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首页> 外文期刊>Oncogene >Interaction with GATA transcription factors provides a mechanism for cell-specific effects of c-Fos
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Interaction with GATA transcription factors provides a mechanism for cell-specific effects of c-Fos

机译：与GATA转录因子的相互作用为c-Fos的细胞特异性作用提供了一种机制

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c-Fos is a multifunctional transcription factor that is involved in cellular proliferation, differentiation and apoptosis. c-Fos is rapidly induced by a variety of hormones, growth factors and other extracellular stimuli, resulting in cell-specific responses. One potential mechanism underlying the cell-specific effects of c-Fos may be its ability to regulate gene expression through interaction with tissue-restricted transcription factors. We report here that c-Fos interacts with the cell-specific GATA proteins to potentiate their ability to transactivate target promoters, via GATA-binding sites. c-Fos is recruited to GATA proteins through direct interaction with their N-terminal activation domain. Neither the leucine zipper nor the DNA-binding domain of c-Fos is required for physical interaction with GATA proteins. Instead, a C-terminal domain located between amino acids 235 and 296, which is conserved in FosB but not in the nontransforming Fos family members, FosB/SF or Fra-1, is essential for c-Fos-GATA interaction. These data suggest that c-Fos may act as an inducible cofactor for cell-specific transcription factors and unravel a novel mechanism for transcriptional regulation by c-Fos, independent of the well-studied AP-1 pathway. The results also raise the possibility that dysregulated interaction with cell-specific transcription factors may be an important component in cellular transformation by nuclear oncogenes.
机译：c-Fos是一种多功能转录因子，参与细胞增殖，分化和凋亡。多种激素，生长因子和其他细胞外刺激物迅速诱导c-Fos，导致细胞特异性反应。 c-Fos的细胞特异性作用的潜在机制之一可能是其通过与组织限制性转录因子的相互作用调节基因表达的能力。我们在这里报告c-Fos与细胞特异性GATA蛋白质相互作用，以增强其通过GATA结合位点激活靶标启动子的能力。 c-Fos通过与其N末端激活域直接相互作用而被募集到GATA蛋白中。与GATA蛋白质的物理相互作用不需要亮氨酸拉链或c-Fos的DNA结合结构域。取而代之的是，位于氨基酸235和296之间的C末端结构域对c-Fos-GATA相互作用至关重要，该氨基酸在FosB中是保守的，但在非转化Fos家族成员FosB / SF或Fra-1中却不保守。这些数据表明c-Fos可能充当细胞特异性转录因子的诱导型辅因子，并揭示了c-Fos进行转录调控的新机制，而与研究的AP-1途径无关。结果也增加了与细胞特异性转录因子相互作用失调的可能性，可能是核癌基因在细胞转化中的重要组成部分。

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