@article{oai:tsukuba.repo.nii.ac.jp:00037757,
 author = {Ohmura, Sakie and 水野, 聖哉 and MIZUNO, Seiya and 大石, 久史 and OISHI, Hisashi and Ku, Chia-Jui and Hermann, Mary and Hosoya, Tomonori and 高橋, 智 and TAKAHASHI, Satoru and Engel, James Douglas},
 issue = {3},
 journal = {The journal of clinical investigation},
 month = {Mar},
 note = {The transcription factor GATA3 is essential for the genesis and maturation of the T cell lineage, and GATA3 dysregulation has pathological consequences. Previous studies have shown that GATA3 function in T cell development is regulated by multiple signaling pathways and that the Notch nuclear effector, RBP-J, binds specifically to the Gata3 promoter. We previously identified a T cell?specific Gata3 enhancer (Tce1) lying 280 kb downstream from the structural gene and demonstrated in transgenic mice that Tce1 promoted T lymphocyte?specific transcription of reporter genes throughout T cell development; however, it was not clear if Tce1 is required for Gata3 transcription in vivo. Here, we determined that the canonical Gata3 promoter is insufficient for Gata3 transcriptional activation in T cells in vivo, precluding the possibility that promoter binding by a host of previously implicated transcription factors alone is responsible for Gata3 expression in T cells. Instead, we demonstrated that multiple lineage-affiliated transcription factors bind to Tce1 and that this enhancer confers T lymphocyte?specific Gata3 activation in vivo, as targeted deletion of Tce1 in a mouse model abrogated critical functions of this T cell?regulatory element. Together, our data show that Tce1 is both necessary and sufficient for critical aspects of Gata3 T cell?specific transcriptional activity.},
 pages = {865--878},
 title = {Lineage-affiliated transcription factors bind the Gata3 Tce1 enhancer to mediate lineage-specific programs},
 volume = {126},
 year = {2016},
 yomi = {ミズノ, セイヤ and オオイシ, ヒサシ and タカハシ, サトル}
}