Evidence map›Paper›PMID 19118012›Full record

ArticleCancer research2009

Cyclin-dependent kinase-3-mediated c-Jun phosphorylation at Ser63 and Ser73 enhances cell transformation.

Yong-Yeon Cho, Faqing Tang, Ke Yao, Chengrong Lu, Feng Zhu, Duo Zheng, Angelo Pugliese, Ann M Bode, Zigang Dong

Open access · greenAbstract read
In one paragraph

Article in Cancer research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

35 citing papers in PubMed, 63 citations in OpenAlex.

  1. Review
  2. CMGC Kinases in Viral Infection and Human Disease.Pathogens (Basel, Switzerland) · 2026
    Review
  3. Review
  4. Review
  5. Article
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  8. Article
  9. Article
  10. Cyclin-dependent kinases: Masters of the eukaryotic universe.Wiley interdisciplinary reviews. RNA · 2023
    Review
  11. Article
  12. Article
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  14. Article
  15. Article
  16. 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

9 authors at 2 institutions in 1 country.

Yong-Yeon ChoThe Hormel Institute, University of Minnesota, 801 16th Avenue Northeast, Austin, MN 55912, USA.
Faqing Tang
Ke Yao
Chengrong Lu
Feng Zhu
Duo Zheng
Angelo Pugliese
Ann M Bode
Zigang Dong
Hormel (United States) · USUniversity of Minnesota · US

Funding

Ultraviolet-Induced Signal TrasductionR01CA077646 · NCI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI DONG, ZIGANG · 1999 to 2010
$2.3M
Anticarcinogenic Mechanisms of Tea ConstituentsR01CA081064 · NCI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI DONG, ZIGANG · 1999 to 2007
$1.9M
Anticarcinogenic Mechanisms of Tea ConstituentsR37CA081064 · NCI · UNIVERSITY OF MINNESOTA · PI DONG, ZIGANG · 2008 to 2012
$1.5M
MOLECULAR MECHANISMS OF ASPIRIN IN CANCER PREVENTIONR29CA074916 · NCI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI DONG, ZIGANG · 1997 to 2001
$222k
NCI NIH HHS CA 74916NCI NIH HHS CA 77646NCI NIH HHS CA 81064NCI NIH HHS R01 CA077646NCI NIH HHS R01 CA081064NCI NIH HHS R29 CA074916NCI NIH HHS R37 CA081064
6 · The paper itself

Abstract

c-Jun is a component of the activator protein-1 (AP-1) complex, which plays a crucial role in the regulation of gene expression, cell proliferation, and cell transformation, as well as cancer development. Herein, we found that cyclin-dependent kinase (Cdk)-3, but not Cdk2 or c-Jun NH(2)-terminal kinase, is a novel kinase of c-Jun induced by stimulation with growth factors such as epidermal growth factor (EGF). Cdk3 was shown to phosphorylate c-Jun at Ser63 and Ser73 in vitro and ex vivo. EGF-induced Cdk3 activation caused c-Jun phosphorylation at Ser63 and Ser73, resulting in increased AP-1 transactivation. Ectopic expression of Cdk3 resulted in anchorage-independent cell transformation of JB6 Cl41 cells induced by EGF and foci formation stimulated by constitutively active Ras (Ras(G12V)), which was mediated by AP-1 in NIH3T3 cells. These results showed that the Cdk3/c-Jun signaling axis plays an important role in EGF-stimulated cell proliferation and cell transformation.

Indexed as

AnimalsCell AdhesionCell Growth ProcessesCell LineCell Transformation, NeoplasticCyclin-Dependent Kinase 3Cyclin-Dependent KinasesEpidermal Growth FactorHumansMiceNIH 3T3 CellsPhosphorylationProto-Oncogene Proteins c-junSerineSignal TransductionTranscription Factor AP-1CDK3 protein, humanCdk3 protein, mouseCyclin-Dependent Kinase 3Cyclin-Dependent KinasesEpidermal Growth FactorProto-Oncogene Proteins c-junSerineTranscription Factor AP-1

Identifiers

PMID19118012
PMCPMC2684448
OpenAlexW2141034990

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.