Cloned (Comment) | Organism |
---|---|
Lfng overexpression in transgenic mouse model | Mus musculus |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Mus musculus | - |
gene lfng | - |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
spleen | - |
Mus musculus | - |
thymocyte | - |
Mus musculus | - |
Synonyms | Comment | Organism |
---|---|---|
LFNG | - |
Mus musculus |
Lunatic Fringe | - |
Mus musculus |
General Information | Comment | Organism |
---|---|---|
malfunction | Lfng modification of EGF12 in the Notch1 ligand-binding domain contributes to, but is not solely responsible for, the cell-nonautonomous inhibition of T cell development caused by transgenic Lfng expression in double-positive thymocytes. O-fucose site in the Notch1 ligand binding domain is partly responsible for the effects of Lfng overexpression | Mus musculus |
physiological function | Notch1 activation by Delta-like Notch ligands is essential to induce T cell commitment and to suppress B cell development from thymus-seeding progenitors. Thymus-seeding progenitor competition for Delta-like ligand DL4 is critically regulated by Lunatic Fringe, which glycosylates epidermal growth factor repeats in the Notch1 extracellular domain to enhance binding avidity for Delta-like ligands. Notch1 activation is also essential for the process of beta-selection, which drives TCRbeta+ CD4/CD8 double-negative 3 precursors to proliferate and generate a large pool of CD4/CD8 double-positive thymocytes. Lunatic Fringe enhances competition for delta-like Notch ligands but does not overcome defective pre-TCR signaling during thymocyte beta-selection in vivo, importance of Lfng-Notch1 interactions in regulating competition of preselection and postselection DN3 thymocytes for DL ligands in vivo, overview. Transgenic Lfng confers a competitive advantage to wild-type but not Rag2-/- DN3 thymocytes. Lfng improves the competitive fitness of Lck-deficient and Ptcra-deficient DN3beta thymocytes | Mus musculus |