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首页> 外文期刊>Cellular & molecular biology letters. >PUMA, a critical mediator of cell death--one decade on from its discovery.
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PUMA, a critical mediator of cell death--one decade on from its discovery.

机译：PUMA是细胞死亡的关键介质-自发现以来已有十年。

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摘要

PUMA (p53 upregulated modulator of apoptosis) is a pro-apoptotic member of the BH3-only subgroup of the Bcl-2 family. It is a key mediator of p53-dependent and p53-independent apoptosis and was identified 10 years ago. The PUMA gene is mapped to the long arm of chromosome 19, a region that is frequently deleted in a large number of human cancers. PUMA mediates apoptosis thanks to its ability to directly bind known anti-apoptotic members of the Bcl-2 family. It mainly localizes to the mitochondria. The binding of PUMA to the inhibitory members of the Bcl-2 family (Bcl-2-like proteins) via its BH3 domain seems to be a critical regulatory step in the induction of apoptosis. It results in the displacement of the proteins Bax and/or Bak. This is followed by their activation and the formation of pore-like structures on the mitochondrial membrane, which permeabilizes the outer mitochondrial membrane, leading to mitochondrial dysfunction and caspase activation. PUMA is involved in a large number of physiological and pathological processes, including the immune response, cancer, neurodegenerative diseases and bacterial and viral infections.
机译：PUMA（凋亡的p53上调调节剂）是Bcl-2家族仅BH3子组的促凋亡成员。它是p53依赖性和p53依赖性细胞凋亡的关键介体，并于10年前被发现。 PUMA基因定位在19号染色体的长臂上，该染色体在许多人类癌症中经常被删除。由于PUMA具有直接结合Bcl-2家族已知抗凋亡成员的能力，因此它可以介导凋亡。它主要定位于线粒体。 PUMA通过其BH3结构域与Bcl-2家族的抑制成员（Bcl-2-样蛋白）的结合似乎是诱导凋亡的关键调控步骤。它导致蛋白质Bax和/或Bak的置换。其后是它们的活化和在线粒体膜上的孔状结构的形成，其透化线粒体外膜，导致线粒体功能障碍和胱天蛋白酶活化。 PUMA参与了许多生理和病理过程，包括免疫应答，癌症，神经退行性疾病以及细菌和病毒感染。

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