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Tlx2 knock-out mice demonstrate lethal intestinal pseudo-obstruction and colonic hyperganglionosis, similar to human intestinal neuronal dysplasia [ 34- 36].
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With the aim of demonstrating lethal mutagenesis as a conceivable approach to treat viral infections in vivo, we investigated whether ribavirin and favipiravir elicit antiviral activities in a mouse model of persistent norovirus infection.
Dose-response studies carried out in wild type (WT; Sv129) mice demonstrated that 3 g/kg of APAP is the submaximal lethal dose in this experimental model.
The lethal phenotypes of both Mdm2 and Mdm4 knockout mice can be completely rescued by p53 null mice, demonstrating that p53 is involved in the developmental lethality of Mdm2 and Mdm4 knockout mice.
The vaccinated mice demonstrated efficient clearance of the virus after challenge and resistance to lethal infection.
In addition, in vivo studies in mice demonstrated that the PEGylated E196 301 can fully protect mice from a lethal dose of cocaine (180 mg/kg, LD100) for at least 3 days, with the average protection time being ∼94 h.
The initial drop in platelet numbers also in IdeS treated mice, demonstrates that the IgG antibodies rapidly bind to the platelets and induce the lethal condition.
All mice demonstrated full visual capability.
The failure to generate a p53 and ASPP2 double knockout mouse demonstrates that ASPP2 and p53 deficiency are synthetic lethal.
In conclusion, we generated Snap23 knockout mice and demonstrated that Snap23 deletion is lethal.
Complete loss of GPI anchors is embryonic lethal in mice, as demonstrated by knockout of Piga, a critical and early GPI biosynthesis enzyme (Kawagoe et al., 1996; Tremml et al., 1999).
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