Intriguingly, selective knockout of CFTR in myeloid cells in another mouse strain led to a basal inflammatory dysfunction that was further accentuated upon infection [93], suggesting that in mice, the impact of CFTR on myeloid cells (including but not limited to neutrophils) may be dependent upon the strain and conditions tested.
Unfortunately, brain-directed overexpression of human soluble IL-1 receptor antagonist in another transgenic mouse strain led to an atrophic phenotype of the brain along with modified levels of APP and PS1 [ 16].
Administration of replication-competent retroviruses to susceptible mouse strains leads to tumor development, as a result of multiple insertion events and the outgrowth of clones containing one or more proviruses activating growth-controlling genes [15].
Genetic divergence between different inbred mouse strains leads to variations in ex vivo and in vivo cardiac function and also infarct size.
Therefore, the large genetic diversity of laboratory mouse strains leads to more transcriptional diversity than is reflected in the reference annotation.
Some strains of adult mice infected with LASV by the intracranial route develop an acute neurological disease, while infection by other routes and in other mouse strains lead to no disease [ 6].
TMEV is a single-stranded RNA virus, and intracranial inoculation of susceptible mouse strains (SJL/J) leads to the development of a chronic-progressive CD4+ T cell-mediated demyelinating disease [4], [5], [6].
This mutation originated in the highly inbred B6 mouse strain, where it leads to consistent pigmentation defects in otherwise normal heterozygotes (primarily a white belly "splotch").
Problems with the storage and maintenance of the huge number of genetically engineered mouse strains have led to an increased need for murine sperm preservation.
Inbred strains of mice exhibit differential susceptibility to lung Carcinogenesis, and genetic crosses between different mouse strains have led to the identification of pulmonary adenoma susceptibility 1 (Pas1) as a major locus regulating predisposition to mutant Kras-driven lung cancer [45].
