| First Author | Yoh K | Year | 2001 |
| Journal | Genes Cells | Volume | 6 |
| Issue | 12 | Pages | 1055-66 |
| PubMed ID | 11737266 | Mgi Jnum | J:128658 |
| Mgi Id | MGI:3767754 | Doi | 10.1046/j.1365-2443.2001.00489.x |
| Citation | Yoh K, et al. (2001) Transgenic over-expression of MafK suppresses T cell proliferation and function in vivo. Genes Cells 6(12):1055-66 |
| abstractText | BACKGROUND: The small Maf proteins regulate gene transcription from Maf recognition elements (MARE). These proteins do not contain a canonical transactivation domain. Depending upon the ratio of small Maf proteins to their partner proteins, which either possess a transactivation domain or not, transcription can be switched on or off. RESULTS: Transgenic mice were generated which over-express the small Maf family member MafK, specifically in the T cell lineage. It was our expectation that the high level of MafK would shift the balance to the formation of MafK homodimer and thereby repress MARE-dependent transcription. The transgenic mice had a shortened life span because of Pneumocystis carinii pneumonia and displayed a decrease in thymocytes and lower IL-2 and IL-4 mRNA expression levels. Analyses by electrophoretic gel mobility shift assay revealed that over-expressed MafK could interact with the proximal AP-1 sequence of IL-2 and the MARE in the IL-4 promoter region. CONCLUSION: These results indicate that when over-expressed, MafK binds to a MARE-like sequence and represses MARE-dependent transcription. Consequently, T cell proliferation and cytokine secretion are affected. The MafK homodimer serves as an important molecular probe for evaluating the role played by cis-acting MAREs in the proliferation and function of T cells. |
