Th2 LCR 缺陷型小鼠中 GATA-3 表达缺陷。
Defective GATA-3 expression in Th2 LCR-deficient mice.
机构信息
Department of Life Science, Sogang University, Seoul 121-742, Republic of Korea.
出版信息
Biochem Biophys Res Commun. 2011 Jul 15;410(4):866-71. doi: 10.1016/j.bbrc.2011.06.080. Epub 2011 Jun 15.
Th2 cell differentiation is critically influenced by transcription factor GATA-3 and by various cis-acting elements including enhancers, silencers and a locus control region (LCR) in the Th2 cytokine locus. Th2 LCR-deficient Th2 cells completely lost the expression of GATA-3 and the phosphorylation of STAT6. Histone 3 lysine 4 (H3-K4) was hypomethylated in the gata3 locus in these cells. GATA-3 and STAT6 bound several regulatory regions in the gata3 locus and transactivated the expression of the gata3 gene. These results suggest that Th2 differentiation program stimulates feed-forward regulation of gata3 gene expression.
Th2 细胞分化受到转录因子 GATA-3 和各种顺式作用元件（包括增强子、沉默子和 Th2 细胞因子基因座中的 locus control region，LCR）的严格调控。Th2 LCR 缺陷型 Th2 细胞完全丧失了 GATA-3 的表达和 STAT6 的磷酸化。这些细胞中 gata3 基因座的组蛋白 3 赖氨酸 4（H3-K4）低甲基化。GATA-3 和 STAT6 结合 gata3 基因座的几个调节区域，并反式激活 gata3 基因的表达。这些结果表明，Th2 分化程序刺激 gata3 基因表达的正反馈调节。
Zotero 插件