Regulation of mitochondrial nutrient and energy metabolism by BCL-2 family proteins

被引:111
作者
Gimenez-Cassina, Alfredo [1 ,2 ]
Danial, Nike N. [1 ,2 ]
机构
[1] Dana Farber Canc Inst, Dept Canc Biol, Boston, MA 02215 USA
[2] Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA 02115 USA
基金
美国国家卫生研究院;
关键词
BCL-2; proteins; mitochondria; OXPHOS; glucose; fatty acids; metabolism; CARNITINE PALMITOYLTRANSFERASE I; FATTY-ACID OXIDATION; CELL-DEATH; OUTER-MEMBRANE; KETOGENIC DIET; BAX OLIGOMERIZATION; INSULIN-SECRETION; RESPIRATORY-CHAIN; VDAC STRUCTURE; BETA-CELLS;
D O I
10.1016/j.tem.2015.02.004
中图分类号
R5 [内科学];
学科分类号
100201 [内科学];
摘要
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.
引用
收藏
页码:165 / 175
页数:11
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