Regulation of mitochondrial nutrient and energy metabolism by BCL-2 family proteins.
Cells have evolved a highly integrated network of mechanisms to coordinate cellular survival/death, proliferation, differentiation, and repair with metabolic states. It is therefore not surprising that proteins with canonical roles in cell death/survival also modulate nutrient and energy metabolism and vice versa. The finding that many BCL-2 (B cell lymphoma 2) proteins reside at mitochondria or can translocate to this organelle has long motivated investigation into their involvement in normal mitochondrial physiology and metabolism. These endeavors have led to the discovery of homeostatic roles for BCL-2 proteins beyond apoptosis. We predominantly focus on recent findings that link select BCL-2 proteins to carbon substrate utilization at the level of mitochondrial fuel choice, electron transport, and metabolite import independent of their cell death regulatory function.
Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02215, USA; Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA. Electronic address: alfredo.gimenez-cassina@ki.se.
Alfredo
A
Giménez-Cassina
Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02215, USA; Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA. Electronic address: nika_danial@dfci.harvard.edu.
Nika N
NN
Danial
D000818:Animals; D004032:Diet / Q000009:adverse effects; D002149:Energy Intake; D004734:Energy Metabolism; D006706:Homeostasis; D006801:Humans; D008928:Mitochondria / Q000201:enzymology / Q000378:metabolism*; D008954:Models, Biological; D010085:Oxidative Phosphorylation; D021381:Protein Transport; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism*
D019253:Proto-Oncogene Proteins c-bcl-2
BCL-2 proteins; OXPHOS; fatty acids; glucose; metabolism; mitochondria