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首页> 外文期刊>Journal of Leukocyte Biology: An Official Publication of the Reticuloendothelial Society >Functional regulation of GATA-2 by acetylation.
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Functional regulation of GATA-2 by acetylation.

机译：通过乙酰化对GATA-2的功能调节。

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摘要

The transcription factor GATA-2 is expressed in hematopoietic stem and progenitor cells and is functionally implicated in their survival and proliferation. In the present study, we show that GATA-2 exists as an acetylated protein in immature precursor cells, KG1. GATA-2 was acetylated in vitro by p300 and GCN5. We have identified multiple acetylation sites by p300 on GATA-2, which include sites outside the zinc finger domain. We confirmed that GATA-2 acetylation occurred in transiently transfected 293T cells at sites similar to those induced by p300 in vitro. We have successfully shown that acetylation of GATA-2 in vitro increased its DNA-binding activity. In addition, GATA-2 displayed a transcriptional synergism with p300 that was impaired by mutation of each acetylation site. More importantly, each mutation in the acetylation sites of GATA-2 abolished its growth inhibitory effect on an interleukin-3-dependent progenitor, 32D. We conclude that acetylation provides multiple control points for the regulation of GATA-2 function.
机译：转录因子GATA-2在造血干细胞和祖细胞中表达，并在功能上牵涉其生存和增殖。在本研究中，我们表明GATA-2作为未成熟前体细胞KG1中的乙酰化蛋白存在。 GATA-2在体外被p300和GCN5乙酰化。我们已经在GATA-2上通过p300鉴定了多个乙酰化位点，其中包括锌指结构域之外的位点。我们证实，GATA-2乙酰化发生在瞬时转染的293T细胞中，其位置与体外p300诱导的位置相似。我们已经成功地证明了体外GATA-2的乙酰化增加了其DNA结合活性。另外，GATA-2显示出与p300的转录协同作用，但由于每个乙酰化位点的突变而受损。更重要的是，GATA-2乙酰化位点的每个突变都消除了其对白介素3依赖性祖细胞32D的生长抑制作用。我们得出结论，乙酰化为调节GATA-2功能提供了多个控制点。

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