Evidence map›Paper›PMID 24180340›Full record

ReviewAntioxidants & redox signaling2014

Cell cycle regulators guide mitochondrial activity in radiation-induced adaptive response.

Aris T Alexandrou, Jian Jian Li

Open access · greenAbstract readReview
In one paragraph

Review in Antioxidants & redox signaling, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

20 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Article
  3. Low-Dose Non-Targeted Effects and Mitochondrial Control.International journal of molecular sciences · 2023
    Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Ionizing Radiation and Translation Control: A Link to Radiation Hormesis?International journal of molecular sciences · 2020
    Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Potential Modulation of Sirtuins by Oxidative Stress.Oxidative medicine and cellular longevity · 2016
    Review
  17. Article
  18. Article
  19. Article
  20. Review
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

2 authors at 1 institution in 1 country.

Aris T AlexandrouDepartment of Radiation Oncology, NCI-Designated Comprehensive Cancer Center, University of California at Davis , Sacramento, California.
Jian Jian Li
University of California, Davis · US

Funding

Target MKP-1 for Therapy-Resistant Breast Cancer Stem CellsR01CA152313 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI LI, JIAN JIAN · 2011 to 2015
$1.9M
NF-kB-mediated HER-2 overexpression in radioresistant breast cancer stem cells?R01CA133402 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI LI, JIAN JIAN · 2009 to 2013
$1.5M
NCI NIH HHS CA152313NCI NIH HHS R01 CA133402NCI NIH HHS R01 CA152313
6 · The paper itself

Abstract

significanceThere are accruing concerns on potential genotoxic agents present in the environment including low-dose ionizing radiation (LDIR) that naturally exists on earth's surface and atmosphere and is frequently used in medical diagnosis and nuclear industry. Although its long-term health risk is being evaluated and remains controversial, LDIR is shown to induce temporary but significant adaptive responses in mammalian cells and animals. The mechanisms guiding the mitochondrial function in LDIR-induced adaptive response represent a unique communication between DNA damage and cellular metabolism. Elucidation of the LDIR-regulated mitochondrial activity may reveal new mechanisms adjusting cellular function to cope with hazardous environmental stress. RECENT ADVANCES: Key cell cycle regulators, including Cyclin D1/CDK4 and Cyclin B1/cyclin-dependent kinase 1 (CDK1) complexes, are actively involved in the regulation of mitochondrial functions via phosphorylation of their mitochondrial targets. Accumulating new evidence supports a concept that the Cyclin B1/CDK1 complex acts as a mediator in the cross talk between radiation-induced DNA damage and mitochondrial functions to coordinate cellular responses to low-level genotoxic stresses. CRITICAL ISSUES: The LDIR-mediated mitochondrial activity via Cyclin B1/CDK1 regulation is an irreplaceable network that is able to harmonize vital cellular functions with adjusted mitochondrial metabolism to enhance cellular homeostasis. FUTURE DIRECTIONS: Further investigation of the coordinative mechanism that regulates mitochondrial activities in sublethal stress conditions, including LDIR, will reveal new insights of how cells cope with genotoxic injury and will be vital for future targeted therapeutic interventions that reduce environmental injury and cancer risk.

Indexed as

Radiation, IonizingAdaptation, BiologicalAnimalsApoptosisCell CycleCell Cycle ProteinsCyclin-Dependent KinasesCyclinsHumansMitochondriaMitochondrial DynamicsMolecular ChaperonesOxidation-ReductionOxidative PhosphorylationProtein TransportRadiation DosageCell Cycle ProteinsCyclin-Dependent KinasesCyclinsMolecular Chaperones

Identifiers

PMID24180340
PMCPMC3936506
OpenAlexW1885513881

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.