Volume 3 Issue 6
Jun.  2012
Turn off MathJax
Article Contents
Junbing Wu, Shengyi Peng, Rong Wu, Yumin Hao, Guangju Ji, Zengqiang Yuan. Generation of Calhm1 knockout mouse and characterization of calhm1 gene expression[J]. Protein&Cell, 2012, 3(6): 470-480. doi: 10.1007/s13238-012-2932-6
Citation: Junbing Wu, Shengyi Peng, Rong Wu, Yumin Hao, Guangju Ji, Zengqiang Yuan. Generation of Calhm1 knockout mouse and characterization of calhm1 gene expression[J]. Protein&Cell, 2012, 3(6): 470-480. doi: 10.1007/s13238-012-2932-6

Generation of Calhm1 knockout mouse and characterization of calhm1 gene expression

doi: 10.1007/s13238-012-2932-6
Funds:

This work was supported by the National Basic Research Program (973 Program) (Grant No. 2009CB918704) and the National Natural Science Foundation of China (Grant Nos. 81125010 and 81030025). Human tissue was provided by Chinese PLA General Hospital. Calhm1 knockout mouse was generated at Model Animal Research Center of Nanjing University. Thank Dr. Fuchou Tang from Peking University for the help of the absolute real-time RT-PCR.

  • Received Date: 2012-04-08
  • Rev Recd Date: 2012-04-24
  • Alzheimer's disease (AD) is the most common neurodegenerative disease among elderly people worldwide. Several genes have been validated to be associated with AD, and calcium homeostasis modulator 1 (Calhm1) is the latest suspected one. To investigate the biological and pathological function of Calhm1 systematically, we generated a Calhm1 conventional knockout mouse. However, both the male and female of elderly Calhm1 knockout (KO) mice showed similar ability to their wild type littermates in spatial learning and memory retrieving. Surprisingly, we found that Calhm1 mRNA could not be detected in mouse brains at different ages, although it is expressed in the human brain tissues. We further found that CpG islands (CGIs) of both mouse and human Calhm1 were hypermethylated, whereas CGI of mouse Calhm2 was hypomethylated. In addition, transcriptional active marker H3K4Di occupied on promoters of human Calhm1 and mouse Calhm2 at a considerable level in brain tissues, while the occupancy of H3K4Di on promoter of mouse Calhm1 was rare. In sum, we found that mouse Calhm1 was of rare abundance in brain tissues. So it might not be suitable to utilize the knockout murine model to explore biological function of Calhm1 in the pathogenesis of AD.
  • loading
  • 加载中

Catalog

    通讯作者: 陈斌, bchen63@163.com
    • 1. 

      沈阳化工大学材料科学与工程学院 沈阳 110142

    1. 本站搜索
    2. 百度学术搜索
    3. 万方数据库搜索
    4. CNKI搜索

    Article Metrics

    Article views (170) PDF downloads(245) Cited by()
    Proportional views
    Related

    /

    DownLoad:  Full-Size Img  PowerPoint
    Return
    Return