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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Myc-interacting protein 1 target gene profile: A link to microtubules, extracellular signal-regulated kinase, and cell growth
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Myc-interacting protein 1 target gene profile: A link to microtubules, extracellular signal-regulated kinase, and cell growth

机译：Myc相互作用蛋白1目标基因概况：与微管，细胞外信号调节激酶和细胞生长的联系

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摘要

To study the role of the transcription factor Myc-interacting protein 1 (MIZ-1) in activating various target genes after induction with the microtubule disrupting agent T113242, we have used small interfering RNA duplexes (siRNAs) to knockdown the expression of MIZ-1. As expected, depletion of MIZ-1 resulted in the inhibition of T113242-dependent activation of the low-density lipoprotein receptor (LDLR) gene in hepatocytes. Cells transfected with MIZ-1 siRNAs also exhibited growth arrest. In addition, inhibition of the extracellular signal-regulated kinase (ERK) pathway inhibited T113242-induced nuclear accumulation of MIZ-1 and activation of LDLR. Gene expression microarray analysis under various induction conditions identified other T113242-activated genes affected by a decrease in MIZ-1 and inhibition of the ERK pathway. We also found that the accumulation of MIZ-1 in the nucleus is influenced by cell-cell contact and/or growth. Taken together, our studies suggest that MIZ-1 regulates a specific set of genes that includes LDLR and that the ERK pathway plays a role in the activation of target promoters by MIZ-1.
机译：为了研究转录因子Myc相互作用蛋白1（MIZ-1）在微管破坏剂T113242诱导后激活各种靶基因中的作用，我们使用了小分子干扰RNA双链体（siRNA）来抑制MIZ-1的表达。如所预期的，MIZ-1的耗尽导致抑制肝细胞中低密度脂蛋白受体（LDLR）基因的T113242依赖性激活。用MIZ-1 siRNA转染的细胞也表现出生长停滞。此外，细胞外信号调节激酶（ERK）途径的抑制抑制了T113242诱导的MIZ-1的核蓄积和LDLR的激活。在各种诱导条件下的基因表达微阵列分析确定了受MIZ-1减少和ERK途径抑制影响的其他T113242激活基因。我们还发现，MIZ-1在细胞核中的积累受到细胞与细胞接触和/或生长的影响。两者合计，我们的研究表明，MIZ-1调节包括LDLR在内的一组特定基因，而ERK途径在MIZ-1激活靶标启动子中起作用。

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