Evidence map›Paper›PMID 23599428›Full record

ArticleThe Journal of biological chemistry2013

Protein kinase C δ increases Kruppel-like factor 4 protein, which drives involucrin gene transcription in differentiating keratinocytes.

Yap Ching Chew, Gautam Adhikary, Wen Xu, Gerald M Wilson, Richard L Eckert

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.1field-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

25 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. ACTL6A suppresses p21Oncogenesis · 2021
    Article
  5. Review
  6. Cellular consequences of arginine methylation.Cellular and molecular life sciences : CMLS · 2019
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Interleukin-4 Downregulation of Involucrin Expression in Human Epidermal Keratinocytes Involves Stat6 Sequestration of the Coactivator CREB-Binding Protein.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2016
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Krüppel-like factors 4 and 5 expression and their involvement in differentiation of oral carcinomas.International journal of clinical and experimental pathology · 2015
    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 1 institution in 1 country.

Yap Ching ChewDepartment of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA.
Gautam Adhikary
Wen Xu
Gerald M Wilson
Richard L Eckert
University of Maryland, Baltimore · US

Funding

Polycomb genes and keratinocyte functionR01AR053851 · NIAMS · UNIVERSITY OF MARYLAND BALTIMORE · PI ECKERT, RICHARD L. · 2008 to 2012
$2.2M
MAP KINASES REGULATE INVOLUCRIN GENE EXPRESSIONR01AR046494 · NIAMS · UNIVERSITY OF MARYLAND BALTIMORE · PI ECKERT, RICHARD L. · 2000 to 2010
$1.9M
NIAMS NIH HHS R01 AR046494NIAMS NIH HHS R01 AR053851
6 · The paper itself

Abstract

KLF4 is a member of the Kruppel-like factor family of transcriptional regulators. KLF4 has been shown to be required for normal terminal differentiation of keratinocytes, but the molecular mechanism whereby KLF4 regulates genes associated with the differentiation process has not been studied. In the present study, we explore the impact of KLF4 on expression of involucrin, a gene that is specifically expressed in differentiated keratinocytes. KLF4 overexpression and knockdown studies show that involucrin mRNA and protein level correlates directly with KLF4 level. Moreover, studies of mutant KLF4 proteins indicate that transcriptionally inactive forms do not increase involucrin expression. PKCδ is a regulator of keratinocyte differentiation that increases expression of differentiation-associated target genes, including involucrin. Overexpression of KLF4 augments the PKCδ-dependent increase in involucrin expression, whereas KLF4 knockdown attenuates this response. The KLF4 induction of human involucrin (hINV) promoter activity is mediated via KLF4 binding to a GC-rich element located in the hINV promoter distal regulatory region, a region of the promoter required for in vivo involucrin expression. Mutation of the GC-rich element, an adjacent AP1 factor binding site, or both sites severely attenuates the response. Moreover, loss of KLF4 in an epidermal equivalent model of differentiation results in loss of hINV expression. These studies suggest that KLF4 is part of a multiprotein complex that interacts that the hINV promoter distal regulatory region to drive differentiation-dependent hINV gene expression in epidermis.

Indexed as

Cell DifferentiationCells, CulturedChromatin ImmunoprecipitationGC Rich SequenceHumansKeratinocytesKruppel-Like Factor 4Kruppel-Like Transcription FactorsPromoter Regions, GeneticProtein Kinase C-deltaProtein PrecursorsResponse ElementsRNA, MessengerTranscriptional ActivationTranscription, GeneticinvolucrinKLF4 protein, humanKruppel-Like Factor 4Kruppel-Like Transcription FactorsProtein Kinase C-deltaProtein PrecursorsRNA, MessengerCell DifferentiationGene ExpressionKeratinocytesKruppel-like Factor (KLF)Protein Kinase C (PKC)

Identifiers

PMID23599428
PMCPMC3682575
OpenAlexW1484463029

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.