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In our mouse model, only a single dose of oxaliplatin caused a significant increase in serum ALT and AST levels, which was restored by addition of ursolic acid in a dose-dependent manner, strongly suggesting its liver protective effect.

In our mouse model, only the expression of IL-6 was promoted by radiation.

In a Tsc1 +/− mouse model, only 53 and 37% of cyst epithelial cells were positive for phospho- mTOR and phospho-S6 immunostaining, respectively, compared with >90% of cystadenomas and renal cell carcinomas that stained positively for both markers.

Similarly, in the curves from the mean rate of ROS fluorescence, the rat model had two large O2– bursts, whereas the mouse model only had one, which is ∼60% smaller.

Although this mouse model only recapitulates the biochemical imbalances of the disease and some molecular features in very old animals, it represents the best tool available to investigate the pathomechanisms of MNGIE (Torres-Torronteras et al, 2014).

These data suggest that p53R270H induces tumours with basal-like characteristics, which are strikingly different from the mammary tumours developed in the p53lox/lox mouse model, as the p53lox/lox mouse model only gave rise to CK8-positive tumours.

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Of the HIS mouse models, only the NSG/CD34+ mouse has been characterized for its neuropathology.

Compared to previously described animal models, mouse models only enable moderate experimental throughput.

Among different α-syn Tg mouse models, only a few exhibit overt degeneration of nigrostriatal DA fibers and even fewer show loss of nigral DA neurons (Dawson et al. 2010; Lee et al. 2002; Masliah et al. 2000).

While the link between genotoxic stress and hair graying has been established using mouse models, only correlative data from human patients are available in regards to life-long UV exposure and hair loss [ 40, 45].

The findings presented here clearly demonstrated that Fmr1-KO mice model only some specific autistic-like deficits.

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