Evidence map›Paper›PMID 15743817›Full record

ArticleMolecular and cellular biology2005

Congenital semilunar valvulogenesis defect in mice deficient in phospholipase C epsilon.

Makoto Tadano, Hironori Edamatsu, Susumu Minamisawa, Utako Yokoyama, Yoshihiro Ishikawa, Noboru Suzuki, Hiromitsu Saito, Dongmei Wu, Misa Masago-Toda, Yuriko Yamawaki-Kataoka and 5 more

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.2field-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

29 citing papers in PubMed, 76 citations in OpenAlex.

  1. Increase of intracellular ZnScientific reports · 2025
    Article
  2. Review
  3. Review
  4. Review
  5. Molecular regulation of PLCβ signaling.Methods in enzymology · 2023
    Review
  6. Phospholipase Cε insufficiency causes ascending aortic aneurysm and dissection.American journal of physiology. Heart and circulatory physiology · 2022
    Article
  7. Article
  8. Phospholipase C.Advances in experimental medicine and biology · 2020
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Review
  20. What chick and mouse models have taught us about the role of the endocardium in congenital heart disease.Birth defects research. Part A, Clinical and molecular teratology · 2011
    Review
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

15 authors at 3 institutions in 1 country.

Makoto TadanoDivision of Molecular Biology, Department of Molecular and Cellular Biology, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan.
Hironori Edamatsu
Susumu Minamisawa
Utako Yokoyama
Yoshihiro Ishikawa
Noboru Suzuki
Hiromitsu Saito
Dongmei Wu
Misa Masago-Toda
Yuriko Yamawaki-Kataoka
Tomiyoshi Setsu
Toshio Terashima
Sakan Maeda
Takaya Satoh
Tohru Kataoka
Yokohama City University · JPMie University · JPKobe University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Phospholipase Cepsilon is a novel class of phosphoinositide-specific phospholipase C, identified as a downstream effector of Ras and Rap small GTPases. We report here the first genetic analysis of its physiological function with mice whose phospholipase Cepsilon is catalytically inactivated by gene targeting. The hearts of mice homozygous for the targeted allele develop congenital malformations of both the aortic and pulmonary valves, which cause a moderate to severe degree of regurgitation with mild stenosis and result in ventricular dilation. The malformation involves marked thickening of the valve leaflets, which seems to be caused by a defect in valve remodeling at the late stages of semilunar valvulogenesis. This phenotype has a remarkable resemblance to that of mice carrying an attenuated epidermal growth factor receptor or deficient in heparin-binding epidermal growth factor-like growth factor. Smad1/5/8, which is implicated in proliferation of the valve cells downstream of bone morphogenetic protein, shows aberrant activation at the margin of the developing semilunar valve tissues in embryos deficient in phospholipase Cepsilon. These results suggest a crucial role of phospholipase Cepsilon downstream of the epidermal growth factor receptor in controlling semilunar valvulogenesis through inhibition of bone morphogenetic protein signaling.

Indexed as

AllelesAnimalsAortic ValveAortopulmonary Septal DefectBone Morphogenetic ProteinsCardiomyopathy, DilatedDNA-Binding ProteinsErbB ReceptorsGene TargetingHeart Valve DiseasesHeart VentriclesMiceMice, Mutant StrainsMutationPhosphoinositide Phospholipase CPhosphoproteinsBone Morphogenetic ProteinsDNA-Binding ProteinsErbB ReceptorsPhosphoinositide Phospholipase Cphospholipase C epsilonPhosphoproteinsSmad1 ProteinSmad1 protein, mouseSmad5 ProteinSmad5 protein, mouseSmad8 ProteinSmad9 protein, mouseSmad ProteinsTrans-ActivatorsType C Phospholipases

Identifiers

PMID15743817
PMCPMC1061609
OpenAlexW2122668945

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.