Evidence map›Paper›PMID 10473625›Full record

ArticleThe Journal of biological chemistry1999

Regulation of the Dlx3 homeobox gene upon differentiation of mouse keratinocytes.

G T Park, M I Morasso

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

19 citing papers in PubMed, 46 citations in OpenAlex.

  1. Chromatin Landscape Governing Murine Epidermal Differentiation.The Journal of investigative dermatology · 2023
    Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Theria-specific homeodomain and cis-regulatory element evolution of the Dlx3-4 bigene cluster in 12 different mammalian species.Journal of experimental zoology. Part B, Molecular and developmental evolution · 2012
    Article
  8. Article
  9. Epidermal ablation of Dlx3 is linked to IL-17-associated skin inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2011
    Article
  10. Article
  11. Article
  12. Article
  13. Dlx genes, p63, and ectodermal dysplasias.Birth defects research. Part C, Embryo today : reviews · 2005
    Review
  14. Article
  15. Article
  16. Article
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  18. 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

2 authors at 1 institution in 1 country.

G T ParkLaboratory of Skin Biology, NIAMS, National Institutes of Health, Bethesda, Maryland 20892, USA.
M I Morasso
National Institutes of Health · US

Funding

REGULATION OF EPIDERMAL DIFFERENTIATIONZ01AR041124 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI MORASSO, MARIA I · 2000 to 2008
$1.9M
NIAMS NIH HHS Z01 AR041124-06
6 · The paper itself

Abstract

The Distal-less Dlx3 homeodomain gene is expressed in terminally differentiated murine epidermal cells, and there is evidence to support an essential role as a transcriptional regulator of the terminal differentiation process in these cells. In an attempt to determine the factors that induce Dlx3 gene expression, we have cloned the 1.2-kilobase pair proximal region of murine gene and analyzed its cis-regulatory elements and potential trans-acting factors. The proximal region of the Dlx3 gene has a canonical TATA box and CCAAT box, and the transcription start site was located 205 base pairs upstream from the initiation of translation site. Serial deletion analysis showed that the region between -84 and -34 confers the maximal promoter activity both in undifferentiated and differentiated primary mouse keratinocytes. Gel retardation assays and mutational analysis demonstrated that the transcriptional regulator NF-Y (also referred to as CBF) binds to a CCAAT box motif within this region and is responsible for the majority of the Dlx3 promoter activity. In addition, an Sp1-binding site was located immediately upstream of transcription start site that acts as a positive regulatory element of the Dlx3 promoter, independent of the CCAAT box motif. Importantly, elements residing between +30 to +60 of the Dlx3 gene are responsible for the Ca(2+)-dependent induction of Dlx3 during keratinocyte differentiation.

Indexed as

Gene Expression RegulationGenes, HomeoboxAnimalsBase SequenceCalciumCCAAT-Enhancer-Binding ProteinsCell DifferentiationCells, CulturedCloning, MolecularDNADNA-Binding ProteinsHomeodomain ProteinsKeratinocytesMiceMolecular Sequence DataMutagenesis, Site-DirectedCalciumCCAAT-Enhancer-Binding ProteinsDistal-less homeobox proteinsDNADNA-Binding ProteinsHomeodomain ProteinsSp1 Transcription FactorTranscription Factors

Identifiers

PMID10473625
PMCPMC1317293
OpenAlexW2084925528

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.