| Literature DB >> 19757169 |
Lei Cai1, Yan Li, Feng Liu, Wei Zhang, Binliang Huo, Wei Zheng, Rui Ding, Jiyuan Guo, Qingchuan Zhao, Kefeng Dou.
Abstract
The RNA editing adenosine deaminase gene (ADAR1) expression is wide-spread in lymphocytes. We explore the mechanism of ADAR1 regulation on the function of T primary lymphocytes when rejection occurs by knock-down the expression of ADAR1 in mouse T primary lymphocytes in mixed lymphocyte cultures. The changes of cell proliferation, the expression of ADAR1 and the cell cycle related genes cyclin D1 and A1, cell cycle and apoptosis analysis and mouse gene expression profiles was evaluated. We found that treatment with ADAR1-specific siRNA inhibited allogenic antigen stimulated T cell proliferation, arrested T cell cycle at G(0)/G(1) phases and promoted T cell apoptosis, which was associated with down-regulation of some related key genes transcription. These findings suggest that ADAR1 is essential for the maintenance of function of T lymphocytes during acute rejection. The mechanism underlying ADAR1's action might include editing of a currently unknown substrate and interacting with other proteins.Entities:
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Year: 2009 PMID： 19757169 DOI： 10.1007/s11033-009-9804-z
Source DB: PubMed Journal: Mol Biol Rep ISSN： 0301-4851 Impact factor: 2.316