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Overexpression of IL-10 in a transgenic mouse model leads to macrophage-mediated demyelinating polyneuropathy.
Our findings indicate that Pten inactivation in this mouse model leads to accumulation of the novel identified luminal epithelial progenitor cells by a drastic change of the differentiation/proliferation balance of these cells.
JNK activation in a transgenic mouse model leads to down-regulation of Cx43, slowing of ventricular conduction, contractile dysfunction and congestive heart failure.
Acetylation of FOXO1 was also decreased in KI mice, indicating that overexpression of Sirt1 in this mouse model leads to increased SIRT1 activity in vivo (Fig. 1f).
The recently published data revealing that withdrawal of miR-21 in a mouse model leads to complete regression of tumors [ 13], make miR-21 a promising therapeutic target, particularly in glioblastoma where effective treatment modalities are still lacking.
In further support of this hypothesis, ablation of Bax in the human G93A SOD1 transgenic mouse model leads to complete dissociation between motor neuron soma death and motor dysfunction via distal denervation (47).
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In line with these findings, pancreas-specific Bmal1 knockout in a different mouse model led to impaired insulin secretion [ 14].
Deletion of basal cell maker p63 in mouse model led to absence of basal cells in prostate explants [ 2– 4].
Interestingly, prevention of FAO dysfunction in a gene-targeted mouse model led to increased contractile function, attenuation of hypertrophy and reduction of fibrosis after cardiac pressure overload.
Transgenic expression of BCAR1 in the MMTV-ERBB2 mouse model led to shorter latency of tumor formation compared with expression of ERRB2 alone.
In vivo administration of N6022 in the OVA mouse model led to a significant decrease in active, nuclear NFκB p65 subunit within mouse lung tissue when compared to vehicle.
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