In addition to the smaller right ventricles found in Cdc42 knockout mice, we also noted that the inactivation of Cdc42 resulted in ventricle wall evagination.
To reveal any potential toxic effect of BN-PEG on the liver and heart of the treated mice, we also carried out the test of blood biochemistry.
Along with HDC−/− mice, we also used histamine H1-/H2-receptor gene-double knockout (H1R−/−/H2R−/−) mice generated by crossbreeding of H1-receptor null mice and H2-receptor null mice.
For adult mice, we also tested the effect of previous participation to the challenge as pups.
In the MKS1 mutant mice we also found decreased expression of a key olfactory protein (AC3).
Prior to development of T-ALL in our TLX1 mice, we also identified a partial block in T-cell differentiation.
In addition, since mitophagy was activated in Lck-Casp9DN mice, we also examined oncogenesis in tumor-prone mice with impaired autophagy (Beclin 1+/−).
To better understand the metabolic phenotype of dmpk−/− mice, we also analyzed the impact of DMPK in the IGF1-receptor intracellular trafficking.
In our uninfected control mice, we also noticed that the normalized running distance was significantly higher in female mice (p = 0.021).
In the WTTg mice, we also observed a significant limitation in their ability to associate mild aversive stimulus with the environmental context but not with an auditory cue.
Finally, since Rae-1 expression is circadianly regulated in the liver of C57BL/6 mice, we also addressed the role of each promoter region in this circadian rhythm.
