T helper cell fate specified by kinase-mediated interaction of T-bet with GATA-3
T helper cell fate specified by kinase-mediated interaction of T-bet with GATA-3
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DOI：
10.1126/science.1103336
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发表时间：
2005-01-21
期刊：
影响因子：
56.9
通讯作者：
Glimcher, LH
中科院分区：
文献类型：
--
作者：
Hwang, ES;Szabo, SJ;Glimcher, LH
细胞谱系特化取决于基因激活和基因沉默，在辅助性T细胞祖细胞分化为Th1或Th2效应细胞的过程中，这需要两种相互拮抗的转录因子T - bet和GATA - 3的作用。T - bet对Th1细胞的发育至关重要，GATA - 3在Th2细胞发育中起同等作用。我们报道T - bet通过两种转录因子之间由酪氨酸激酶介导的相互作用抑制Th2谱系定向，这种相互作用干扰GATA - 3与其靶DNA的结合。这些结果为转录因子的酪氨酸磷酸化在确定一个共同祖细胞的不同命运方面提供了一种新的功能。
Cell Lineage specification depends on both gene activation and gene silencing, and in the differentiation of T helper progenitors to Th1 or Th2 effector cells, this requires the action of two opposing transcription factors, T-bet and GATA-3. T-bet is essential for the development of Th1 cells, and GATA-3 performs an equivalent role in Th2 development. We report that T-bet represses Th2 lineage commitment through tyrosine kinase-mediated interaction between the two transcription factors that interferes with the binding of GATA-3 to its target DNA. These results provide a novel function for tyrosine phosphorylation of a transcription factor in specifying alternate fates of a common progenitor cell.