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首页> 外文期刊>Cell cycle >FOXP3 actively represses transcription by recruiting the HAT/HDAC complex.
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FOXP3 actively represses transcription by recruiting the HAT/HDAC complex.

机译：FOXP3通过募集HAT / HDAC复合物来积极抑制转录。

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摘要

The Forkhead box protein P3 (FOXP3) is a master cell lineage modulator in CD4(+)CD25(+) natural regulatory T cell (Treg) development. The Treg set of cells, also called T suppressor cells, play an essential role in natural Treg-mediated suppression of various types of immune cells. Suppression can be manifest by a cell-cell contact set of events, and recent evidence also supports soluble mediators. FOXP3 was previous identified as a passive transcriptional repressor which associates with nuclear factor of activated T-cells, cytoplasmic, and calcineurin-dependent 2 (NFATc2) as well as several other transcriptional factors including nuclear factor kappa-B (NFkappaB) and acute myeloid leukemia 1(AML1)/runt-related transcription factor 1(RUNX1). We found FOXP3 could actively repress transcription by recruiting distinct histone acetyltransferases and histone deacetylases to function as a co-repressor complex. The identification of enzymatic factors operative as essential participants in FOXP3-mediated transcriptional repression provides a practical basis for therapeutically modulating the activity of FOXP3 in immune suppression. Here we briefly summarize recent progress in our understanding of the biochemistry of FOXP3-mediated transcriptional regulation.
机译：叉头盒蛋白P3（FOXP3）是CD4（+）CD25（+）自然调节性T细胞（Treg）发育中的主细胞谱系调节剂。 Treg细胞集，也称为T抑制细胞，在天然Treg介导的各种类型免疫细胞的抑制中起重要作用。抑制作用可以通过一系列的细胞-细胞接触事件来体现，最近的证据也支持可溶性介体。 FOXP3先前被鉴定为被动转录阻遏物，与激活的T细胞，胞质和钙调神经磷酸酶依赖性2（NFATc2）的核因子以及其他几个转录因子有关，包括核因子kappa-B（NFkappaB）和急性髓性白血病1（AML1）/与矮子相关的转录因子1（RUNX1）。我们发现FOXP3可以通过募集不同的组蛋白乙酰转移酶和组蛋白脱乙酰酶来积极抑制转录，以充当共抑制复合物。识别作为FOXP3介导的转录抑制必不可少的参与者的酶因子，为在免疫抑制中治疗性调节FOXP3的活性提供了实用的依据。在这里，我们简要总结了我们对FOXP3介导的转录调控的生物化学的理解的最新进展。

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