NDLI: p53 protein-mediated up-regulation of MAP kinase phosphatase 3 (MKP-3) contributes to the establishment of the cellular senescent phenotype through dephosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2).

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p53 protein-mediated up-regulation of MAP kinase phosphatase 3 (MKP-3) contributes to the establishment of the cellular senescent phenotype through dephosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2).

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p53 protein-mediated up-regulation of MAP kinase phosphatase 3 (MKP-3) contributes to the establishment of the cellular senescent phenotype through dephosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2).

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Zhang, Hui Chi, Yuan Yao, Jian Zhang, Xiling Gao, Kun
Description	Author Affiliation: Zhang H ( From the Department of Molecular Signaling, University of Yamanashi, Yamanashi 409-3898, Japan and the Trauma Research Center, First Hospital Affiliated to the Chinese PLA General Hospital, Beijing 100037, China.); Chi Y ( From the Department of Molecular Signaling, University of Yamanashi, Yamanashi 409-3898, Japan and.); Gao K ( From the Department of Molecular Signaling, University of Yamanashi, Yamanashi 409-3898, Japan and.); Zhang X ( From the Department of Molecular Signaling, University of Yamanashi, Yamanashi 409-3898, Japan and.); Yao J ( From the Department of Molecular Signaling, University of Yamanashi, Yamanashi 409-3898, Japan and yao@yamanashi.ac.jp.)
Abstract	Growth arrest is one of the essential features of cellular senescence. At present, the precise mechanisms responsible for the establishment of the senescence-associated arrested phenotype are still incompletely understood. Given that ERK1/2 is one of the major kinases controlling cell growth and proliferation, we examined the possible implication of ERK1/2. Exposure of normal rat epithelial cells to etoposide caused cellular senescence, as manifested by enlarged cell size, a flattened cell body, reduced cell proliferation, enhanced ß-galactosidase activity, and elevated p53 and p21. Senescent cells displayed a blunted response to growth factor-induced cell proliferation, which was preceded by impaired ERK1/2 activation. Further analysis revealed that senescent cells expressed a significantly higher level of mitogen-activated protein phosphatase 3 (MKP-3, a cytosolic ERK1/2-targeted phosphatase), which was suppressed by blocking the transcriptional activity of the tumor suppressor p53 with pifithrin- . Inhibition of MKP-3 activity with a specific inhibitor or siRNA enhanced basal ERK1/2 phosphorylation and promoted cell proliferation. Apart from its role in growth arrest, impairment of ERK1/2 also contributed to the resistance of senescent cells to oxidant-elicited cell injury. These results therefore indicate that p53-mediated up-regulation of MKP-3 contributes to the establishment of the senescent cellular phenotype through dephosphorylating ERK1/2. Impairment of ERK1/2 activation could be an important mechanism by which p53 controls cellular senescence.
ISSN	00219258
e-ISSN	1083351X
Journal	Journal of Biological Chemistry
Issue Number	2
Volume Number	290
Language	English
Publisher	American Society for Biochemistry and Molecular Biology (United States)
Publisher Date	2015-01-09
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Cell Aging Genetics Dual Specificity Phosphatase 6 Biosynthesis Mitogen-Activated Protein Kinase 3 Tumor Suppressor Protein P53 Animals Cell Cycle Cell Line Cell Proliferation Oxidative Stress Phosphorylation RNA, Small Interfering Transcriptional Activation Research Support, Non-U.S. Gov't Biochemistry Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology

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p53 Protein-mediated Up-regulation of MAP Kinase Phosphatase 3 (MKP-3) Contributes to the Establishment of the Cellular Senescent Phenotype through Dephosphorylation of Extracellular Signal-regulated Kinase 1/2 (ERK1/2)

p53 Protein-mediated Up-regulation of MAP Kinase Phosphatase 3 (MKP-3) Contributes to the Establishment of the Cellular Senescent Phenotype through Dephosphorylation of Extracellular Signal-regulated Kinase 1/2 (ERK1/2)*

The Mechanism of Dephosphorylation of Extracellular Signal-regulated Kinase 2 by Mitogen-activated Protein Kinase Phosphatase 3

Substrate Recognition Domains within Extracellular Signal-regulated Kinase Mediate Binding and Catalytic Activation of Mitogen-activated Protein Kinase Phosphatase-3

Mechanism of Mitogen-activated Protein Kinase Phosphatase-3 Activation by ERK2

Mechanistic Basis for Catalytic Activation of Mitogen-activated Protein Kinase Phosphatase 3 by Extracellular Signal-regulated Kinase

Prolonged Nuclear Retention of Activated Extracellular Signal-regulated Kinase 1/2 Is Required for Hepatocyte Growth Factor-induced Cell Motility

MAP Kinase-dependent Degradation of p27Kip1 by Calpains in Choroidal Melanoma Cells REQUIREMENT OF p27Kip1 NUCLEAR EXPORT

Cell Surface Expression of the Major Amyloid-β Peptide (Aβ)-degrading Enzyme, Neprilysin, Depends on Phosphorylation by Mitogen-activated Protein Kinase/Extracellular Signal-regulated Kinase Kinase (MEK) and Dephosphorylation by Protein Phosphatase 1a

p53 protein-mediated up-regulation of MAP kinase phosphatase 3 (MKP-3) contributes to the establishment of the cellular senescent phenotype through dephosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2).

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p53 protein-mediated up-regulation of MAP kinase phosphatase 3 (MKP-3) contributes to the establishment of the cellular senescent phenotype through dephosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2).