These mice also show normal levels of anxiety-like behaviors, social interaction, and repetitive behaviors.
The Cbfa1-deficient mice also show an abnormality in cartilage development.
Cntnap2 KO mice also show abnormalities in myelin formation, consistent with a hypo-connectivity model of ASD.
The sfx/sfx mice also show reduced femoral cortical density and diaphyseal circumference, as well as a paucity of mature osteoblasts on bone surfaces.
HO-2−/− mice also show attenuated ventilatory responses to hypoxia (10% O2) with normal responses to hypercapnia (10% CO2), suggesting the impaired oxygen sensing.
Moreover, these mice also show low and variable levels of T-cell-dependent antibody reShultzs (Shultz et al., 2007).
Bcl-2 null mice also show defects in subpopulation of neurons during neonatal period (Michaelidis et al., 1996).
ECE-2 KO mice also show more rapid development of tolerance with prolonged morphine treatment and fewer signs of naloxone-precipitated withdrawal.
Isolated thymic T cells from the transgenic mice also show a dramatically decreased survival rate when evaluated in culture under conditions that do not favor activation.
Hyperuricemic, leptin receptor deficient mice also show excessive hepatic XOR expression suggesting that leptin receptor signaling may also down regulate hepatic XOR expression[67].
(Studies of mice also show that exposure to continually loud environments also damaged their auditory nerve fibers).
