1] The Walter and Eliza Hall Institute of Medical Research and Department of Medical Biology, University of Melbourne, 1G Royal Parade, Parkville, Victoria 3052, Australia. [2].
The Walter and Eliza Hall Institute of Medical Research and Department of Medical Biology, University of Melbourne, 1G Royal Parade, Parkville, Victoria 3052, Australia.
Nat Rev Mol Cell Biol. 2014 Jan;15(1):49-63. doi: 10.1038/nrm3722.
The BCL-2 protein family determines the commitment of cells to apoptosis, an ancient cell suicide programme that is essential for development, tissue homeostasis and immunity. Too little apoptosis can promote cancer and autoimmune diseases; too much apoptosis can augment ischaemic conditions and drive neurodegeneration. We discuss the biochemical, structural and genetic studies that have clarified how the interplay between members of the BCL-2 family on mitochondria sets the apoptotic threshold. These mechanistic insights into the functions of the BCL-2 family are illuminating the physiological control of apoptosis, the pathological consequences of its dysregulation and the promising search for novel cancer therapies that target the BCL-2 family.
BCL-2 蛋白家族决定了细胞对凋亡的定向，凋亡是一种古老的细胞自杀程序，对于发育、组织平衡和免疫至关重要。凋亡过少会促进癌症和自身免疫性疾病；凋亡过多会加重缺血状况并导致神经退行性病变。我们讨论了阐明 BCL-2 家族成员如何在线粒体上相互作用来设定凋亡阈值的生化、结构和遗传研究。这些对 BCL-2 家族功能的机制见解正在阐明凋亡的生理控制、其失调的病理后果以及针对 BCL-2 家族的新型癌症治疗方法的有希望的探索。
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