Mounting evidence from a number of mouse models proves the existence of this p53-dependent checkpoint in vivo.
Within the constraints of the experimental design employed here, the HFA mice model proved to be acceptable for studying dose-related effects of tetracycline on human intestinal microflora.
However, combining studies in humans and studies in mouse models has proved useful in identifying candidate genes for human developmental respiratory control disorders and providing pathogenic information.
More recently, analysis of knockout mouse models has proved the involvement of host genes like CD81 in the malaria liver stage [18].
The use of mouse models has proved fundamental in revealing the essential role of VLA-4 in fetal and adult hematopoiesis (reviewed in [ 56, 61]).
Transgenic mouse models have proved useful in understanding the physiological role of individual sodium channels, and there has been significant progress in the development of subtype selective inhibitors of sodium channels.
Although the idea that missense mutations can confer oncogenic properties to p53, in contrast to a mere loss-of-function, has been around for many years(22 24), only specific mouse models have proved that mutant p53 gain-of-function (GOF defined as the ability of p53 missense mutants to actively contribute to tumor progression and aggressiveness indeed affects tumorigenesis in vivo.
These FRDA mouse models have proved useful in studies of FRDA disease mechanisms (Chan et al., 2013; Hayashi et al., 2014; Sahdeo et al., 2014; Shan et al., 2013), potential novel FRDA drug therapies (Li et al., 2013; Sandi et al., 2011; Tomassini et al., 2012) and cell-based therapeutic research (Jones et al., 2013; Jones et al., 2015).
Genetically engineered tumor-prone mouse models have proven to be powerful tools in understanding many aspects of carcinogenesis, including epigenetics.
However, translation of disease pathology into mouse models has proven to be challenging, primarily due to the complex genetic architecture of schizophrenia and the difficulties in the re-creation of susceptibility alleles in the mouse genome.
