miR-29b 在神经元成熟过程中被激活，并靶向 BH3 仅基因以限制细胞凋亡。
miR-29b is activated during neuronal maturation and targets BH3-only genes to restrict apoptosis.
机构信息
Department of Cell and Developmental Biology, University of North Carolina, Chapel Hill, North Carolina 27599, USA.
出版信息
Genes Dev. 2011 Jan 15;25(2):125-30. doi: 10.1101/gad.1975411.
Abstract
The execution of apoptosis is critical for proper development of the nervous system. However, it is equally important that neurons strictly inhibit apoptosis after development to ensure their survival throughout the lifetime of the organism. Here we show that a microRNA, miR-29b, is markedly induced with neuronal maturation and functions as a novel inhibitor of neuronal apoptosis. The prosurvival function of miR-29b is mediated by targeting genes in the proapoptotic BH3-only family. Our results identify a unique strategy evolved by maturing neurons that uses a single microRNA to inhibit the multiple, redundant BH3-only proteins that are key initiators of apoptosis.
摘要
细胞凋亡的执行对于神经系统的正常发育至关重要。然而，神经元在发育后严格抑制细胞凋亡，以确保其在整个生命周期中的存活，这同样重要。在这里，我们表明一种 microRNA，miR-29b，在神经元成熟时明显被诱导，并作为神经元凋亡的新型抑制剂发挥作用。miR-29b 的生存促进功能是通过靶向凋亡 BH3 仅家族中的基因来介导的。我们的结果确定了成熟神经元进化出的一种独特策略，即使用单个 microRNA 抑制多个冗余的 BH3 仅蛋白，这些蛋白是凋亡的关键起始因子。
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