Mutant mouse models, genetically-engineered or spontaneous-mutations, serve as valuable tools for biomedical research.
The development of mutant mouse models of candidate risk genes and the examination of mutant mouse phenotypes allow direct associations to be made between these genes, specific pathological processes, and behavioral phenotypes, and hence, shed light on genetic contributions to the pathophysiology of schizophrenia.
Two Fto mutant mouse models have been reported before [31], [32].
Furthermore, the role of GRP94 is human diseases such as cancer, diabetes and neurodegeneration can be also achieved through the use of the mutant mouse models.
The phenotypes displayed by mutant mouse models and human syndromes associated with a loss of imprinting of certain genes demonstrate, in many cases, conservation of imprinted gene function and regulation between mouse and man [2], [3].
Therefore we used a systematic approach to investigate the specific role of NPY signalling on bone homeostasis employing several NPY mutant mouse models including specific re-introduction of NPY into the hypothalamus of otherwise NPY deficient adult mice.
Intriguingly, the mutant mouse models of many clock genes, such as Arntl, Clock, Npas2, Cry1 and Cry2, also have alterations in sleep duration and homeostasis [52], [53], [54], [55].
As it is able to analyze global metabolic changes in biofluids it is an appropriate tool for comparing GHR mutant mouse models and allows us to integrate metabolite data with our previous microarray study [19].
Results from our current work with the two mutant mouse models, the PtenloxP/loxP; GCre+ mice and PtenloxP/loxP; Zp3-Cre+ mice that carry Pten deficiency in oocytes of primordial and primary follicles, respectively, indicate that PTEN/PI3K Akt signaling in oocytes is critically important for maintenance of the primordial follicle pool.
Mutant mouse models provide an opportunity to better understand the molecular pathology that drives these diseases.
Therefore, to validate our hypothesis, we generated two additional PKD mutant mouse models.
