Evidence map›Paper›PMID 19717565›Full record

ArticleThe Journal of biological chemistry2009

p63 Suppresses non-epidermal lineage markers in a bone morphogenetic protein-dependent manner via repression of Smad7.

Laura De Rosa, Dario Antonini, Giustina Ferone, Monia T Russo, Paul B Yu, Rong Han, Caterina Missero

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.3field-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

28 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Molecular Mechanisms of p63-Mediated Squamous Cancer Pathogenesis.International journal of molecular sciences · 2019
    Review
  7. Article
  8. Master regulatory role of p63 in epidermal development and disease.Cellular and molecular life sciences : CMLS · 2018
    Review
  9. Protein aggregation of the p63 transcription factor underlies severe skin fragility in AEC syndrome.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. p53/p63/p73 in the epidermis in health and disease.Cold Spring Harbor perspectives in medicine · 2014
    Review
  17. Article
  18. Induced multipotency in adult keratinocytes through down-regulation of ΔNp63 or DGCR8.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  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

7 authors at 3 institutions in 2 countries.

Laura De RosaCEINGE Biotecnologie Avanzate, via Comunale Margherita 482, 80145 Napoli, Italy.
Dario Antonini
Giustina Ferone
Monia T Russo
Paul B Yu
Rong Han
Caterina Missero
Ceinge Biotecnologie Avanzate (Italy) · ITHarvard University · USSDN Istituto di Ricerca Diagnostica e Nucleare · IT

Funding

The role of the BMP type II receptor in vascular functionK08HL079943 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI YU, PAUL B · 2006 to 2010
$672k
NHLBI NIH HHS K08 HL079943Telethon GGP06243
6 · The paper itself

Abstract

p63, a p53 family member, plays an essential role in epidermal development by regulating its transcriptional program. Here we report a previously uncovered role of p63 in controlling bone morphogenetic protein (BMP) signaling, which is required for maintaining low expression levels of several non-epidermal genes. p63 represses transcription of the inhibitory Smad7 and activates Bmp7, thereby sustaining BMP signaling. In the absence of p63, compromised BMP signaling leads to inappropriate non-epidermal gene expression in postnatal mouse keratinocytes and in embryonic epidermis. Reactivation of BMP signaling by Smad7 knockdown and/or, to a lesser extent, by BMP treatment suppresses expression of non-epidermal genes in the absence of p63. Canonical BMP/Smad signaling is essential for control of non-epidermal genes as use of a specific inhibitor, or simultaneous knockdown of Smad1 and Smad5 counteract suppression of non-epidermal genes. Our data indicate that p63 prevents ectopic expression of non-epidermal genes by a mechanism involving Smad7 repression and, to a lesser extent, Bmp7 induction, with consequent enhancement of BMP/Smad signaling.

Indexed as

Epidermal CellsAnimalsBiomarkersBone Morphogenetic Protein 7Bone Morphogenetic ProteinsCell LineageCells, CulturedGene Expression RegulationKeratinocytesMicePhosphoproteinsSignal TransductionSmad7 ProteinTrans-ActivatorsBiomarkersBone Morphogenetic Protein 7Bone Morphogenetic ProteinsPhosphoproteinsSmad7 ProteinSMAD7 protein, humanTrans-ActivatorsTrp63 protein, mouse

Identifiers

PMID19717565
PMCPMC2781612
OpenAlexW2056838445

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.