Evidence map›Paper›PMID 15169892›Full record

ArticleMolecular and cellular biology2004

Targeted inactivation of serum response factor in the developing heart results in myocardial defects and embryonic lethality.

Ara Parlakian, David Tuil, Ghislaine Hamard, Geneviève Tavernier, Daniele Hentzen, Jean-Paul Concordet, Denise Paulin, Zhenlin Li, Dominique Daegelen

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers.

0numbers the graph read from it
0cells of the map it votes in
94citing papers in PubMed
5.5field-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

94 citing papers in PubMed, 205 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. IL-2 delivery to CD8Nature communications · 2024
    Article
  7. Review
  8. Article
  9. Cardiac Transcription Factors and Regulatory Networks.Advances in experimental medicine and biology · 2024
    Review
  10. Article
  11. Sarcomere maturation: function acquisition, molecular mechanism, and interplay with other organelles.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2022
    Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article

34 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

9 authors at 3 institutions in 1 country.

Ara ParlakianLaboratoire de Biologie Moléculaire de la Différenciation, Université Paris 7, 75005 Paris, France.
David Tuil
Ghislaine Hamard
Geneviève Tavernier
Daniele Hentzen
Jean-Paul Concordet
Denise Paulin
Zhenlin Li
Dominique Daegelen
Laboratoire de Biologie du Développement · FRInserm · FRUniversité Paris Cité · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Serum response factor (SRF) is at the confluence of multiple signaling pathways controlling the transcription of immediate-early response genes and muscle-specific genes. There are active SRF target sequences in more than 50 genes expressed in the three muscle lineages including normal and diseased hearts. However, the role of SRF in heart formation has not been addressed in vivo thus far due to the early requirement of SRF for mesoderm formation. We have generated a conditional mutant of SRF by using Cre-LoxP strategy that will be extremely useful to study the role of SRF in embryonic and postnatal cardiac functions, as well as in other tissues. This report shows that heart-specific deletion of SRF in the embryo by using a new beta MHC-Cre transgenic mouse line results in lethal cardiac defects between embryonic day 10.5 (E10.5) and E13.5, as evidenced by abnormally thin myocardium, dilated cardiac chambers, poor trabeculation, and a disorganized interventricular septum. At E9.5, we found a marked reduction in the expression of essential regulators of heart development, including Nkx2.5, GATA4, myocardin, and the SRF target gene c-fos prior to overt maldevelopment. We conclude that SRF is crucial for cardiac differentiation and maturation, acting as a global regulator of multiple developmental genes.

Indexed as

AnimalsApoptosisBase SequenceCell DivisionDNA, ComplementaryFemaleFetal DeathFetal HeartGene Expression Regulation, DevelopmentalGene TargetingGestational AgeHeart Defects, CongenitalMiceMice, Inbred C57BLMice, Inbred DBAMice, TransgenicDNA, ComplementarySerum Response FactorTranscription Factors

Identifiers

PMID15169892
PMCPMC419888
OpenAlexW2154993940

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.