Elf-1 binds to GGAA elements on the FcRγ promoter and represses its expression
Elf-1 binds to GGAA elements on the FcRγ promoter and represses its expression
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DOI：
10.4049/jimmunol.179.7.4884
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发表时间：
2007-10-01
影响因子：
4.4
通讯作者：
Tsokos, George C.
中科院分区：
文献类型：
--
作者：
Juang, Yuang-Taung;Sumibcay, Laarni;Tsokos, George C.
已有研究表明，当TCR Zeta链减少时，T细胞中铁受体(FCR)伽马链上调。我们证明Elf-1，而不是其他ETS家族转录因子，与位于FCRγ启动子转录起始点上游200bp内的GGAA位点结合。强制表达Elf-1会抑制FCR-γ的表达，而用小干扰RNA Elf-1沉默其表达则会增加FCR-γ的表达。ELF-1是第一个被证实参与FCR-γ转录调控的转录因子，不表达ELF-1的细胞，如人类系统性红斑狼疮T细胞，将表达FCR-Gamma链。
The Fe receptor (FcR) gamma-chain has been shown to be up-regulated in T cells when the TCR zeta-chain is decreased. We demonstrate that Elf-1, but not other Ets family transcription factors, bind to a cluster of GGAA sites located within the 200 bp upstream from the transcription initiation site of the FcR gamma promoter. Forced expression of Elf-1 results in the suppression of FcR gamma expression, whereas silencing its expression with small interfering RNA Elf-1 results in increased FcR gamma expression. Elf-1 represents the first transcription factor identified to be involved in the transcriptional regulation of FcR gamma, and cells that fail to express Elf-1, as is the case with human systemic lupus erythematosus T cells, will express FcR gamma-chain.