[1]杨依然,刘钟,毛一凡,等.酪蛋白激酶-2相互作用蛋白1基于磷脂酰肌醇3-激酶/蛋白激酶B/哺乳动物雷帕霉素靶蛋白通路参与绝经后骨质疏松症发生发展过程中细胞自噬的机制[J].中医正骨,2018,30(04):59-62.
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酪蛋白激酶-2相互作用蛋白1基于磷脂酰肌醇3-激酶/蛋白激酶B/哺乳动物雷帕霉素靶蛋白通路参与绝经后骨质疏松症发生发展过程中细胞自噬的机制()
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《中医正骨》[ISSN:1001-6015/CN:41-1162/R]

卷:
第30卷
期数:
2018年04期
页码:
59-62
栏目:
综述
出版日期:
2018-04-20

文章信息/Info

作者:
杨依然1刘钟1毛一凡1程晓光2孙迎春3史晓林4
1.浙江中医药大学,浙江 杭州 310053; 2.北京积水潭医院,北京 100035; 3.中国康复研究中心,首都医科大学,北京 100068; 4.浙江中医药大学附属第二医院,浙江 杭州 310005
关键词:
骨质疏松绝经后 自噬 酪蛋白激酶Ⅱ 磷酸肌醇3-激酶 蛋白激酶类 哺乳动物雷帕霉素靶蛋白 综述
摘要:
自噬及自噬相关蛋白在骨代谢平衡中具有十分重要的作用,是当前骨质疏松研究的重要方向。磷脂酰肌醇3-激酶(phosphatidylinositol-3 kinase,PI3K)/蛋白激酶B(protein kinase B,Akt)/哺乳动物雷帕霉素靶(mammalian target of rapamycin,mTOR)信号通路是细胞自噬的经典信号通路,不仅对成骨细胞和破骨细胞的功能有间接调节作用,而且直接参与了成骨细胞矿化和破骨细胞褶皱缘形成。酪蛋白激酶-2相互作用蛋白(casein kinase 2 interacting protein,CKIP)1可通过增强Smad 泛素化调节因子的泛素连接酶活性抑制成骨,是重要的骨形成负调节因子,也可抑制PI3K/Akt/mTOR信号通路。但目前对CKIP-1与PI3K/Akt/mTOR信号通路参与细胞自噬的研究较少,且大多集中在肿瘤方面。对于CKIP-1基于PI3K/Akt/mTOR信号通路参与绝经后骨质疏松症发生发展过程中细胞自噬的机制,目前仍存在很多值得研究的问题。

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备注/Memo

备注/Memo:
基金项目:国家自然科学基金项目(81573754) 通讯作者:史晓林 E-mail:xlshi-2002@163.com
更新日期/Last Update: 2018-08-24