In addition, we used a model system where mice have been genetically engineered to express GFP in cells of the osteoblastic lineage, facilitating identification and visualisation of these cells.
Reports in various cell systems and mice have stressed the importance of macroautophagy for cell survival in various neurodegenerative diseases and suggest induction of macroautophagy as a therapeutic strategy, while other studies suggest that suppression of macroautophagy is protective [28] [35].
30 Utilizing the Cre-lox system, ChAT Cre mice have selectively reduced levels of SMN protein in motor neurons (levels produced by two copies of SMN2) in motor neurons and other cells have control levels of SMN.
In this paper, we reveal that the IRG resistance system in mice has a scale of polymorphic complexity that rivals the MHC, and that a resistant IRG haplotype in the mouse can counter polymorphic virulence factors in the parasite, generating a host phenotype that is permissive for encystment, and thus for the propagation, of virulent strains.
A recent study, in which 66 G4C2 repeats were expressed in the central nervous system of mice, has shown that nuclear RNA foci, DPR inclusions and TDP-43 pathology were present in the cortex and hippocampus of mice, suggesting that the repeat itself, possibly through foci formation, RAN translation or another mechanisms entirely, caused aberrant TDP-43 deposition [ 23].
Bak fl/fl Bax −/− mice were crossed with the vav-Cre transgenic mice to generate mice lacking Bax and Bak only in the hematopoietic system; Mcl-1+/− mice have been previously described.
NMUR2 is expressed primarily in the central nervous system, and Nmur2-deficient mice have been shown to have impaired responses to pain in some assays; in contrast, these pain responses were normal in Nmur1-deficient mice [ 20].
The most powerful application of the transposon systems in mice has been to identify genes that promote cancer (Collier and Largaespada, 2007).
The development of Cre- lox conditional knockout systems in mice has allowed cell- and tissue-specific HIF-1α and HIF-2α knockout models to be created that have been instrumental in our understanding of the roles of hypoxia and HIF in specific cell types and tissues (Cramer et al., 2003; Kapitsinou et al., 2014; Schipani et al., 2001).
Mice carrying TH null mutations (Th −/−), die in utero due to the failure in the development of the cardiovascular system, but heterozygous TH deficient mice have a normal life span [Zhou et al., 1995].
