TOPK通过抑制HDAC1和HDAC2活性调节短暂性脑缺血后小胶质细胞极化

来源 :2016年中国生命电子学术年会 | 被引量 : 0次 | 上传用户：alex_tan01

【摘要】

：

研究背景和目的：T-LAK 源性的蛋白激酶(TOPK)是一种最新发现的蛋白激酶，是促丝裂原活化蛋白激酶家族的一员。我们前期的研究发现TOPK 对于脑缺血再灌注损伤具有保护作用。因此，本研究的目的是观察TOPK 是否参与小胶质细胞M1/M2 表型的极化，以及潜在的表观遗传学机制。研究方法：本实验采用的动物模型是C57 小鼠短暂性大脑中动脉栓塞术(tMCAO)。用蛋白免疫印迹及免疫荧光染色观察TOPK

【作者】

：

韩子萍赵海苹陶真王荣亮吉训明罗玉敏

【机构】

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首都医科大学宣武医院,北京100053

【出处】

：

2016年中国生命电子学术年会

【发表日期】

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2016年5期

【关键词】

：

TOPK HDAC1 HDAC2 胶质细胞极化

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TOPK通过抑制HDAC1和HDAC2活性调节短暂性脑缺血后小胶质细胞极化

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