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Mice were engineered to express a human receptor to poliovirus (hPVR).
Regarding Bmp8b TG mice, WT SV129*C57Bl/6J mixed strain mice were engineered to express the murine Bmp8b gene from the apolipoprotein 2 (Fabpromoteroter.
PI16-deficient mice were engineered and found to generate higher levels of processed chemerin than wildtype mice.
Transgenic (TG; FVB/N background) mice were engineered to express rat CRNK under control of the α-myosin heavy chain promoter, and crossed with FVB/N mice with cardiomyocyte-specific expression of caPKCε to create double TG mice.
To compare CD40 and LMP1-mediated events in vivo, transgenic mice were engineered to express mouse CD40 (mCD40tg) or a protein with extracellular mCD40 and cytoplasmic LMP1 (mCD40-LMP1tg).
As an alternative approach to inhibiting calcineurin in the hearts of intact animals, transgenic mice were engineered to overexpress a human cDNA encoding the calcineurin-binding protein, myocyte-enriched calcineurin-interacting protein-1 (hMCIP1) under control of the cardiac-specific, alpha-myosin heavy chain promoter (alpha-MHC).
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Mice that were engineered to express two copies of this dominant-negative Jak2 protein died in utero.
Mice with targeted disruption of NF90 were engineered.
Mice had been engineered to carry a mutation in MTM1, the gene involved in X-linked myotubular myopathy.
Mice have been engineered, which lack global PPP1R15A and/or PPP1R15B (23, 23).
Mice that are engineered with telomere dysfunction, or defects in DNA damage checkpoints or DNA repair, may therefore represent better models for comparative oncogenomics [287].
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