组蛋白H3K9去甲基化酶KDM3B对ANGPT1的转录抑制作用。
Transcriptional repression of ANGPT1 by histone H3K9 demethylase KDM3B.
作者信息
Han Arim, Chae Yun-Cheol, Park Jin Woo, Kim Kee-Beom, Kim Ji-Young, Seo Sang-Beom
机构信息
Department of Life Science, College of Natural Sciences, Chung-Ang University, Seoul 156-756, Korea.
出版信息
BMB Rep. 2015 Jul;48(7):401-6. doi: 10.5483/bmbrep.2015.48.7.188.
Here we report that the H3K9 demethylase KDM3B represses transcription of the angiogenesis regulatory gene, ANGPT1. Negative regulation of ANGPT1 by KDM3B is independent of its Jumonji (JmjC) domain-mediated H3K9 demethylase activity. We demonstrate that KDM3B downregulates ANGPT1 via interaction with SMRT, and suggest that the repressor complex is formed at the promoter area of ANGPT1. Using MTT and wound healing assays, depletion of KDM3B was found to increase cell proliferation and cell motility, indicating that KDM3B has a role in angiogenesis.
在此我们报告，H3K9去甲基化酶KDM3B可抑制血管生成调节基因ANGPT1的转录。KDM3B对ANGPT1的负调控独立于其Jumonji（JmjC）结构域介导的H3K9去甲基化酶活性。我们证明KDM3B通过与SMRT相互作用下调ANGPT1，并表明在ANGPT1的启动子区域形成了抑制复合物。使用MTT和伤口愈合试验，发现KDM3B的缺失会增加细胞增殖和细胞迁移，表明KDM3B在血管生成中发挥作用。
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