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首页> 外文期刊>Molecular and Cellular Biology >Overexpression of RelA in transgenic mouse thymocytes: specific increase in levels of the inhibitor protein I kappa B alpha.
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Overexpression of RelA in transgenic mouse thymocytes: specific increase in levels of the inhibitor protein I kappa B alpha.

机译：RelA在转基因小鼠胸腺细胞中的过表达：抑制蛋白IκBα的水平特异性增加。

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RelA (p65) is one of the strongest activators of the Rel/NF-kappa B family. As a first step to elucidate the mechanisms that regulate its activity in vivo, we have generated transgenic mice overexpressing RelA in the thymus. Although the levels of RelA were significantly increased in thymocytes of transgenic mice, the overall NF-kappa B-binding activity in unstimulated cells was not augmented compared with that in control thymocytes. This could be explained by the dramatic increase of endogenous I kappa B alpha levels observed in RelA-overexpressing cells in both cytoplasmic and nuclear compartments. The ikba mRNA levels were not augmented by overexpressed RelA, but I kappa B alpha inhibitor was found to be stabilized through association with RelA. Although a fraction of RelA was associated with cytoplasmic p105, no changes in the precursor levels were observed. Upon stimulation of RelA-overexpressing thymocytes with phorbol 12-myristate 13-acetate and lectin (phytohemaglutinin), different kappa B-binding complexes, including RelA homodimers, were partially released from I kappa B alpha. Association of RelA with I kappa B alpha prevented complete degradation of the inhibitor. No effect of phorbol 12-myristate 13-acetate-lectin treatment was detected on RelA associated with p105. Our data indicate that cytoplasmic retention of overexpressed RelA by I kappa B alpha is the major in vivo mechanism controlling the potential excess of NF-kappa B activity in long-term RelA-overexpressing thymocytes.
机译：RelA（p65）是Rel /NF-κB家族最强的激活剂之一。为阐明调节其在体内活性的机制的第一步，我们已经产生了在胸腺中过表达RelA的转基因小鼠。尽管在转基因小鼠的胸腺细胞中RelA水平显着增加，但是与对照胸腺细胞相比，未刺激细胞中的总NF-κB结合活性并未增加。这可以通过在细胞质和核区室中过表达RelA的细胞中观察到的内源性IκBα水平急剧增加来解释。过表达的RelA不能增加ikba mRNA的水平，但是我发现I kappa B alpha抑制剂通过与RelA结合而稳定。尽管一部分RelA与细胞质p105有关，但未观察到前体水平的变化。用佛波醇12-肉豆蔻酸酯13-乙酸酯和凝集素（植物血凝素）刺激过表达RelA的胸腺细胞后，不同的Kappa B结合复合物（包括RelA同型二聚体）会从I Kappa Bα中部分释放。 RelA与IκBα的缔合阻止了抑制剂的完全降解。在与p105有关的RelA上未检测到佛波12-肉豆蔻酸酯13-乙酸-凝集素处理的作用。我们的数据表明，Ikappa B alpha过度表达的RelA的细胞质保留是控制长期过度表达RelA的胸腺细胞中潜在的NF-κB活性过量的主要体内机制。

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