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Updated: May 12, 2026

Examining BCL-2 Family Function with Large Unilamellar Vesicles
Published on: October 5, 2012
Functions of BCL-X L at the Interface between Cell Death and Metabolism
Judith Michels1, Oliver Kepp, Laura Senovilla
1INSERM, U848, Institut Gustave Roussy, Pavillon de Recherche 1, 39 Rue Camille Desmoulins, 94805 Villejuif, France ; Université Paris Sud/Paris XI, 94805 Villejuif, France ; Institut Gustave Roussy, 94805 Villejuif, France.
Abstract:
The BCL-2 homolog BCL-XL, one of the two protein products of BCL2L1, has originally been characterized for its prominent prosurvival functions. Similar to BCL-2, BCL-XL binds to its multidomain proapoptotic counterparts BAX and BAK, hence preventing the formation of lethal pores in the mitochondrial outer membrane, as well as to multiple BH3-only proteins, thus interrupting apical proapoptotic signals. In addition, BCL-XL has been suggested to exert cytoprotective functions by sequestering a cytosolic pool of the pro-apoptotic transcription factor p53 and by binding to the voltage-dependent anion channel 1 (VDAC1), thereby inhibiting the so-called mitochondrial permeability transition (MPT). Thus, BCL-XL appears to play a prominent role in the regulation of multiple distinct types of cell death, including apoptosis and regulated necrosis. More recently, great attention has been given to the cell death-unrelated functions of BCL-2-like proteins. In particular, BCL-XL has been shown to modulate a number of pathophysiological processes, including-but not limited to-mitochondrial ATP synthesis, protein acetylation, autophagy and mitosis. In this short review article, we will discuss the functions of BCL-XL at the interface between cell death and metabolism.
Insights
BCL-XL protein regulates cell death and has additional roles in cell metabolism, including ATP synthesis and autophagy. This review explores BCL-XL
Area of Science:
- Molecular Biology
- Cell Biology
- Biochemistry
Background:
- BCL-XL, a BCL-2 homolog, is known for its prosurvival functions.
- It inhibits apoptosis by binding to BAX, BAK, and BH3-only proteins.
- BCL-XL also has proposed roles in inhibiting p53 and VDAC1, affecting mitochondrial permeability transition (MPT).
Purpose of the Study:
- To review the multifaceted functions of BCL-XL.
- To discuss BCL-XL's role at the intersection of cell death and metabolism.
- To highlight recently discovered cell death-unrelated functions of BCL-XL.
Main Methods:
- Literature review of existing research on BCL-XL.
- Analysis of studies investigating BCL-XL's interactions and functions.
- Synthesis of findings related to cell death and metabolic processes.
Main Results:
- BCL-XL regulates apoptosis and regulated necrosis.
- Emerging evidence shows BCL-XL influences mitochondrial ATP synthesis, protein acetylation, autophagy, and mitosis.
- BCL-XL's functions extend beyond cell death regulation into cellular metabolism.
Conclusions:
- BCL-XL is a key regulator of cell death pathways.
- BCL-XL plays significant roles in cellular metabolism, independent of its death-regulating functions.
- Further research into BCL-XL's metabolic roles is warranted.
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