Evidence map›Paper›PMID 25101980›Full record

ArticlePloS one2014

Deoxycytidine kinase augments ATM-Mediated DNA repair and contributes to radiation resistance.

Yuri L Bunimovich, Evan Nair-Gill, Mireille Riedinger, Melissa N McCracken, Donghui Cheng, Jami McLaughlin, Caius G Radu, Owen N Witte

Open access · goldAbstract read
In one paragraph

Article in PloS one, 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 18% 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, 31 citations in OpenAlex.

  1. Review
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  16. Human Biodistribution and Radiation Dosimetry ofJournal of nuclear medicine : official publication, Society of Nuclear Medicine · 2017
    Article
  17. The Role of Deoxycytidine Kinase (dCK) in Radiation-Induced Cell Death.International journal of molecular sciences · 2016
    Article
  18. [18F]CFA as a clinically translatable probe for PET imaging of deoxycytidine kinase activity.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  19. Nucleotide salvage deficiencies, DNA damage and neurodegeneration.International journal of molecular sciences · 2015
    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

8 authors at 2 institutions in 1 country.

Yuri L BunimovichDepartment of Molecular and Medical Pharmacology, University of California Los Angeles, Los Angeles, California, United States of America; Crump Institute for Molecular Imaging, University of California Los Angeles, Los Angeles, California, United States of America.
Evan Nair-GillDepartment of Molecular and Medical Pharmacology, University of California Los Angeles, Los Angeles, California, United States of America.
Mireille RiedingerDepartment of Molecular and Medical Pharmacology, University of California Los Angeles, Los Angeles, California, United States of America.
Melissa N McCrackenDepartment of Molecular and Medical Pharmacology, University of California Los Angeles, Los Angeles, California, United States of America.
Donghui ChengHoward Hughes Medical Institute, University of California Los Angeles, Los Angeles, California, United States of America.
Jami McLaughlinDepartment of Microbiology, Immunology, and Molecular Genetics, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, United States of America.
Caius G RaduDepartment of Molecular and Medical Pharmacology, University of California Los Angeles, Los Angeles, California, United States of America; Crump Institute for Molecular Imaging, University of California Los Angeles, Los Angeles, California, United States of America; Ahmanson Translational Imaging Division, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, United States of America.
Owen N WitteDepartment of Molecular and Medical Pharmacology, University of California Los Angeles, Los Angeles, California, United States of America; Howard Hughes Medical Institute, University of California Los Angeles, Los Angeles, California, United States of America; Eli and Edythe Broad Center for Regenerative Medicine and Stem Cell Research, University of California Los Angeles, Los Angeles, California, United States of America; Department of Microbiology, Immunology, and Molecular Genetics, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, United States of America.
University of California, Los Angeles · USHoward Hughes Medical Institute · US

Funding

Women's CancersP30CA016042 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Samuel Wheeler French · 1985 to 2026
$134.5M
UCLA Center for Biological RadioprotectorsU19AI067769 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI MCBRIDE, WILLIAM H. · 2005 to 2019
$44.6M
UCLA Scholars in Oncologic Molecular lmaging (SOMI)R25CA098010 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI PHELPS, MICHAEL E · 2003 to 2013
$5.0M
NCI NIH HHS P30 CA016042NCI NIH HHS R25 CA098010NCI NIH HHS R25T CA098010NIAID NIH HHS NIH 5T32 AI06567NIAID NIH HHS U19 AI067769NIAID NIH HHS U19AI067769
6 · The paper itself

Abstract

Efficient and adequate generation of deoxyribonucleotides is critical to successful DNA repair. We show that ataxia telangiectasia mutated (ATM) integrates the DNA damage response with DNA metabolism by regulating the salvage of deoxyribonucleosides. Specifically, ATM phosphorylates and activates deoxycytidine kinase (dCK) at serine 74 in response to ionizing radiation (IR). Activation of dCK shifts its substrate specificity toward deoxycytidine, increases intracellular dCTP pools post IR, and enhances the rate of DNA repair. Mutation of a single serine 74 residue has profound effects on murine T and B lymphocyte development, suggesting that post-translational regulation of dCK may be important in maintaining genomic stability during hematopoiesis. Using [(18)F]-FAC, a dCK-specific positron emission tomography (PET) probe, we visualized and quantified dCK activation in tumor xenografts after IR, indicating that dCK activation could serve as a biomarker for ATM function and DNA damage response in vivo. In addition, dCK-deficient leukemia cell lines and murine embryonic fibroblasts exhibited increased sensitivity to IR, indicating that pharmacologic inhibition of dCK may be an effective radiosensitization strategy.

Indexed as

AnimalsAtaxia Telangiectasia Mutated ProteinsB-LymphocytesCell Line, TumorDeoxycytidineDeoxycytidine KinaseDeoxyribonucleosidesDNA DamageDNA RepairGenomic InstabilityHematopoiesisHumansMiceMice, Inbred BALB CMice, KnockoutMutagenesis, Site-DirectedAtaxia Telangiectasia Mutated ProteinsDeoxycytidineDeoxycytidine KinaseDeoxyribonucleosides

Identifiers

PMID25101980
PMCPMC4125169
OpenAlexW1990443176

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.