ArticleGenesis (New York, N.Y. : 2000)2014
Generation of a Cre knock-in into the Myocardin locus to mark early cardiac and smooth muscle cell lineages.
Article in Genesis (New York, N.Y. : 2000), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
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.
Who cites it
2 citing papers in PubMed, 5 citations in OpenAlex.
- Differential regulation of cranial and cardiac neural crest by serum response factor and its cofactors.eLife · 2022Article
- Myocardin in biology and disease.Journal of biomedical research · 2015Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The molecular events that control cell fate determination in cardiac and smooth muscle lineages remain elusive. Myocardin is an important transcription cofactor that regulates cell proliferation, differentiation, and development of the cardiovascular system. Here, we describe the construction and analysis of a dual Cre and enhanced green fluorescent protein (EGFP) knock-in mouse line in the Myocardin locus (Myocd(KI)). We report that the Myocd(KI) allele expresses the Cre enzyme and the EGFP in a manner that recapitulates endogenous Myocardin expression patterns. We show that Myocardin expression marks the earliest cardiac and smooth muscle lineages. Furthermore, this genetic model allows for the identification of a cardiac cell population, which maintains both Myocardin and Isl-1 expression, in E7.75-E8.0 embryos, highlighting the contribution and merging of the first and second heart fields during cardiogenesis. Therefore, the Myocd(KI) allele is a unique tool for studying cardiovascular development and lineage-specific gene manipulation.
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Registered trials
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