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首页> 美国卫生研究院文献>Molecular and Cellular Biology >Transcription enhancer factor 1 interacts with a basic helix-loop-helix zipper protein Max for positive regulation of cardiac alpha-myosin heavy-chain gene expression.
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Transcription enhancer factor 1 interacts with a basic helix-loop-helix zipper protein Max for positive regulation of cardiac alpha-myosin heavy-chain gene expression.

机译：转录增强因子1与基本的螺旋-环-螺旋拉链蛋白Max相互作用以积极调节心脏α-肌球蛋白重链基因的表达。

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The M-CAT binding factor transcription enhancer factor 1 (TEF-1) has been implicated in the regulation of several cardiac and skeletal muscle genes. Previously, we identified an E-box-M-CAT hybrid (EM) motif that is responsible for the basal and cyclic AMP-inducible expression of the rat cardiac alpha-myosin heavy chain (alpha-MHC) gene in cardiac myocytes. In this study, we report that two factors, TEF-1 and a basic helix-loop-helix leucine zipper protein, Max, bind to the alpha-MHC EM motif. We also found that Max was a part of the cardiac troponin T M-CAT-TEF-1 complex even when the DNA template did not contain an apparent E-box binding site. In the protein-protein interaction assay, a stable association of Max with TEF-1 was observed when glutathione S-transferase (GST)-TEF-1 or GST-Max was used to pull down in vitro-translated Max or TEF-1, respectively. In addition, Max was coimmunoprecipitated with TEF-1, thus documenting an in vivo TEF-1-Max interaction. In the transient transcription assay, overexpression of either Max or TEF-1 resulted a mild activation of the alpha-MHC-chloramphenicol acetyltransferase (CAT) reporter gene at lower concentrations and repression of this gene at higher concentrations. However, when Max and TEF-1 expression plasmids were transfected together, the repression mediated by a single expression plasmid was alleviated and a three- to fourfold transactivation of the alpha-MHC-CAT reporter gene was observed. This effect was abolished once the EM motif in the promoter-reporter construct was mutated, thus suggesting that the synergistic transactivation function of the TEF-1-Max heterotypic complex is mediated through binding of the complex to the EM motif. These results demonstrate a novel association between Max and TEF-1 and indicate a positive cooperation between these two factors in alpha-MHC gene regulation.
机译：M-CAT结合因子转录增强因子1（TEF-1）已牵涉到几个心肌和骨骼肌基因的调控。以前，我们确定了一个E-box-M-CAT杂种（EM）基序，该基元负责大鼠心肌α-肌球蛋白重链（alpha-MHC）基因在心肌细胞中的基础和环状AMP诱导表达。在这项研究中，我们报告两个因素，TEF-1和一个基本的螺旋-环-螺旋亮氨酸拉链蛋白Max，结合到alpha-MHC EM主题。我们还发现，即使DNA模板不包含明显的E-box结合位点，Max也是心肌肌钙蛋白T M-CAT-TEF-1复合物的一部分。在蛋白质相互作用试验中，当使用谷胱甘肽S-转移酶（GST）-TEF-1或GST-Max下拉体外翻译的Max或TEF-1时，观察到Max与TEF-1稳定关联，分别。另外，Max与TEF-1共免疫沉淀，因此证明了体内TEF-1-Max相互作用。在瞬时转录分析中，Max或TEF-1的过度表达在较低浓度下会导致α-MHC-氯霉素乙酰转移酶（CAT）报告基因的轻度激活，在较高浓度下会抑制该基因。然而，当Max和TEF-1表达质粒一起被转染时，由单个表达质粒介导的抑制被减轻，并且观察到α-MHC-CAT报告基因的三至四倍反式激活。一旦启动子-报道基因构建体中的EM基序发生突变，这种作用就被消除，因此表明TEF-1-Max异型复合物的协同反式激活功能是通过复合物与EM基序的结合而介导的。这些结果表明Max和TEF-1之间的新型关联，并表明这两个因素在αMHC基因调控中的积极合作。

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