity during apoptosis.

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Examining BCL-2 Family Function with Large Unilamellar Vesicles

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Published on: October 5, 2012

Identifying Inhibitors of the HBx-DDB1 Interaction Using a Split Luciferase Assay System

Identifying Inhibitors of the HBx-DDB1 Interaction Using a Split Luciferase Assay System

Published on: December 21, 2019

Area of Science:

Biochemistry
Molecular Biology
Cell Biology

Background:

The BCL2 protein family regulates apoptosis.
Key questions involve interactions between pro- and antiapoptotic members and mitochondrial membrane translocation.

Purpose of the Study:

To quantify molecular interactions between BH3-interacting domain death agonist (BID) and BCL2 family protein BCL(XL) in solution and membranes.
To elucidate the role of the membrane in modulating these interactions.

Main Methods:

Fluorescence correlation spectroscopy (FCS) was employed.
Interactions between BID (full-length and truncated tBID) and BCL(XL) truncated at the C terminus (BCL(XL)DeltaCt) were quantified.

Main Results:

Only the active form, tBID, binds to BCL(XL)DeltaCt.
Membrane environments significantly promote the binding between tBID and BCL(XL)DeltaCt.
A BH3 peptide from BID partially disrupts the tBID-BCL(XL) complex in lipid bilayers, unlike in solution.

Conclusions:

tBID-BCL(XL) interactions differ in solution versus lipid membranes.
BCL(XL) likely inhibits tBID predominantly at the membrane surface.
Membranes play an underestimated, active role in modulating BCL2 protein interactions.