Evidence map›Paper›PMID 17164422›Full record

ArticleDevelopment (Cambridge, England)2007

Dusp6 (Mkp3) is a negative feedback regulator of FGF-stimulated ERK signaling during mouse development.

Chaoying Li, Daryl A Scott, Ekaterina Hatch, Xiaoyan Tian, Suzanne L Mansour

Open access · bronzeAbstract read
In one paragraph

Article in Development (Cambridge, England), 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 174 papers.

0numbers the graph read from it
0cells of the map it votes in
174citing papers in PubMed
5.6field-weighted citation impact, top 3% 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

174 citing papers in PubMed, 283 citations in OpenAlex.

  1. Article
  2. Article
  3. FGF family in health and disease.Molecular biomedicine · 2026
    Review
  4. Review
  5. Breast Cancer Progression by the FGF/FGFR Axis: A Metabolic Perspective.Journal of mammary gland biology and neoplasia · 2025
    Review
  6. Review
  7. Static morphogen scaling enables proportional growth in a tissue growth model inspired by axolotl limb regeneration.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Genetic factors underlying Mandibular prognathism: insights from recent human and animal studies.Mammalian genome : official journal of the International Mammalian Genome Society · 2025
    Review
  14. Article
  15. Nuclear envelope budding inhibition slows down progerin-induced aging process.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

114 more citing papers are in PubMed but not listed here.

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.

Chaoying LiDepartment of Human Genetics, University of Utah, 15 N 2030 E RM 2100, Salt Lake City, UT 84112-5330, USA.
Daryl A Scott
Ekaterina Hatch
Xiaoyan Tian
Suzanne L Mansour
University of Utah · US

Funding

TRAINING PROGRAM IN GENETICST32GM007464 · NIGMS · UNIVERSITY OF UTAH · PI GRUNWALD, DAVID J., STANFIELD, GILLIAN · 1985 to 2020
$6.1M
FORMING AND PATTERNING THE VERTEBRATE INNER EARR01DC004185 · NIDCD · UNIVERSITY OF UTAH · PI SCHOENWOLF, GARY C · 2000 to 2009
$3.8M
GENES INVOLVED IN INNER EAR DEVELOPMENTR01DC002043 · NIDCD · UNIVERSITY OF UTAH · PI MANSOUR, SUZANNE L · 1993 to 2012
$3.1M
NIDCD NIH HHS R01 DC002043NIDCD NIH HHS R01 DC004185NIDCD NIH HHS R01DC02043NIDCD NIH HHS R01DC04185NIGMS NIH HHS T32 GM007464
6 · The paper itself

Abstract

Mitogen-activated protein kinase (MAPK) pathways are major mediators of extracellular signals that are transduced to the nucleus. MAPK signaling is attenuated at several levels, and one class of dual-specificity phosphatases, the MAPK phosphatases (MKPs), inhibit MAPK signaling by dephosphorylating activated MAPKs. Several of the MKPs are themselves induced by the signaling pathways they regulate, forming negative feedback loops that attenuate the signals. We show here that in mouse embryos, Fibroblast growth factor receptors (FGFRs) are required for transcription of Dusp6, which encodes MKP3, an extracellular signal-regulated kinase (ERK)-specific MKP. Targeted inactivation of Dusp6 increases levels of phosphorylated ERK, as well as the pERK target, Erm, and transcripts initiated from the Dusp6 promoter itself. Finally, the Dusp6 mutant allele causes variably penetrant, dominant postnatal lethality, skeletal dwarfism, coronal craniosynostosis and hearing loss; phenotypes that are also characteristic of mutations that activate FGFRs inappropriately. Taken together, these results show that DUSP6 serves in vivo as a negative feedback regulator of FGFR signaling and suggest that mutations in DUSP6 or related genes are candidates for causing or modifying unexplained cases of FGFR-like syndromes.

Indexed as

Feedback, PhysiologicalSignal TransductionAllelesAnimalsCell LineDual Specificity Phosphatase 6Embryo, MammalianEmbryonic Stem CellsExtracellular Signal-Regulated MAP KinasesFemaleFibroblast Growth FactorsGene Expression Regulation, DevelopmentalGene TargetingMiceMice, Inbred C57BLMutationDual Specificity Phosphatase 6Dusp6 protein, mouseExtracellular Signal-Regulated MAP KinasesFibroblast Growth FactorsProtein Tyrosine PhosphatasesReceptors, Fibroblast Growth Factor

Identifiers

PMID17164422
PMCPMC2424197
OpenAlexW2139626362

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.