To verify whether ELuc can be used at the single-cell level to quantify gene expression in tissues, we generated transgenic mice that expressed ELuc under the control of the mBmal1 clock gene promoter [18].
To find out if prions could replicate in muscle tissue independently, the scientists created mice that "expressed" or made normal prions in muscle but nowhere else in the body.
Teaming up with researchers at other institutions, Chen's lab created a new line of mice that expressed too much of that one glutamate receptor.
In that study, thymocytes from diabetic mice that expressed lower VLA-5 and VLA-6 levels did not show altered migration ability in vitro, indicating that only lower integrin expression on the cell surface is not sufficient to hinder migration.
Double Tg (dTg) mice that expressed both Ig and sHEL transgenes were produced by intercrossing IgTg and sHEL mice.
Surprisingly, significant lifespan extension was observed in both MCAT transgenic lines but not in other transgenic mice that expressed catalase in the peroxisome or nucleus.
These mice were bred with mice that expressed the Cre recombinase gene under the control of the murine Agrp promoter [10].
Using the Müllerian inhibiting substance type II receptor (MISIIR) promoter, we generated transgenic mice that expressed activated PIK3CA in the Müllerian epithelium.
Transgenic mice that expressed TLX1 under the control of the Eµ enhancer developed B-cell lymphomas instead of T-ALL [29].
Furthermore, to investigate whether Foxo1 acts downstream of PDK1 in AGRP neurons, we generated Pdk1 knockout mice that expressed an AGRP neuron-specific, transactivation-defective form of Foxo1 (Δ256Foxo1), which lacks a carboxyl terminal transactivation domain and can compete with endogenous Foxos and inhibit expression of the target genes of Foxos [6], [7], [8].
We obtained eight founder mice that expressed the mutant (A339T) Gsdma transgene and two founder mice that expressed the wild-type Gsdma transgene.
