Evidence map›Paper›PMID 28732181›Full record

ArticleJournal of dental research2017

IRF6 and SPRY4 Signaling Interact in Periderm Development.

Y A Kousa, R Roushangar, N Patel, A Walter, P Marangoni, R Krumlauf, O D Klein, B C Schutte

Open access · greenAbstract read
In one paragraph

Article in Journal of dental research, 2017. 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
3.3field-weighted citation impact, top 8% 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, 32 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Neural crest and periderm-specific requirements ofbioRxiv : the preprint server for biology · 2024
    Article
  8. Article
  9. Article
  10. Article
  11. The Mafb cleft-associated variant H131Q is not required for palatogenesis in the mouse.Developmental dynamics : an official publication of the American Association of Anatomists · 2021
    Article
  12. Journal of dental research · 2020
    Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. IRF6 and AP2A Interaction Regulates Epidermal Development.The Journal of investigative dermatology · 2018
    Article
  19. 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

8 authors at 3 institutions in 1 country.

Y A Kousa1 Department of Biochemistry and Molecular Biology, Michigan State University, East Lansing, MI, USA.
R Roushangar1 Department of Biochemistry and Molecular Biology, Michigan State University, East Lansing, MI, USA.
N Patel2 Pediatrics and Human Development, Michigan State University, East Lansing, MI, USA.
A Walter2 Pediatrics and Human Development, Michigan State University, East Lansing, MI, USA.
P Marangoni3 Departments of Orofacial Sciences and Pediatrics and Institute for Human Genetics, University of California, San Francisco, San Francisco, CA, USA.
R Krumlauf4 Stowers Institute for Medical Research, Kansas City, MO, USA.
O D Klein3 Departments of Orofacial Sciences and Pediatrics and Institute for Human Genetics, University of California, San Francisco, San Francisco, CA, USA.
B C Schutte2 Pediatrics and Human Development, Michigan State University, East Lansing, MI, USA.
Michigan State University · USUniversity of California, San Francisco · USStowers Institute for Medical Research · US

Funding

CLONING AND CHARACTERIZATION OF THE VAN DER WOUDE GENER01DE013513 · NIDCR · UNIVERSITY OF IOWA · PI SCHUTTE, BRIAN C · 2000 to 2009
$2.6M
Role of Irf6 in palatal epitheliumF31DE022696 · NIDCR · MICHIGAN STATE UNIVERSITY · PI KOUSA, YOUSSEF A · 2012 to 2013
$60k
NIDCR NIH HHS F31 DE022696NIDCR NIH HHS R01 DE013513
6 · The paper itself

Abstract

Rare mutations in IRF6 and GRHL3 cause Van der Woude syndrome, an autosomal dominant orofacial clefting disorder. Common variants in IRF6 and GRHL3 also contribute risk for isolated orofacial clefting. Similarly, variants within genes that encode receptor tyrosine kinase (RTK) signaling components, including members of the FGF pathway, EPHA3 and SPRY2, also contribute risk for isolated orofacial clefting. In the mouse, loss of Irf6 or perturbation of Fgf signaling leads to abnormal oral epithelial adhesions and cleft palate. Oral adhesions can result from a disruption of periderm formation. Here, we find that IRF6 and SPRY4 signaling interact in periderm function. We crossed Irf6 heterozygous ( Irf6

Indexed as

Abnormalities, MultipleAnimalsCleft LipCleft PalateCystsDisease Models, AnimalInterferon Regulatory FactorsJaw AbnormalitiesLipMiceMice, TransgenicMouth AbnormalitiesMutationNerve Tissue ProteinsPhenotypeSignal TransductionInterferon Regulatory FactorsIRF6 protein, mouseNerve Tissue ProteinsSpry4 protein, mousecleft lip with or without cleft palate nonsyndromicGRHL3 proteinoral adhesionspopliteal pterygium syndromereceptor protein-tyrosine kinasesVan der Woude syndrome

Identifiers

PMID28732181
PMCPMC5613880
OpenAlexW2738765931

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.