Evidence map›Paper›PMID 10811845›Full record

ArticleThe Journal of clinical investigation2000

Disruption of ECE-1 and ECE-2 reveals a role for endothelin-converting enzyme-2 in murine cardiac development.

H Yanagisawa, R E Hammer, J A Richardson, N Emoto, S C Williams, S i Takeda, D E Clouthier, M Yanagisawa

Open access · greenAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

64 citing papers in PubMed, 190 citations in OpenAlex.

  1. Article
  2. Review
  3. Endothelin signaling in development.Development (Cambridge, England) · 2023
    Review
  4. Article
  5. Double outlet right ventricle.Frontiers in pediatrics · 2023
    Review
  6. Review
  7. Review
  8. Endothelins in inflammatory neurological diseases.Pharmacology & therapeutics · 2019
    Review
  9. Pulmonary artery smooth muscle cell HIF-1α regulates endothelin expression via microRNA-543.American journal of physiology. Lung cellular and molecular physiology · 2018
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Dermal lymphatic dilation in a mouse model of alopecia areata.Experimental and molecular pathology · 2016
    Article
  17. Endothelin.Pharmacological reviews · 2016
    Review
  18. Article
  19. Review
  20. Article

4 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

8 authors at 2 institutions in 2 countries.

H YanagisawaHoward Hughes Medical Institute, Department of Biochemistry, University of Texas Southwestern Medical Center, Dallas 75390-9050, USA.
R E Hammer
J A Richardson
N Emoto
S C Williams
S i Takeda
D E Clouthier
M Yanagisawa
The University of Texas Southwestern Medical Center · USKobe University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endothelin-converting enzyme-1 and -2 (ECE-1 and -2) are membrane-bound metalloproteases that can cleave biologically the inactive endothelin-1 (ET-1) precursor to form active ET-1 in vitro. We previously reported developmental defects in specific subsets of neural crest-derived tissues, including branchial arch-derived craniofacial structures, aortic arch arteries, and the cardiac outflow tract in ECE-1 knockout mice. To examine the role of ECE-2 in cardiovascular development, we have now generated a null mutation in ECE-2 by homologous recombination. ECE-2 null mice develop normally, are healthy into adulthood, are fertile in both sexes, and live a normal life span. However, when they are bred into an ECE-1-null background, defects in cardiac outflow structures become more severe than those in ECE-1 single knockout embryos. In addition, ECE-1(-/-); ECE-2(-/-) double null embryos exhibited abnormal atrioventricular valve formation, a phenotype never seen in ECE-1 single knockout embryos. In the developing mouse heart, ECE-2 mRNA is expressed in the endocardial cushion mesenchyme from embyronic day (E) 12.5, in contrast to the endocardial expression of ECE-1. Levels of mature ET-1 and ET-2 in whole ECE-1(-/-); ECE-2(-/-) embryos at E12.5 do not differ appreciably from those of ECE-1(-/-) embryos. The significant residual ET-1/ET-2 in the ECE-1(-/-); ECE-2(-/-) embryos indicates that proteases distinct from ECE-1 and ECE-2 can carry out ET-1 activation in vivo.

Indexed as

AnimalsAspartic Acid EndopeptidasesBase SequenceDNA PrimersEndothelin-1Endothelin-2Endothelin-Converting EnzymesFemaleFetal HeartGene Expression Regulation, DevelopmentalGene Expression Regulation, EnzymologicHeart Defects, CongenitalIn Situ HybridizationIn Vitro TechniquesMaleMetalloendopeptidasesAspartic Acid EndopeptidasesDNA PrimersEce1 protein, mouseEce2 protein, mouseEndothelin-1Endothelin-2Endothelin-Converting EnzymesMetalloendopeptidasesRNA, Messenger

Identifiers

PMID10811845
PMCPMC315458
OpenAlexW1985592940

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.