Of these three miRNAs, only miR-221 is predicted to regulate murine ATF6 mRNA, and in βENaC-Tg mice, expression of miR-221 is increased in native airway tissues (tracheal and bronchial tissues) compared to wild-type mice.
In these mice, expression of the tetracycline-transactivator is driven by the TIE2 promoter, which has been shown to be active in hematopoietic stem cells [16], [17].
When the clone was subcutaneously injected into nude male mice, expression of miR-17* in vivo was induced by administering Dox containing water.
After a single intravenous administration of P140 into MRL/lpr mice, expression of several genes was down-regulated (Figure 5A and 5C).
To further compare the effects of down-regulation of mTOR signaling by rapamycin to alterations seen in hippocampal slices from Tg2576 mice, expression of selective synaptic proteins was examined in the presence of rapamycin.
The results suggest that in adult mice expression of this selected group of genes with functions related to ATE is predictive of the level of fat mass that existed at 10 days of age.
In Mutyh−/− mice, expression of hMOX1, IL-17A and NOX1 was 2-fold lower (P<0.05) and IL-6 (P = 0.02) was 2-fold higher than in wt mice (Figure 2).
In these mice, expression of the mutated p110δ protein and the other PI3K subunits was equivalent to that of the wild-type (WT) proteins in brain homogenate (Figure S2), demonstrating the absence of compensatory PI3K expression.
In mice, expression of 250 CUG repeats within a heterologous RNA gives rise to DM1-like phenotypes thus demonstrating that expanded CUG repeat transcripts are themselves toxic to cells [3].
Indeed, spontaneous convulsive seizures were observed occasionally in KO mice, expression of seizure-sensitive markers in the hippocampus was abnormal and these animals showed an increased sensitivity to chemo-convulsants.
In mice, expression of Alx3 is highly localized and the characteristic expression pattern suggests an important role in patterning of neural-crest derived mesenchyme and shaping of craniofacial structures [64].
