Evidence map›Paper›PMID 17227291›Full record

ArticleCell proliferation2007

Constitutive histone H2AX phosphorylation and ATM activation are strongly amplified during mitogenic stimulation of lymphocytes.

T Tanaka, M Kajstura, H D Halicka, F Traganos, Z Darzynkiewicz

Abstract read
In one paragraph

Article in Cell proliferation, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

39 citing papers in PubMed, 62 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Manipulating DNA damage-response signaling for the treatment of immune-mediated diseases.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  7. Article
  8. Article
  9. In search of antiaging modalities: evaluation of mTOR- and ROS/DNA damage-signaling by cytometry.Cytometry. Part A : the journal of the International Society for Analytical Cytology · 2014
    Review
  10. Article
  11. Review
  12. DNA damage signaling, impairment of cell cycle progression, and apoptosis triggered by 5-ethynyl-2'-deoxyuridine incorporated into DNA.Cytometry. Part A : the journal of the International Society for Analytical Cytology · 2013
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Induction of DNA damage signaling by oxidative stress in relation to DNA replication as detected using "click chemistry".Cytometry. Part A : the journal of the International Society for Analytical Cytology · 2011
    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

5 authors at 2 institutions in 1 country.

T TanakaBrander Cancer Research Institute and Department of Pathology, New York Medical College, Valhalla, NY 10595, USA.
M Kajstura
H D Halicka
F Traganos
Z Darzynkiewicz
New York Medical College · USCancer Research Institute · US

Funding

PROBES FOR FLOW CYTOMETRYR01CA028704 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI DARZYNKIEWICZ, ZBIGNIEW · 1985 to 2014
$6.0M
NCI NIH HHS R01 CA028704NCI NIH HHS R01 CA 28704
6 · The paper itself

Abstract

objectivesWe recently postulated that constitutive activation of Ataxia Telangiectasia, Mutated (CAA) and constitutive histone H2AX phosphorylation (CHP) seen in cells not treated with genotoxic agents are the events triggered by DNA damage caused by endogenous reactive oxygen species (ROS), the product of mitochondrial oxidative metabolism. The aim of this study was to seek further evidence in support of this postulate, namely to test whether the levels of CAA and CHP correlate with cells metabolic activity. MATERIALS &

methodsPeripheral blood lymphocytes are non-cycling (G(0)) cells characterized by minimal rate of oxidative metabolism. A dramatic rise in transcriptional and translational activity, an increase in number of mitochondria, and induction of DNA replication, occur during their mitogenic stimulation. This classic model of cell activation was chosen to study a possible correlation between CAA and CHP versus metabolic activity and generation of ROS.

resultsThe levels of CAA and CHP in lymphocytes were increased many-fold during their stimulation. This increase was paralleled by the rise in extent of endogenously generated ROS. The growth of stimulated lymphocytes in the presence glucose antimetabolite 2-deoxy-D-glucose led to markedly lowered translational activity, decreased ROS generation and correspondingly attenuated CHA and CAA.

conclusionsThe present data are consistent with our postulate that CHP and CAA report DNA damage by endogenous oxidants whose level correlates with metabolic activity. Because cumulative DNA damage by ROS generated via oxidative metabolism is considered the key mechanism responsible for cell ageing and senescence the data imply that these processes are delayed in G(0) quiescent lymphocytes or stem cells as compared with proliferating cells.

Indexed as

Lymphocyte ActivationAgedAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsCells, CulturedDNADNA-Binding ProteinsHistonesHumansMaleMiddle AgedModels, BiologicalPhosphorylationProtein Serine-Threonine KinasesRNATumor Suppressor ProteinsAtaxia Telangiectasia Mutated ProteinsATM protein, humanCell Cycle ProteinsDNADNA-Binding ProteinsH2AX protein, humanHistonesProtein Serine-Threonine KinasesRNATumor Suppressor Proteins

Identifiers

PMID17227291
PMCPMC3860878
OpenAlexW2055988020

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.