Evidence map›Paper›PMID 21098032›Full record

ArticleThe Journal of biological chemistry2011

Hyperosmotic stress-induced ATF-2 activation through Polo-like kinase 3 in human corneal epithelial cells.

Ling Wang, Reid Payton, Wei Dai, Luo Lu

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
0.7field-weighted citation impact, top 32% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 38 citations in OpenAlex.

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  19. Polo-like kinases: structural variations lead to multiple functions.Nature reviews. Molecular cell biology · 2014
    Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Ling WangDepartment of Medicine, David Geffen School of Medicine, University of California Los Angeles, Torrance, California 90502, USA.
Reid Payton
Wei Dai
Luo Lu
University of California, Los Angeles · USNew York University · US

Funding

Role of CTCF in EGF_Induced Corneal Epithelial GrowthR01EY015281 · NEI · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · PI LU, LUO · 2004 to 2014
$3.0M
PROTEIN SER/THR KINASE PRK AND CELL CYCLE PROGRESSIONR01CA074229 · NCI · UNIVERSITY OF CINCINNATI · PI DAI, WEI · 1998 to 2007
$2.1M
Mechanisms of Environmental Stress Affecting Corneal Epithelial Wound HealingR01EY018343 · NEI · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · PI LU, LUO · 2007 to 2011
$1.7M
NCI NIH HHS CA074229NCI NIH HHS R01 CA074229NEI NIH HHS EY 018343NEI NIH HHS R01 EY015281NEI NIH HHS R01 EY018343
6 · The paper itself

Abstract

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.

Indexed as

Signal TransductionActivating Transcription Factor 2Active Transport, Cell NucleusCell Line, TransformedCell NucleusEpithelial CellsEpithelium, CornealHumansMAP Kinase Kinase 4Osmotic Pressurep38 Mitogen-Activated Protein KinasesPhosphorylationPolo-like KinasesProtein Serine-Threonine KinasesTranscription Factor AP-1Tumor Suppressor ProteinsActivating Transcription Factor 2ATF2 protein, humanMAP Kinase Kinase 4p38 Mitogen-Activated Protein KinasesPLK3 protein, humanPolo-like KinasesProtein Serine-Threonine KinasesTranscription Factor AP-1Tumor Suppressor Proteins

Identifiers

PMID21098032
PMCPMC3023491
OpenAlexW2172089993

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.