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

Seung Myung Dong; Hyun Jung Byun; Boh Ram Kim; Seung Hoon Lee; Barry Trink; Seung Bae Rho

doi:10.1016/j.cellsig.2012.02.002

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

Seung Myung Dong, Hyun Jung Byun, Boh Ram Kim, Seung Hoon Lee, Barry Trink, Seung Bae Rho

Research output: Contribution to journal › Article › peer-review

7 Scopus citations

Abstract

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.

Original language	English (US)
Pages (from-to)	1208-1214
Number of pages	7
Journal	Cellular Signalling
Volume	24
Issue number	6
DOIs	https://doi.org/10.1016/j.cellsig.2012.02.002
State	Published - Jun 2012
Externally published	Yes

Keywords

BLU
Cell cycle
Cervical tumorigenesis
Pro-apoptosis
Protein-protein interaction
SMEK1

ASJC Scopus subject areas

Cell Biology

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10.1016/j.cellsig.2012.02.002

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title = "Tumor suppressor BLU enhances pro-apoptotic activity of sMEK1 through physical interaction",

abstract = "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.",

keywords = "BLU, Cell cycle, Cervical tumorigenesis, Pro-apoptosis, Protein-protein interaction, SMEK1",

author = "Dong, {Seung Myung} and Byun, {Hyun Jung} and Kim, {Boh Ram} and Lee, {Seung Hoon} and Barry Trink and Rho, {Seung Bae}",

note = "Funding Information: We thank Dr. S.A. Martinis (Department of Biochemistry, University of Illinois at Urbana-Champaign, IL, USA), and Richard Yoo (University of Washington, Seattle, WA, USA) for critical reading of the manuscript. This work was supported by a grant from the National Cancer Center, Korea ( NCC-0910262-3 ).",

year = "2012",

month = jun,

doi = "10.1016/j.cellsig.2012.02.002",

language = "English (US)",

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AU - Dong, Seung Myung

AU - Byun, Hyun Jung

AU - Kim, Boh Ram

AU - Lee, Seung Hoon

AU - Trink, Barry

AU - Rho, Seung Bae

N1 - Funding Information: We thank Dr. S.A. Martinis (Department of Biochemistry, University of Illinois at Urbana-Champaign, IL, USA), and Richard Yoo (University of Washington, Seattle, WA, USA) for critical reading of the manuscript. This work was supported by a grant from the National Cancer Center, Korea ( NCC-0910262-3 ).

PY - 2012/6

Y1 - 2012/6

N2 - 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.

AB - 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.

KW - BLU

KW - Cell cycle

KW - Cervical tumorigenesis

KW - Pro-apoptosis

KW - Protein-protein interaction

KW - SMEK1

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

Abstract

Keywords

ASJC Scopus subject areas

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