PNAS：CRISPR技术帮助创建慢性阻塞性肺病的小鼠模型

2018-03-19 药明康德学术经纬

慢性阻塞性肺病 (chronic obstructive pulmonary diseases， COPD) 影响着全世界10%的人口的生活。其中最主要的遗传原因是由于基因变异导致的α-1抗胰蛋白酶 (α-1 antitrypsin， ATT) 缺乏症，它会造成患者出现遗传性肺气肿 (emphysema) 。

慢性阻塞性肺病 (chronic obstructive pulmonary diseases， COPD) 影响着全世界10%的人口的生活。其中最主要的遗传原因是由于基因变异导致的α-1抗胰蛋白酶 (α-1 antitrypsin， ATT) 缺乏症，它会造成患者出现遗传性肺气肿 (emphysema) 。人类编码ATT蛋白的基因只有一个，而小鼠中最多存在6个基因编码ATT蛋白，这让构建模拟ATT缺乏症的小鼠模型变得非常困难。马萨诸塞大学(University of Massachusetts) 医学院的研究人员利用CRISPR/Cas9基因编辑技术，成功在C57BL/6J小鼠中敲除了所有编码ATT的基因。他们发现这种小鼠模型能够复制人类ATT缺乏症的症状，随着小鼠年龄的增长，它们会自发患上肺气肿。这一独特的小鼠模型不但会是研究ATT缺乏症的有力工具，而且可以帮助对肺气肿和吸烟对肺部影响的研究。

原始出处：

Florie Borel，et al.Editing out five Serpina1 paralogs to create a mouse model of genetic emphysema.PNAS.March 13， 2018. 115 (11) 2788-2793

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2018-07-07 tomyang96

#阻塞#

0 0
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2018-08-05 amy0559

#肺病#

34 0
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2018-03-29 wxl882001

了解一下

63 0
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2018-11-25 drwjr

#PNAS#

29 0
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2018-03-21 yuandd

#CRISPR#

37 0
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2018-03-21 zhouqu_8

#小鼠模型#

30 0
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2018-03-21 ms1779634646866130

#Crispr技术#

31 0

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PNAS：CRISPR技术帮助创建慢性阻塞性肺病的小鼠模型

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