The other 20% of mouse genes lack a strict 1 1 relationship, due to differential expansion in at least one of the two genomes [ 16].
Our results demonstrate that, of the 15 mouse-specific genes lacking human orthologues, three (Mm.235619, Mm.234248, and Mm.190482) are protease inhibitors.
The model used is that of knockout (KO) mice for the α1,3galactosyltransferase gene, lacking the α-gal epitopes and transplanted with wild type mouse heart expressing the α-gal epitope.
For this purpose, wild-type mice and mice lacking the σ1R gene were exposed to partial sciatic nerve ligation and neuropathic pain-related behaviors were investigated.
The α-Gal A gene-disrupted mouse, generated by insertion of a neo cassette in Exon 3 of the mouse Gla gene, lack α-Gal A enzymatic activity but otherwise live a normal lifespan [ 18].
Encouraged, the team injected VEGF and the virus containing a functional copy of the dystrophin gene into mice lacking the gene.
As protoypic models, we investigated experimental autoimmune encephalomyelitis (EAE) in ciliary neurotrophic factor gene knockout mice (CNTF−/− mice) with severe myelin pathology and EAE in beta-2 microglobulin gene knockout mice (β2m−/− mice) lacking CD8-positive T-cells.
Everitt et al.[ 8] used a knockout mouse model to show mice lacking IFITM3 gene display fulminant viral pneumonia on infection with a low-pathogenicity influenza virus.
Gene-targeted mice lacking CCR2 (CCR2−/− mice) exhibit defects in monocyte/macrophage trafficking to sites of inflammation (Kurihara et al, 1997; Boring et al, 1998; Peters et al, 2000).
Similarly, long-term EE improves memory and reduces astrogliosis and brain degeneration in a mouse model lacking the presenilin genes [77].
