REFERENCES
1. Fukushige S, Sauer B. Genomic targeting with a positive-selection lox integration vector allows highly reproducible gene expression in mammalian cells. Proc Natl Acad Sci U S A 1992;89:7905-9.
2. Agah R, Frenkel PA, French BA, Michael LH, Overbeek PA, Schneider MD. Gene recombination in postmitotic cells. Targeted expression of Cre recombinase provokes cardiac-restricted, site-specific rearrangement in adult ventricular muscle in vivo. J Clin Invest 1997;100:169-79.
3. Pugach EK, Richmond PA, Azofeifa JG, Dowell RD, Leinwand LA. Prolonged Cre expression driven by the α-myosin heavy chain promoter can be cardiotoxic. J Mol Cell Cardiol 2015;86:54-61.
4. Metzger D, Clifford J, Chiba H, Chambon P. Conditional site-specific recombination in mammalian cells using a ligand-dependent chimeric Cre recombinase. Proc Natl Acad Sci U S A 1995;92:6991-5.
5. Feil R, Brocard J, Mascrez B, LeMeur M, Metzger D, Chambon P. Ligand-activated site-specific recombination in mice. Proc Natl Acad Sci U S A 1996;93:10887-90.
6. Sohal DS, Nghiem M, Crackower MA, et al. Temporally regulated and tissue-specific gene manipulations in the adult and embryonic heart using a tamoxifen-inducible Cre protein. Circ Res 2001;89:20-5.
7. Koitabashi N, Bedja D, Zaiman AL, et al. Avoidance of transient cardiomyopathy in cardiomyocyte-targeted tamoxifen-induced MerCreMer gene deletion models. Circ Res 2009;105:12-5.
8. Hall ME, Smith G, Hall JE, Stec DE. Systolic dysfunction in cardiac-specific ligand-inducible MerCreMer transgenic mice. Am J Physiol Heart Circ Physiol 2011;301:H253-60.
9. Heinen A, Gödecke S, Flögel U, et al. 4-hydroxytamoxifen does not deteriorate cardiac function in cardiomyocyte-specific MerCreMer transgenic mice. Basic Res Cardiol 2021;116:8.
10. Soonpaa MH, Field LJ. Survey of studies examining mammalian cardiomyocyte DNA synthesis. Circ Res 1998;83:15-26.
11. Cheedipudi SM, Hu J, Fan S, et al. Exercise restores dysregulated gene expression in a mouse model of arrhythmogenic cardiomyopathy. Cardiovasc Res 2020;116:1199-213.
12. Auguste G, Gurha P, Lombardi R, Coarfa C, Willerson JT, Marian AJ. Suppression of activated FOXO transcription factors in the heart prolongs survival in a mouse model of laminopathies. Circ Res 2018;122:678-92.
13. Chen SN, Lombardi R, Karmouch J, et al. DNA damage response/TP53 pathway is activated and contributes to the pathogenesis of dilated cardiomyopathy associated with LMNA (Lamin A/C) mutations. Circ Res 2019;124:856-73.
14. Wingett SW, Andrews S. FastQ Screen: a tool for multi-genome mapping and quality control. F1000Res 2018;7:1338.
15. Dobin A, Davis CA, Schlesinger F, et al. STAR: ultrafast universal RNA-seq aligner. Bioinformatics 2013;29:15-21.
16. Risso D, Ngai J, Speed TP, Dudoit S. Normalization of RNA-seq data using factor analysis of control genes or samples. Nat Biotechnol 2014;32:896-902.
17. Love MI, Huber W, Anders S. Moderated estimation of fold change and dispersion for RNA-seq data with DESeq2. Genome Biol 2014;15:550.
18. Auguste G, Rouhi L, Matkovich SJ, et al. BET bromodomain inhibition attenuates cardiac phenotype in myocyte-specific lamin A/C-deficient mice. J Clin Invest 2020;130:4740-58.
19. Rouhi L, Cheedipudi SM, Chen SN, et al. Haploinsufficiency of Tmem43 in cardiac myocytes activates the DNA damage response pathway leading to a late-onset senescence-associated pro-fibrotic cardiomyopathy. Cardiovasc Res 2021;117:2377-94.
20. Pépin G, Ferrand J, Höning K, et al. Cre-dependent DNA recombination activates a STING-dependent innate immune response. Nucleic Acids Res 2016;44:5356-64.
21. Thyagarajan B, Guimarães M, Groth A, Calos M. Mammalian genomes contain active recombinase recognition sites. Gene 2000;244:47-54.
