Tumor suppressor BLU enhances pro-apoptotic activity of sMEK1 through physical interaction

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• 作者：Seung Myung Dong^a ; ¹ ; Hyun-Jung Byun^a ; ¹ ; Boh-Ram Kim^a ; Seung-Hoon Lee^b ; Barry Trink^c ; Seung Bae Rho^a ; ^{sbrho@ncc.re.kr}
• 关键词：PP4 ; regulatory subunit of protein phosphatase 4 ; MTT ; 3-(4 ; 5-dimethylthiazol-2-yl)-2.5-diphenyl-2H-tetrazolium bromide ; ONPG ; o-nitrophenyl 尾-d-galactopyranoside ; sMEK1 ; suppressor of MEK null 1 ; siRNA ; small interfering RNA
• 刊名：Cellular Signalling
• 出版年：2012
• 期刊代码：42_08986568
• 类别：bio
• 出版时间：June, 2012
• 卷：24
• 期：6
• 页码：1208-1214
• 文件大小：1216 K

摘要

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.