Tumor suppressor BLU enhances pro-apoptotic activity of sMEK1 through physical interaction
Tumor suppressor BLU enhances pro-apoptotic activity of sMEK1 through physical interaction
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DOI：
10.1016/j.cellsig.2012.02.002
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发表时间：
2012-06-01
影响因子：
4.8
通讯作者：
Rho, Seung Bae
中科院分区：
文献类型：
--
作者：
Dong, Seung Myung;Byun, Hyun-Jung;Rho, Seung Bae
BLU 是一种肿瘤抑制因子，通过与细胞成分的结合充当转录调节因子。然而，BLU 在细胞功能中的工作机制尚不清楚。我们发现 BLU 直接与 sMEK1（蛋白磷酸酶 4 的调节亚基）相互作用。此外，我们确定了 BLU 和 sMEK1 之间相互作用所需的结合域。观察到 BLU 的 N 端与 sMEK1 的 C 端相互作用。 sMEK1 表达的 BLU 依赖性增加以及诱导的细胞凋亡活性证实了结合活性。此外，BLU 和 sMEK1 的表达在卵巢和宫颈患者中下调，并且高度甲基化。这些发现表明 BLU 可以通过诱导 sMEK1 介导促凋亡活性。 (c) 2012 Elsevier Inc. 保留所有权利。
BLU is a tumor suppressor that acts as a transcriptional regulator through the association with cellular components. However, the working mechanism of BLU in cellular functions was not understood. We found that BLU directly interacts with sMEK1, a regulatory subunit of protein phosphatase 4. Furthermore, we determined the binding domains that are required for interaction between BLU and sMEK1. The N-terminal of BLU was observed to interact with the C-terminal of sMEK1. Binding activity was confirmed by the BLU-dependent increase of sMEK1 expression, as well as by the induced apoptotic activity. Also, expression of BLU and sMEK1 was down-regulated in ovarian and cervical patients, and was hypermethylated. These findings indicate that BLU can mediate the pro-apoptotic activity through the induction of sMEK1. (c) 2012 Elsevier Inc. All rights reserved.