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Here, we extend that approach to an autochthonous mouse model, namely the Apc min /+ mouse, which develops multiple intestinal adenomas as a result of Wnt pathway activation.

This is a provocative observation given the T-cell-signaling-impaired Skg mouse, which develops an RA-like clinical phenotype on a susceptible genetic background.

In the ob/ob mouse, which develops obesity and type 2 diabetes-like symptoms, expression of mir-21 in liver is downregulated [ 53] suggesting that mir-21 may have different roles depending on the cell type.

48– 52 An exception involving a decrease of AMPAR synaptic transmission is the stargazer mutant mouse, which develops absence epilepsy due to reduced AMPAR-mediated synaptic transmission in inhibitory thalamic reticular nucleus neurons, but not in excitatory relay neurons.

By ENU germline mutagenesis, the Apc Min/+ mouse (which develops multiple intestinal adenomas owing to a point mutation in the Apc gene) was discovered over two decades ago (Moser et al., 1990).

The most commonly used animal model for ALS is the high-copy-number SOD-1 G93A transgenic mouse, which develops hindlimb muscle wasting and paralysis by 120-130 days old.

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We sought to develop and characterize a novel paucibacillary model in mice, which develops necrotic lung granulomas after infection with Mycobacterium tuberculosis.

From postnatal day P5 cochlear development is severely impaired in mutant Igf1−/− mice, which develop a smaller cochlea with an immature tectorial membrane.

The necessity of neurogenin 3 in the development of EC cells has been demonstrated in neurogenin 3−/− mice, which develop without any endocrine cells.

The proof of principle for the importance of STAT1 in impeding the development of tumors came from experiments with MMTV-neu tumor STAT1 null mice, which develop mammary tumors with shorter latency as compared to STAT1-proficient controls [ 8, 9, 11].

To test this idea, the team turned to so-called K/BxN mice, which develop inflammatory arthritis.

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