Publication | Open Access
Mitochondrial proteomic approach reveals galectin-7 as a novel BCL-2 binding protein in human cells
66
Citations
30
References
2011
Year
MitophagyPure Mitochondrial FractionsApoptosisImmunologyCell DeathMolecular BiologyTumor BiologyOxidative StressHuman CellsAutophagyProteomicsCell SignalingProtein Quality ControlMitochondrial DynamicTranslational ProteomicsCell BiologyMitochondrial ProteinsMitochondrial FunctionNatural SciencesApoptosis InitiationCellular BiochemistrySystems BiologyMedicineCell Development
Although the anti-apoptotic activity of Bcl-2 has been extensively studied, its mode of action remains incompletely understood. Deciphering the network of Bcl-2 interacting factors is necessary to better understand the key function of Bcl-2 in apoptosis initiation. To identify novel Bcl-2 mitochondrial partners, we have combined a Bcl-2 immunocapture with a mass spectrometry analysis using highly pure mitochondrial fractions isolated from human cancer cells. We identified at high confidence 127 potential Bcl-2-interacting proteins. Gene ontology mining reveals enrichment for mitochondrial proteins, endoplasmic reticulum-associated proteins, and cytoskeleton-associated proteins. Importantly, we report the identification of galectin-7 (Gal7), a member of a family of β-galactoside-binding lectins that was already known to exhibit a pro-apoptotic function, as a new mitochondrial Bcl-2 interacting partner. Our data further show that endogenous Bcl-2 coimmunoprecipitates with Gal7 and that recombinant Gal7 directly interacts with recombinant Bcl-2. A fraction of Gal7 is constitutively localized at mitochondria in a Bcl-2-dependent manner and sensitizes the mitochondria to the apoptotic signal. In addition, we show that the Bcl-2/Gal7 interaction is abolished following genotoxic stress. Taken together, our findings suggest that the binding of Gal7 to Bcl-2 may constitute a new target for enhancing the intrinsic apoptosis pathway.
| Year | Citations | |
|---|---|---|
Page 1
Page 1