Previously, a recapitulation of the HF differentiation programme was seen in mouse models investigating the development of ectopic HFs (Lo Celso et al, 2004; Silva-Vargas et al, 2005).
The mouse models investigating the role of the FTO gene suggest that pharmacological inhibition of the encoded protein's enzymatic activity might lead to a reduction in adiposity (see above), which is the basis of an anti-obesity drug.
Another interesting study that focuses on colorectal carcinogenesis in the azoxymethane-ApcMin/+ mouse model investigated green tea as well.
Murine models of systemic lupus erythematosus (SLE) have shown apparently contradictory evidence in that either (a) tumor necrosis factor (TNF) expression was low and TNF administration helpful or (b) TNF was high and TNF blockade of therapeutic benefit, depending on the mouse model investigated.
The APP/PS1KI mouse model investigated by Casas et al. (2004) did not only show significant neuron loss (Bayer and Wirths 2008), but also displayed a significant decrease in the numbers of parvalbumin- (PV) and calretinin- (CR) immunoreactive (ir) neurons in the hippocampus (Takahashi et al. 2010).
Apart from vinculin knock-outs, no other mouse model investigating vinculin function has been analysed to date.
Here, we examined whether EC can reduce early brain injury in ICH mouse models and investigated the underlying mechanisms.
To understand the mechanisms behind the high susceptibility to OME in 22q11DS mouse models, we investigated the development of the middle ear and onset of OM in Df1/+ and Tbx1 +/− heterozygous mice.
Lastly, expression of PPL in cholestatic mouse models was investigated using ANIT and BDL; these approaches induce 2 distinct types of cholestasis, cholangiocellular injury-derived (intrahepatic) and obstructive (extrahepatic) cholestasis, respectively [ 35, 36].
For decades immunological research has relied, with variable success, on mouse models to investigate diseases and possible therapeutic interventions.
