Evidence map›Paper›PMID 21559334›Full record

ArticlePloS one2011

CDK-mediated regulation of cell functions via c-Jun phosphorylation and AP-1 activation.

Tony J Vanden Bush, Gail A Bishop

Registry-linked trialOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03220178 (PRECYCLE), which is not on this map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.4field-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.

NCT03220178 phase4terminatednot on this mapstarted 2017, after this paper: background citation

PRECYCLE: Multicenter, Randomized Phase IV Intergroup Trial to Evaluate the Impact of eHealth-based Patient Reported Outcome (PRO) Assessment on Quality of Life in Patients With Hormone Receptor Positive, HER2 Negative Locally Advanced or Metastatic Breast Cancer Treated With Palbociclib and an Aromatase Inhibitor- or Palbociclib and Fulvestrant

TypeinterventionalSponsorPalleos Healthcare GmbHRan2017 to 2021Enrolled532ConditionsBreast NeoplasmArmsPalbociclib, Fulvestrant, Anastrozole, Letrozole, Exemestane
3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. Article
  3. Cyclin-dependent kinases: Masters of the eukaryotic universe.Wiley interdisciplinary reviews. RNA · 2023
    Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Cyclin-dependent kinase 2 controls peripheral immune tolerance.Journal of immunology (Baltimore, Md. : 1950) · 2012
    Article
  16. Article
  17. 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

2 authors at 1 institution in 1 country.

Tony J Vanden BushDepartment of Microbiology, The University of Iowa, Iowa City, Iowa, United States of America.
Gail A Bishop
University of Iowa · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cyclin-dependent kinases (CDKs) and their targets have been primarily associated with regulation of cell-cycle progression. Here we identify c-Jun, a transcription factor involved in the regulation of a broad spectrum of cellular functions, as a newly recognized CDK substrate. Using immune cells from mouse and human, and several complementary in vitro and in vivo approaches including dominant negative protein expression, pharmacologic inhibitors, kinase assays and CDK4 deficient cells, we demonstrate the ability of CDK4 to phosphorylate c-Jun. Additionally, the activity of AP-1, a ubiquitous transcription factor containing phosphorylated c-Jun as a subunit, was inhibited by abrogating CDK4. Surprisingly, the regulation of c-Jun phosphorylation by CDK4 occurred in non-dividing cells, indicating that this pathway is utilized for cell functions that are independent of proliferation. Our studies identify a new substrate for CDK4 and suggest a mechanism by which CDKs can regulate multiple cellular activation functions, not all of which are directly associated with cell cycle progression. These findings point to additional roles of CDKs in cell signaling and reveal potential implications for therapeutic manipulations of this kinase pathway.

Indexed as

AnimalsCD40 AntigensCell CycleCell ProliferationCyclin-Dependent Kinase 4Cyclin-Dependent KinasesHumansImmune SystemInterleukin-6JNK Mitogen-Activated Protein KinasesMembrane GlycoproteinsMicePhosphorylationToll-Like Receptor 7Transcription Factor AP-1CD40 AntigensCDK4 protein, humanCdk4 protein, mouseCyclin-Dependent Kinase 4Cyclin-Dependent KinasesInterleukin-6JNK Mitogen-Activated Protein KinasesMembrane GlycoproteinsTLR7 protein, humanTlr7 protein, mouseToll-Like Receptor 7Transcription Factor AP-1

Identifiers

PMID21559334
PMCPMC3084876
OpenAlexW2014433419

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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.