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中国海洋大学开辟长寿药物研究新途径

2018-01-02 廖洋 中国科学报

近日,中国海洋大学医药学院在《自然—通讯》发表了最新研究成果,发现了长寿基因SIRT1活性调控的新机制。

近日,中国海洋大学医药学院在《自然—通讯》发表了最新研究成果,发现了长寿基因SIRT1活性调控的新机制。

据介绍,SIRT1是一种高度保守的NAD+依赖性的脱乙酰化酶,参与了许多重要的生理和病理过程,如代谢调节、基因组稳定性、衰老等;在多种模式生物中,SIRT1均被证实能延长寿命。然而,SIRT1激活的分子机制并不十分清楚。

O-GlcNAc糖基化修饰是一种细胞内普遍存在、动态可逆的蛋白质翻译后修饰现象。O-GlcNAc可以通过影响蛋白稳定性、细胞定位和酶活性等调节蛋白质功能并在生理和病理过程中发挥重要作用。

该研究成果首次发现了SIRT1蛋白具有O-GlcNAc修饰,且修饰位点是549位的丝氨酸。SIRT1的O-GlcNAc修饰增加其与底物蛋白的亲和力并提高SIRT1的脱乙酰化酶活性。进一步研究表明,在应激(氧化应激、代谢应激和基因毒等)条件下,细胞内SIRT1的O-GlcNAc修饰显着增加,并促进其对p53、FOXO3等靶蛋白的脱乙酰化从而发挥细胞保护作用。

研究组还表明,卡路里限制可能通过O-GlcNAc修饰激活SIRT1而起到细胞保护作用,从而揭示了节食延年益寿的一个新的分子机制。

综上所述,该研究发现了SIRT1活性调控的新机制,首次证明了O-GlcNAc修饰是SIRT1抵抗应激的分子开关,表明O-GlcNAc修饰可能成为抗衰老和老年性疾病的新靶点,为抗老年性疾病药物和长寿药物的研究开辟了新途径,具有重要的理论意义和明确的应用前景。

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    2018-09-02 cenghis
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    2018-01-03 hhh678

    henhao

    0

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    2018-01-02 hhh678

    henhao

    0

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