Evidence map›Paper›PMID 24887096›Full record

ArticleFree radical biology & medicine2014

Polo-like kinase 2 activates an antioxidant pathway to promote the survival of cells with mitochondrial dysfunction.

Jie Li, Wenzhe Ma, Ping-yuan Wang, Paula J Hurley, Fred Bunz, Paul M Hwang

Open access · greenAbstract read
In one paragraph

Article in Free radical biology & medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 23% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

  1. Pooled it
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    Review
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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

6 authors at 3 institutions in 2 countries.

Jie LiCenter for Molecular Medicine, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Wenzhe MaCenter for Molecular Medicine, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA; State Key Laboratory for Quality Research in Chinese Medicine, Macau University of Science and Technology, Macau, China.
Ping-yuan WangCenter for Molecular Medicine, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Paula J HurleyDepartment of Urology, The Johns Hopkins School of Medicine, Baltimore, MD 21287, USA.
Fred BunzRadiation Oncology and Molecular Radiation Sciences, The Johns Hopkins School of Medicine, Baltimore, MD 21287, USA.
Paul M HwangCenter for Molecular Medicine, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA. Electronic address: hwangp@mail.nih.gov.
Johns Hopkins University · USNational Heart Lung and Blood Institute · USNational Institutes of Health · US

Funding

NHLBI Animal Program DivisionZIGHL006020 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI CLARK, TANNIA · 2009 to 2025
$47.3M
Mitochondrial regulation in cardiovascular and cancer biologyZIAHL005101 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI HWANG, PAUL M. · 2009 to 2025
$19.1M
Redox homeostasis in cancer and cardiovascular diseasesZIAHL006051 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI HWANG, PAUL M. · 2010 to 2025
$12.8M
Targeting the ATR pathway in p53-deficient cancersR01CA157535 · NCI · JOHNS HOPKINS UNIVERSITY · PI BUNZ, FRED · 2011 to 2015
$1.7M
Intramural NIH HHS ZIA HL005101NCI NIH HHS R01 CA157535
6 · The paper itself

Abstract

We previously reported that Polo-like kinase 2 (PLK2) is highly expressed in cells with defective mitochondrial respiration and is essential for their survival. Although PLK2 has been widely studied as a cell cycle regulator, we have uncovered an antioxidant function for this kinase that activates the GSK3-NRF2 signaling pathway. Here, we report that the expression of PLK2 is responsive to oxidative stress and that PLK2 mediates antioxidant signaling by phosphorylating GSK3, thereby promoting the nuclear translocation of NRF2. We further show that the antioxidant activity of PLK2 is essential for preventing p53-dependent necrotic cell death. Thus, the regulation of redox homeostasis by PLK2 promotes the survival of cells with dysfunctional mitochondria, which may have therapeutic implications for cancer and neurodegenerative diseases.

Indexed as

Active Transport, Cell NucleusAnimalsAntioxidantsCell Line, TumorCell SurvivalGlycogen Synthase Kinase 3HCT116 CellsHumansMiceMitochondriaNF-E2-Related Factor 2Oxidative StressPhosphorylationProtein Serine-Threonine KinasesRNA InterferenceRNA, Small InterferingAntioxidantsGlycogen Synthase Kinase 3NFE2L2 protein, humanNF-E2-Related Factor 2PLK2 protein, humanProtein Serine-Threonine KinasesRNA, Small InterferingAntioxidantFree radicalsGSK3Mitochondrial dysfunctionNecrosisNRF2Oxidative stressp53Polo-like kinase 2

Identifiers

PMID24887096
PMCPMC4115326
OpenAlexW1980128097

What OpenQuestion holds

Textmetadata
LicenceTDM
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.