Bone resorption and formation in Tshr−/− mice were further enhanced by thyroxine replacement.
To further generate endothelial-specific CD146 knockout mice (CD146EC-KO mice), CD146floxed/floxed mice were further bred to Tek+/Cre mice (Strain Name: B6.Cg-Tg(Tek-cre)12Flv/J, The Jackson Laboratory), which specifically expressed Cre recombinase in ECs.
Tek+/CreCD146floxed/floxed mice (CD146EC-KO mice) were viable, and these mice were further cross-bred with Tek+/+CD146floxed/floxed mice, resulting in 50%% Tek+/CreCD146floxed/floxed mice (CD146EC-KO mice) and 50%% Tek+/+CD146floxed/floxed mice (WT mice).
As Tek+/CreCD146floxed/floxe mice (CD146EC-KO mice) were viable, these mice were further bred to Tek+/+CD146floxed/floxed mice (WT mice), resulting in 50%% CD146EC-KO mice and 50 % WT mice, both of which were used for subsequent investigations (Fig. 1B).
These mice were further crossed with an IL-14α transgenic mouse to study the combined effect of PTEN deletion, PI-3K inhibition and expression of IL-14α (a cytokine originally identified as a B cell growth factor) in CD19+ B cell lymphoproliferation and response to LPS stimulation.
The experimentation has been designed as two steps: firstly, the normal male and female mice were compared with male and female C57-AMPK gene knocked-out mice, respectively; then the differences between male C57-AMPK gene knocked-out mice and female C57-AMPK gene knocked-out mice were further detected.
The resulting MMTV-neu/beclin1+/+ or +/− mice were further crossed with ODD-luciferase mice.
Brains from PDGF-AL and wt mice were further analyzed by routine histology.
Tnf−/− mice were further backcrossed into congenic C57BL/6 background (N10).
The Shp2+/− mice were further crossed with UBC-GFP mice to generate Shp2+/−:GFP mice.
The enhanced apoptotic thymocytes in CkbTg mice were further confirmed by TUNEL assay (Figure 4B).
