Endoplasmic reticulum (ER) stress response to tissue damage reduces protein synthesis in the ER, enhances protein degradation of damaged or misfolded proteins, and selectively induces expression of protective proteins. Thbs4 (thrombospondin 4) is one of the protective proteins upregulated in conjunction with ER stress responses in diseased hearts. 

These transgenic mice conditionally express mouse Thbs4 from a tetracycline-responsive element (TRE; tetO) and mouse Myh6 (myosin, heavy polypeptide 6, cardiac muscle, alpha; also known as alpha MHC) minimal promoter. When combined with cardiac-specific Myh6-tTA, removal of dietary doxycyline enables overexpression of THBS4 in the heart and protects animals from protein aggregation-dependent cardiomyopathy. Double transgenic tetO/tTA mice show a large expansion of the ER and post-ER vesicles in the heart.

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These transgenic mice conditionally express mouse Thbs4 from a tetracycline-responsive element (TRE; tetO) and mouse Myh6 (myosin, heavy polypeptide 6, cardiac muscle, alpha; also known as alpha MHC) minimal promoter. When combined with a tTA or rtTA allele, conditional, tissue-specific expression of THBS4 can be enabled.

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FVB-Tg(tetO-Thbs4)17.7Jmol/J Frozen Embryo