pubmed-article:21098032 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:21098032 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
pubmed-article:21098032 | lifeskim:mentions | umls-concept:C1364684 | lld:lifeskim |
pubmed-article:21098032 | lifeskim:mentions | umls-concept:C1182610 | lld:lifeskim |
pubmed-article:21098032 | lifeskim:mentions | umls-concept:C1413549 | lld:lifeskim |
pubmed-article:21098032 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
pubmed-article:21098032 | pubmed:issue | 3 | lld:pubmed |
pubmed-article:21098032 | pubmed:dateCreated | 2011-1-17 | lld:pubmed |
pubmed-article:21098032 | 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. | lld:pubmed |
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pubmed-article:21098032 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21098032 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21098032 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:21098032 | pubmed:language | eng | lld:pubmed |
pubmed-article:21098032 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21098032 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:21098032 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:21098032 | pubmed:month | Jan | lld:pubmed |
pubmed-article:21098032 | pubmed:issn | 1083-351X | lld:pubmed |
pubmed-article:21098032 | pubmed:author | pubmed-author:JayMM | lld:pubmed |
pubmed-article:21098032 | pubmed:author | pubmed-author:RohJ RJR | lld:pubmed |
pubmed-article:21098032 | pubmed:author | pubmed-author:WangLingL | lld:pubmed |
pubmed-article:21098032 | pubmed:author | pubmed-author:PaytonReidR | lld:pubmed |
pubmed-article:21098032 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:21098032 | pubmed:day | 21 | lld:pubmed |
pubmed-article:21098032 | pubmed:volume | 286 | lld:pubmed |
pubmed-article:21098032 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:21098032 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:21098032 | pubmed:pagination | 1951-8 | lld:pubmed |
pubmed-article:21098032 | pubmed:dateRevised | 2011-8-1 | lld:pubmed |
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pubmed-article:21098032 | pubmed:meshHeading | pubmed-meshheading:21098032... | lld:pubmed |
pubmed-article:21098032 | pubmed:year | 2011 | lld:pubmed |
pubmed-article:21098032 | pubmed:articleTitle | Hyperosmotic stress-induced ATF-2 activation through Polo-like kinase 3 in human corneal epithelial cells. | lld:pubmed |
pubmed-article:21098032 | pubmed:affiliation | Department of Medicine, David Geffen School of Medicine, University of California Los Angeles, Torrance, California 90502, USA. | lld:pubmed |
pubmed-article:21098032 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:21098032 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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