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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
3
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pubmed:dateCreated |
2011-1-17
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pubmed:abstractText |
Elevated extracellular solute concentration (hyperosmotic stress) perturbs cell function and stimulates cell responses by evoking MAPK cascades and activating AP-1 transcription complex resulting in alterations of gene expression, cell cycle arrest, and apoptosis. The results presented here demonstrate that hyperosmotic stress elicited increases in ATF-2 phosphorylation through a novel Polo-like kinase 3 (Plk3) pathway in human corneal epithelial (HCE) cells. We found in hyperosmotic stress-induced HCE cells that Plk3 transferred to the nuclear compartment and was colocalized with ATF-2 in nuclei. Kinase activity of Plk3 was significantly activated by hyperosmotic stimulation. Further downstream, active Plk3 phosphorylated ATF-2 at the Thr-71 site in vivo and in vitro. Overexpression of Plk3 and its mutants enhanced hyperosmotic stress-induced ATF-2 phosphorylation. In contrast, suppression of Plk3 by knocking down Plk3 mRNA effectively diminished the effect of hyperosmotic stress-induced ATF-2 phosphorylation. The effect of hyperosmotic stress-induced activation of Plk3 on ATF-2 transcription factor function was also examined in CRE reporter-overexpressed HCE cells. Our results for the first time reveal that hyperosmotic stress can activate the Plk3 signaling pathway that subsequently regulates the AP-1 complex by directly phosphorylating ATF-2 independent from the effects of JNK and p38 activation.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
1083-351X
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:day |
21
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pubmed:volume |
286
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1951-8
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pubmed:dateRevised |
2011-8-1
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pubmed:meshHeading |
pubmed-meshheading:21098032-Activating Transcription Factor 2,
pubmed-meshheading:21098032-Active Transport, Cell Nucleus,
pubmed-meshheading:21098032-Cell Line, Transformed,
pubmed-meshheading:21098032-Cell Nucleus,
pubmed-meshheading:21098032-Epithelial Cells,
pubmed-meshheading:21098032-Epithelium, Corneal,
pubmed-meshheading:21098032-Humans,
pubmed-meshheading:21098032-MAP Kinase Kinase 4,
pubmed-meshheading:21098032-Osmotic Pressure,
pubmed-meshheading:21098032-Phosphorylation,
pubmed-meshheading:21098032-Protein-Serine-Threonine Kinases,
pubmed-meshheading:21098032-Signal Transduction,
pubmed-meshheading:21098032-Transcription Factor AP-1,
pubmed-meshheading:21098032-p38 Mitogen-Activated Protein Kinases
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pubmed:year |
2011
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pubmed:articleTitle |
Hyperosmotic stress-induced ATF-2 activation through Polo-like kinase 3 in human corneal epithelial cells.
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pubmed:affiliation |
Department of Medicine, David Geffen School of Medicine, University of California Los Angeles, Torrance, California 90502, USA.
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pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Extramural
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