Genetically engineered mice, gene profiling, expression assays and in vitro analysis using cultured embryonic neurons are combined to test the temporal impact of NGF/TrkA and Runx1 activity on genes that define the nonpeptidergic lineage.
The lack of an overt mammary gland phenotype in the K6a/b double knockout mice was not unexpected, because it has been difficult to demonstrate the functional properties of most markers used to isolate and characterize stem and progenitor cells by means of gene deletion in genetically engineered mice.
Here we review the contribution of genetically engineered mice (BSP gene knockout and overexpression) to the understanding of the role of BSP in the bone organ.
Studies to separate the role of each α2-AR subtype (α2A, α2B, and α2C) have used genetically engineered mice with disrupted genes for each subtype, or gene treatment in rats with antisense-oligodeoxynucleotides targeting a specific gene sequence.
In genetically engineered mice, some genes that are clearly associated with specific human tumors (e.g., RB1 in retinoblastoma and NF2 in meningiomas and schwannomas) have no such effect.
Using TLR-deleted macrophage cell lines generated from the bone marrow of genetically engineered mice (TLR4 gene-deficient, MyD88- and TLR2-knockout mice) and wild-type control mice, we found that TLR2-deleted macrophages exhibit increased ability to contain Candida albicans infection compared to TLR2+/+ counterpart.
Finally, verification of newly discovered genes is possible in genetically engineered mice (e.g. transgenic and conditional knockout mice).
These studies are taking advantage of the availability of genetically engineered mice, in which genes encoding for specific NOS are deleted.
Observations in humans with specific mutations in fibulin genes, together with results from genetically engineered mice and data from human cardiovascular tissue suggest that the fibulin family of proteins play important functional roles in the cardiovascular system.
He and his colleagues created genetically engineered mice that lack the gene coding for FSH.
