| First Author | Li M | Year | 2012 |
| Journal | PLoS One | Volume | 7 |
| Issue | 11 | Pages | e49841 |
| PubMed ID | 23185455 | Mgi Jnum | J:228409 |
| Mgi Id | MGI:5706909 | Doi | 10.1371/journal.pone.0049841 |
| Citation | Li M, et al. (2012) MCPIP1 down-regulates IL-2 expression through an ARE-independent pathway. PLoS One 7(11):e49841 |
| abstractText | IL-2 plays a key role in the survival and proliferation of immune cells, especially T lymphocytes. Its expression is precisely regulated at transcriptional and posttranscriptional level. IL-2 is known to be regulated by RNA binding proteins, such as tristetraprolin (TTP), via an AU-rich element (ARE) in the 3'-untranslated region (3'UTR) to influence the stability of mRNA. MCPIP1, identified as a novel RNase, can degrade IL-6, IL-12 and TNF-alpha mRNA by an ARE-independent pathway in the activation of macrophages. Here, we reported that MCPIP1 was induced in the activation of T lymphocytes and negatively regulated IL-2 gene expression in both mouse and human primary T lymphocytes through destabilizing its mRNA. A set of Luciferase reporter assay demonstrated that a non-ARE conserved element in IL-2 3'UTR, which formed a stem-loop structure, responded to MCPIP1 activity.RNA immunoprecipitation and Biotin pulldown experiments further suggested that MCPIP1 could modestly bind to IL-2 mRNA. Taken together, these data demonstrate that MCPIP1 down-regulates IL-2 via an ARE-independent pathway. |
