ArticleGenesis (New York, N.Y. : 2000)2015
Generation of a tamoxifen inducible Tnnt2MerCreMer knock-in mouse model for cardiac studies.
Article in Genesis (New York, N.Y. : 2000), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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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.
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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.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- A narrow developmental window defines PKN2's essential role in ventricular chamber morphogenesis.Communications biology · 2026Article
- Lem2 is essential for cardiac development by maintaining nuclear integrity.Cardiovascular research · 2023Article
- Prerequisite endocardial-mesenchymal transition for murine cardiac trabecular angiogenesis.Developmental cell · 2023Article
- Optimization of tamoxifen-induced gene regulation in cardiovascular research.The journal of cardiovascular aging · 2022Article
- ETV1 activates a rapid conduction transcriptional program in rodent and human cardiomyocytes.Scientific reports · 2018Article
- Generation and Analysis of Striated Muscle Selective LINC Complex Protein Mutant Mice.Methods in molecular biology (Clifton, N.J.) · 2018Article
- Resident c-kit(+) cells in the heart are not cardiac stem cells.Nature communications · 2015Article
- A Murine Myh6MerCreMer Knock-In Allele Specifically Mediates Temporal Genetic Deletion in Cardiomyocytes after Tamoxifen Induction.PloS one · 2015Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Tnnt2, encoding thin-filament sarcomeric protein cardiac troponin T, plays critical roles in heart development and function in mammals. To develop an inducible genetic deletion strategy in myocardial cells, we generated a new Tnnt2:MerCreMer (Tnnt2(MerCreMer/+)) knock-in mouse. Rosa26 reporter lines were used to examine the specificity and efficiency of the inducible Cre recombinase. We found that Cre was specifically and robustly expressed in the cardiomyocytes at embryonic and adult stages following tamoxifen induction. The knock-in allele on Tnnt2 locus does not impact cardiac function. These results suggest that this new Tnnt2(MerCreMer/+) mouse could be applied towards the temporal genetic deletion of genes of interests in cardiomyocytes with Cre-LoxP technology. The Tnnt2(MerCreMer/+) mouse model also provides a useful tool to trace myocardial lineage during development and repair after cardiac injury.
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Registered trials
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