Evidence map›Paper›PMID 21177849›Full record

ArticleThe Journal of biological chemistry2011

Regulation of Krüppel-like factor 4 by the anaphase promoting complex pathway is involved in TGF-beta signaling.

Dong Hu, Yong Wan

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

33 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. APC/CCellular and molecular life sciences : CMLS · 2019
    Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. The critical role of Krüppel-like factors in kidney disease.American journal of physiology. Renal physiology · 2017
    Review
  16. Article
  17. Article
  18. Review
  19. Article
  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

2 authors at 1 institution in 1 country.

Dong HuDepartment of Cell Biology and Physiology and University of Pittsburgh Cancer Institute, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213, USA.
Yong Wan
UPMC Hillman Cancer Center · US

Funding

University of Pittsburgh Clinical and Translational Science InstituteUL1TR000005 · NCATS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI REIS, STEVEN E · 2012 to 2015
$50.8M
Interplay between Cdh1/APC and Rad17 in DNA damage checkpoints and carcinogenesisR01CA154695 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI WAN, YONG · 2011 to 2015
$1.5M
Activation of APC by TGF-beta Suppresses Breast CancerR01CA115943 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI WAN, YONG · 2005 to 2009
$1.2M
NCATS NIH HHS UL1 TR000005NCI NIH HHS CA115943NCI NIH HHS R01 CA115943NCI NIH HHS R01 CA154695
6 · The paper itself

Abstract

Krüppel-like factor 4 (KLF4), a zinc finger-containing transcriptional factor, regulates a variety of biological processes, including cell proliferation, differentiation, apoptosis, and stem cell reprogramming. Post-translational modifications of KLF4, including phosphorylation, acetylation, and sumoylation, regulate its transcriptional activity. Most recent studies also demonstrate that KLF4 is targeted for ubiquitin-dependent proteolysis during cell cycle progression. However, the underlying mechanism remains largely unknown. In this study, we demonstrated that KLF4 is profoundly degraded in response to TGF-β signaling. We have identified the Cdh1-anaphase promoting complex as a putative E3 ligase that governs TGF-β-induced KLF4 degradation. The TGF-β-induced KLF4 degradation is mediated by the destruction box on the KLF4. Either depletion of Cdh1 by RNA interference or stabilization of KLF4 by disruption of its destruction box significantly attenuates TGF-β-induced ubiquitylation and degradation. In addition, depletion of Cdh1 or stabilization of KLF4 antagonizes TGF-β-induced activation of transcription. Determining the role of KLF4 proteolysis in response to TGF-β signaling has opened a new perspective to understand the TGF-β signaling pathway.

Indexed as

Adenomatous Polyposis Coli ProteinAnaphaseAntigens, CDCadherinsDown-RegulationHEK293 CellsHumansKruppel-Like Factor 4Kruppel-Like Transcription FactorsMutagenesisPlasminogen Activator Inhibitor 1Proteasome Endopeptidase ComplexProtein StabilitySignal TransductionTranscriptional ActivationTransfectionAdenomatous Polyposis Coli ProteinAntigens, CDAPC protein, humanCadherinsCDH1 protein, humanKLF4 protein, humanKruppel-Like Factor 4Kruppel-Like Transcription FactorsPlasminogen Activator Inhibitor 1Proteasome Endopeptidase ComplexTransforming Growth Factor betaUbiquitin-Protein Ligases

Identifiers

PMID21177849
PMCPMC3044944
OpenAlexW2055337546

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.