| First Author | Endo T | Year | 2010 |
| Journal | Mol Endocrinol | Volume | 24 |
| Issue | 6 | Pages | 1267-73 |
| PubMed ID | 20375239 | Mgi Jnum | J:162258 |
| Mgi Id | MGI:4818523 | Doi | 10.1210/me.2010-0056 |
| Citation | Endo T, et al. (2010) Runx2 deficiency in mice causes decreased thyroglobulin expression and hypothyroidism. Mol Endocrinol 24(6):1267-73 |
| abstractText | We recently reported on the overexpression of Runx2 (Cbfa1/AML3), an osteoblast-specific transcription factor, in human papillary thyroid cancer tissues. We report here that normal thyrocytes also express Runx2 and that Runx2(+/-) mice are in a hypothyroid state. To clarify the mechanism, we studied the effects of small interfering RNA-mediated silencing of Runx2 on thyroid-specific gene expression in FRTL-5 cells. Lowering the levels of Runx2 had no effect on the amount of Na(+)/I(-) symporter mRNA but markedly decreased the amount of thyroglobulin (Tg) mRNA. A Runx2 binding consensus sequence is present on the Tg gene promoter, and gel-shift assay revealed that Runx2 binds to this region. Reporter assay showed that deletion of the region or introduction of a mutation into the binding site significantly impairs promoter function. These results indicate that Runx2 deficiency in mice causes decreased Tg expression and a novel type of hypothyroidism. |
