Temporally Regulated and Tissue-Specific Gene Manipulations in the Adult and Embryonic Heart Using a Tamoxifen-Inducible Cre Protein

By D. Sohal, M. Nghiem, M. Crackower, S. Witt, T. Kimball, Kevin M. Tymitz, Josef M. Penninger, J. Molkentin. Circulation Research, 2001

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The role of autophagy in cardiomyocytes in the basal state and in response to hemodynamic stress (2007, background): “with transgenic mice ( MerCreMer ) which express the Cre recombinase in a tamoxifen-inducible and cardiomyocyte-specific manne”
Neuregulin1/ErbB4 signaling induces cardiomyocyte proliferation and repair of heart injury. (2009, neutral): “We used the a-MHC-MerCreMer strain (Sohal et al., 2001) to delete the loxP-flanked exon 2 of ErbB4 (Golub et al., 2004).”
Evidence from a genetic fate-mapping study that stem cells refresh adult mammalian cardiomyocytes after injury (2007, methodology): “We generated double-transgenic MerCreMer-ZEG mice by crossbreeding transgenic B6129-Tg( Myh6-cre/Esr1 )1Jmk/J (hereafter referred to as MerCreMer) mice, in which the cardiomyocyte-specific α-myosin heavy chain ( Myh6 ) promoter drives expression of a 4-OH-tamoxifen-inducible Cre recombinase fusion p”
Fibroblast-specific TGF-β-Smad2/3 signaling underlies cardiac fibrosis. (2017, neutral): “Here, we deleted Smad2/3 from the adult heart using the α -myosin heavy chain ( α MHC) MCM-containing transgene (40) to determine whether canonical Smad2/3 signaling within cardiomyocytes might similarly affect the cardiac fibrotic response with pressure overload.”