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Cardiac-specific activation of Cre expression at late fetal development

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Opherk,  Jan-Patrick
Department of Cell Physiology, Max Planck Institute for Medical Research, Max Planck Society;

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Yampolsky,  Pessah
Department of Cell Physiology, Max Planck Institute for Medical Research, Max Planck Society;
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

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Koenen,  Michael
Department of Cell Physiology, Max Planck Institute for Medical Research, Max Planck Society;

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Zehelein,  Jörg
Department of Cell Physiology, Max Planck Institute for Medical Research, Max Planck Society;
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

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Citation

Opherk, J.-P., Yampolsky, P., Hardt, S. E., Schoels, W., Katus, H. A., Koenen, M., et al. (2007). Cardiac-specific activation of Cre expression at late fetal development. Biochemical and Biophysical Research Communications, 359(2), 209-213. doi:10.1016/j.bbrc.2007.05.045.


Cite as: http://hdl.handle.net/11858/00-001M-0000-002C-ACC4-7
Abstract
In a first step towards dissecting molecular mechanisms that contribute to the development of cardiac diseases, we have generated transgenic mice that express a Cre-GFP fusion protein under the transcriptional control of a 4.3kb murine cardiac Troponin I gene (cTnI) promoter. Cre-GFP expression, similar in three transgenic lines, is described in one line. In mouse embryos, transgenic for the Cre-GFP and ROSA lacZ reporter allele, first Cre-mediated recombination appeared at 16.5 dpc selectively at the heart. Like the endogenous cTnI gene, transgenic Cre expression showed a slow rise through fetal development that increased neonatally. Bitransgenic hearts, stained at 30 days of age, showed intense signals in ventricular and atrial myocytes while no recombination occurred in other tissues. The delayed onset of Cre activity in cTnI-Cre mice could provide a useful genetic tool to evaluate the function of loxP targeted cardiac genes without interference of recombination during early heart development.