Evidence map›Paper›PMID 10468599›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1999

Three new allelic mouse mutations that cause skeletal overgrowth involve the natriuretic peptide receptor C gene (Npr3).

J Jaubert, F Jaubert, N Martin, L L Washburn, B K Lee, E M Eicher, J L Guénet

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

49 citing papers in PubMed, 139 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. The Natriuretic Peptide System: A Single Entity, Pleiotropic Effects.International journal of molecular sciences · 2023
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. The Genetic Architecture of High Bone Mass.Frontiers in endocrinology · 2020
    Review
  15. Article
  16. Observational
  17. Article
  18. Review
  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.

J JaubertUnité de Génétique des Mammifères, Institut Pasteur, 25 Rue du Docteur Roux, 75724 Paris Cedex 15, France.
F Jaubert
N Martin
L L Washburn
B K Lee
E M Eicher
J L Guénet
Hôpital Necker-Enfants Malades · FRJackson Laboratory · USInstitut Pasteur · FR

Funding

MUTANT GENE RESOURCEP40RR001183 · NCRR · JACKSON LABORATORY · PI DONAHUE, LEAH RAE B · 1985 to 2011
$16.3M
Mammalian Sex Determining GenesR01GM020919 · NIGMS · JACKSON LABORATORY · PI EICHER, EVA M · 1985 to 2006
$3.3M
CYTOGENETICS OF THE MOUSER37GM020919 · NIGMS · JACKSON LABORATORY · PI EICHER, EVA M · 1992 to 2001
$1.5M
MINORITY PREDOCTORAL FELLOWSHIP PROGRAMF31GM020919 · NIGMS · YALE UNIVERSITY · PI DRAYTON, DANIELLE L · 2000 to 2004
$158k
NCRR NIH HHS P40 RR001183NCRR NIH HHS RR01183NIGMS NIH HHS F31 GM020919NIGMS NIH HHS GM20919NIGMS NIH HHS R01 GM020919NIGMS NIH HHS R37 GM020919
6 · The paper itself

Abstract

In 1979, a BALB/cJ mouse was identified with an exceptionally long body. This phenotype was found to be caused by a recessive mutation, designated longjohn (lgj), that mapped to the proximal region of chromosome 15. Several years later, a mouse with a similarly elongated body was identified in an outbred stock after chemical mutagenesis with ethylnitrosourea. This phenotype also was caused by a recessive mutation, designated strigosus (stri). The two mutations were found to be allelic. A third allele was identified in a DBA/2J mouse and was designated longjohn-2J (lgj(2J)). Analysis of skeletal preparations of stri/stri mice indicated that the endochondral ossification process was slightly delayed, resulting in an extended proliferation zone. A recent study reported that mice overexpressing brain natriuretic peptide, one of the members of the natriuretic peptide family, exhibit a skeletal-overgrowth syndrome with endochondral ossification defects. The Npr3 gene coding for type C receptor for natriuretic peptides (NPR-C), which is mainly involved in the clearance of the natriuretic peptides, mapped in the vicinity of our mouse mutations and thus was a candidate gene. The present study reports that all three mutations involve the Npr3 gene and provides evidence in vivo that there is a natriuretic-related bone pathway, underscoring the importance of natriuretic peptide clearance by natriuretic peptide type C receptor.

Indexed as

Chromosome MappingAllelesAmino Acid SequenceAnimalsBody ConstitutionBone and BonesCattleGenes, RecessiveGuanylate CyclaseHumansMiceMice, Inbred BALB CMice, Mutant StrainsMolecular Sequence DataRatsReceptors, Atrial Natriuretic Factoratrial natriuretic factor receptor CGuanylate CyclaseReceptors, Atrial Natriuretic Factor

Identifiers

PMID10468599
PMCPMC17879
OpenAlexW2029416726

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.