Evidence map›Paper›PMID 22589537›Full record

ArticleThe Journal of biological chemistry2012

Elevated cyclin G2 expression intersects with DNA damage checkpoint signaling and is required for a potent G2/M checkpoint arrest response to doxorubicin.

Maike Zimmermann, Aruni S Arachchige-Don, Michaela S Donaldson, Robert F Dallapiazza, Colleen E Cowan, Mary C Horne

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.1field-weighted citation impact, top 8% 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, 60 citations in OpenAlex.

  1. Review
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  9. Article
  10. Cyclin G2 Is Involved in the Proliferation of Placental Trophoblast Cells and Their Interactions with Endothelial Cells.Medical science monitor : international medical journal of experimental and clinical research · 2020
    Article
  11. Article
  12. Article
  13. Atypical cyclins: the extended family portrait.Cellular and molecular life sciences : CMLS · 2020
    Review
  14. Article
  15. Article
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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 2 institutions in 1 country.

Maike ZimmermannDepartment of Pharmacology, University of California, Davis, California 95616, USA.
Aruni S Arachchige-Don
Michaela S Donaldson
Robert F Dallapiazza
Colleen E Cowan
Mary C Horne
University of Iowa · USUniversity of California, Davis · US

Funding

Staff InvestigatorsP30CA093373 · NCI · UNIVERSITY OF CALIFORNIA DAVIS · PI Laura Marcu · 2002 to 2026
$84.9M
Pilot--Role of Reactive Oxygen Species in Aging-Associated CancerP20CA103672 · NCI · UNIVERSITY OF IOWA · PI WALLACE, ROBERT BRUCE · 2003 to 2007
$3.1M
NCI NIH HHS P20 CA103672NCI NIH HHS P20CA103672NCI NIH HHS P30 CA093373
6 · The paper itself

Abstract

To maintain genomic integrity DNA damage response (DDR), signaling pathways have evolved that restrict cellular replication and allow time for DNA repair. CCNG2 encodes an unconventional cyclin homolog, cyclin G2 (CycG2), linked to growth inhibition. Its expression is repressed by mitogens but up-regulated during cell cycle arrest responses to anti-proliferative signals. Here we investigate the potential link between elevated CycG2 expression and DDR signaling pathways. Expanding our previous finding that CycG2 overexpression induces a p53-dependent G(1)/S phase cell cycle arrest in HCT116 cells, we now demonstrate that this arrest response also requires the DDR checkpoint protein kinase Chk2. In accord with this finding we establish that ectopic CycG2 expression increases phosphorylation of Chk2 on threonine 68. We show that DNA double strand break-inducing chemotherapeutics stimulate CycG2 expression and correlate its up-regulation with checkpoint-induced cell cycle arrest and phospho-modification of proteins in the ataxia telangiectasia mutated (ATM) and ATM and Rad3-related (ATR) signaling pathways. Using pharmacological inhibitors and ATM-deficient cell lines, we delineate the DDR kinase pathway promoting CycG2 up-regulation in response to doxorubicin. Importantly, RNAi-mediated blunting of CycG2 attenuates doxorubicin-induced cell cycle checkpoint responses in multiple cell lines. Employing stable clones, we test the effect that CycG2 depletion has on DDR proteins and signals that enforce cell cycle checkpoint arrest. Our results suggest that CycG2 contributes to DNA damage-induced G(2)/M checkpoint by enforcing checkpoint inhibition of CycB1-Cdc2 complexes.

Indexed as

AnimalsAntibiotics, AntineoplasticAtaxia Telangiectasia Mutated ProteinsCDC2 Protein KinaseCell Cycle ProteinsCell DivisionCheckpoint Kinase 2Cyclin BCyclin B1Cyclin-Dependent KinasesCyclin G2DNA-Binding ProteinsDNA DamageDoxorubicinG2 PhaseGenes, cdcAntibiotics, AntineoplasticAtaxia Telangiectasia Mutated ProteinsATM protein, humanAtm protein, mouseCCNB1 protein, humanCCNG2 protein, humanCDC2 Protein KinaseCDK1 protein, humanCell Cycle ProteinsCheckpoint Kinase 2CHEK2 protein, humanChek2 protein, mouseCyclin BCyclin B1Cyclin-Dependent KinasesCyclin G2DNA-Binding ProteinsDoxorubicinOncogene Protein p21(ras)Protein Serine-Threonine KinasesRNA, Small InterferingTP53 protein, humanTumor Suppressor Protein p53Tumor Suppressor Proteins

Identifiers

PMID22589537
PMCPMC3391138
OpenAlexW2012595248

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.